diff --git "a/PMC_clustering_938.jsonl" "b/PMC_clustering_938.jsonl" new file mode 100644--- /dev/null +++ "b/PMC_clustering_938.jsonl" @@ -0,0 +1,834 @@ +{"text": "Scientific Reports 10.1038/s41598-020-60928-0, published online 04 March 2020Correction to: This Article contains a typographical error in the Acknowledgements section.\u201cThis work was supported under the Science for Clear Energy (S4CE) project\u201dshould read:\u201cThis work was supported under the Science for Clean Energy (S4CE) project\u201d"} +{"text": "Scientific Reports 10.1038/s41598-019-47814-0, published online 06 August 2019Correction to: This Article contains an error in Figure 2A, where there was an image processing error.https://www.rndsystems.com/products/human-ldlr-antibody_af2148#product-details). Therefore, the text in the Results, under the subheading \u201cHuman LDLR is proteolytically cleaved in its extracellular ligand binding domain\u201d,The product datasheet for antibody AF2148 has been updated, and the target region of this antibody has been specified as Asp193-Arg788 raised against the entire ectodomain of LDLR\u2026\u201dshould read:\u201c\u2026 antibody AF2148 (R&D Systems) raised against amino acids 193-788 of LDLR\u2026\u201dThe correct Figure 2A appears below as Figure"} +{"text": "In the article titled \u201cThe Effectiveness, Tolerability, and Safety of Different 1-Day Bowel Preparation Regimens for Pediatric Colonoscopy\u201d ["} +{"text": "Scientific Reportshttps://doi.org/10.1038/s41598-020-72409-5, published online 21 September 2020Correction to: This Article contains an error in Figure\u00a03, where the last image in panel (a) is incorrectly labelled \u2018Uninfected ECD\u2019. The correct Figure\u00a03 appears below as Figure"} +{"text": "ScientificReports10.1038/s41598-017-09785-y, published online 30 August 2017Correction to: This Article contains typographical errors in Table6.The reference sequences of ACTA2 and MYH11, \u2018NM_001141945\u2019and \u2018NM_001040114\u2019 were incorrectly given as \u2018NM_001613\u2019 and\u2018NM_002474\u2019, respectively."} +{"text": "A metabolic hallmark of many cancers is the increase in glucose consumption coupled to excessive lactate production. Mindful that L-lactate originates only from pyruvate, the question arises as to how can this be sustained in those tissues where pyruvate kinase activity is reduced due to dimerization of PKM2 isoform or inhibited by oxidative/nitrosative stress, posttranslational modifications or mutations, all widely reported findings in the very same cells. Hereby 17 pathways connecting glucose to lactate bypassing pyruvate kinase are reviewed, some of which transit through the mitochondrial matrix. An additional 69 converging pathways leading to pyruvate and lactate, but not commencing from glucose, are also examined. The minor production of pyruvate and lactate by glutaminolysis is scrutinized separately. The present review aims to highlight the ways through which L-lactate can still be produced from pyruvate using carbon atoms originating from glucose or other substrates in cells with kinetically impaired pyruvate kinase and underscore the importance of mitochondria in cancer metabolism irrespective of oxidative phosphorylation. In huma(2) Glc \u2192\u2192\u2192 methylglyoxal \u2192\u2192\u2192 pyruvate: This may occur through four different routes involving aldehyde dehydrogenase 9, zinc binding alcohol dehydrogenase domain containing two [more recently renamed to prostaglandin reductase 3 ] and at (3) Glc \u2192\u2192\u2192 PEP \u2192 pyruvate: the terminal reaction is catalyzed by tartrate-resistant acid phosphatases (TRAP), the molecular identity of which remained unknown well after their biochemical characterization ; they ar(4) Glc \u2192\u2192\u2192 PEP; PEP + GalNAc \u2192 GalNAc-1P + pyruvate: Terminal reaction catalyzed by N-acetylgalactosamine kinase isoforms 1 or 2 . These e(5) Glc \u2192\u2192\u2192 3-PG \u2192 2-PG (by phosphoglucomutase 1 or 2) \u2192 glycerate [probably through 2-phosphoglyceric acid phosphatase ] \u2192 3-OH-(6) Glc \u2192\u2192\u2192 3-PG \u2192 phosphohydroxypyruvate (Php), catalyzed by phosphoglycerate dehydrogenase; Php + Ala \u2192 phosphoserine (Pser) + pyruvate, catalyzed by phosphoserine aminotransferase (PSAT) : PSAT ov(7) Glc \u2192\u2192\u2192 3-PG \u2192Php ; Php + Ala (or Glu) \u2192 Pser + pyruvate (or \u2192Kg); the latter reaction is catalyzed by phosphoserine aminotransferase; Pser \u2192 Ser \u2192 pyruvate, catalyzed by serine dehydratase or serin(8) Glc \u2192\u2192\u2192 Glyoxal \u2192\u2192\u2192 glyoxylate ; glyoxyl(9) Glc \u2192\u2192\u2192 3-PG \u2192Php ; Php + Glu \u2192 Pser + \u2192Kg; latter reaction catalyzed by phosphoserine aminotransferase; \u2192Kg + Ala \u2192 Glu + pyruvate, catalyzed by alanine aminotransferase .in vivo glyoxylate entry into the mitochondria, (2) reversibility of the matrix phosphoenolpyruvate carboxykinase (PCK2), and (3) reversibility of the mitochondrial pyruvate carrier (MPC). Regarding glyoxylate, I was unable to find information on its transport across the inner mitochondrial membrane; however, it is known that it can be processed by the matrix-localized AGXT2 . PCK2 exin vivo . Regardiin vivo , pigeon in vivo , guinea in vivo , rabbit in vivo , chickenin vivo , and bulin vivo . Howeverin vivo , demonst in vivo ; relevan in vivo ; further in vivo ; indeed in vivo ; however in vivo . Mindful(10) Glc \u2192\u2192\u2192 glyoxal \u2192\u2192\u2192 glyoxylate: Glyoxylate enters the mitochondria; glyoxylate + Ala \u2192 Gly + pyruvate through AGXT2. Pyruvate may exit the mitochondria through the MPC .via mitochondrial PEPCK evoking PEP transport across the inner mitochondrial membrane has also been demonstrated by the group of Kibbey ((11) Glc \u2192\u2192\u2192 PEP which enters the mitochondria; PEP transport across the inner membrane of mammalian mitochondria has been demonstrated to occur by the tricarboxylate carrier by f Kibbey ; PEP \u2192 O(12) Glc \u2192\u2192\u2192 PEP; PEP enters the mitochondria through the means outlined in pathway 11. PEP \u2192 OAA by PCK2; OAA \u2192 pyruvate by FAHD1 , 2015. FME2 knockdown suppresses tumor growth in lung cancer Glc \u2192\u2192\u2192 PEP; PEP enters the mitochondria through the means outlined in pathway 11; PEP \u2192 OAA by PCK2; OAA \u2192 Mal by MDH2; Mal \u2192 pyruvate by ME2,3 . Pyruvatg cancer , while Mc cancer .ME1 knockdown inhibits the growth of colon cancer cells ((14) Glc \u2192\u2192\u2192 PEP; PEP enters the mitochondria through the means outlined in pathway 11; PEP \u2192 OAA by PCK2; OAA \u2192 Mal by MDH2; Mal exits the mitochondria; Mal \u2192 pyruvate by ME1 . ME1 knoer cells , and itser cells . In the er cells .(15) Glc \u2192\u2192\u2192 PEP; PEP enters the mitochondria through the means outlined in pathway 11; PEP \u2192 OAA by PCK2; OAA + acetyl-CoA \u2192 citrate by CS; citrate exits the mitochondria through the dicarboxylate carrier; citrate + ATP + CoASH \u2192 acetyl-coA + ADP + Pi + OAA by ACLY ; OAA \u2192 M(16) Glc \u2192\u2192\u2192 PEP; PEP enters the mitochondria through the means outlined in pathway 11; PEP \u2192 OAA by PCK2; OAA + Glu \u2192\u2192Kg + Asp by GOT2; Asp exits the mitochondria; Asp + \u2192Kg \u2192 Glu + OAA by GOT1; OAA \u2192 Mal by MDH1; Mal \u2192 pyruvate by ME1 .CLYBL was reported to be overexpressed in 465 out of 38,258 tumor samples in the COSMIC database8.(17) Glc \u2192\u2192\u2192 PEP; PEP enters the mitochondria through the means outlined in pathway 11; PEP \u2192 OAA by PCK2; OAA + acetyl-CoA \u2192 citrate by CS; citrate \u2192 cis-aconitate, intermediate of ACO2 reaction; cis-aconitate \u2192 itaconate by cADC; itaconate + CoASH + ATP (or GTP) \u2192 itaconyl-CoA + Pi + ADP (or GDP) by SUCL ; itaconyThese pathways are shown in (18) Ser \u2192 pyruvate, catalyzed by SDS or SDSL .(19) Ser \u2192\u2192\u2192 PEP; PEP \u2192 pyruvate; terminal reaction catalyzed by tartrate-resistant acid phosphatase .(20) Ser \u2192\u2192\u2192 PEP; PEP + GalNAc \u2192 GalNAc-1P + pyruvate. The terminal reaction is catalyzed by N-acetylgalactosamine kinase isoforms 1 or 2 .(21) Ala \u2192 pyruvate, catalyzed by L-amino-acid oxidases (LAAO) : SeveralMYC-dependent manner ((22) Ala + 2-oxoglrm \u2192 Gln + pyruvate, catalyzed by glutamine-pyruvate transaminase (GPAT) . GPAT ist manner .(23) Ala + 2-Oml \u2192 Aml + pyruvate, catalyzed by alanine-ketomalonate transaminase (ALXT) . I was uMYC-dependent manner ((24) Ala + \u03b1Kg \u2192 Glu + pyruvate, catalyzed by GPT: GPT\u2014similar to GPAT\u2014is upregulated in many cancers in a t manner .(25) Ala + OAA \u2192 Asp + pyruvate; enzyme unknown .(26) Ala + Glyoxylate \u2192 Gly + pyruvate, catalyzed by alanine-glyoxylate aminotransferase .(27) Ala + 3-OH-pyr \u2192 Ser + pyruvate, catalyzed by alanine-glyoxylate aminotransferase .(28) Thr \u2192 Gly + acetaldehyde, catalyzed by SHMT1 ; Gly + 5(29) Asp + \u03b1Kg \u2192 Glu + OAA, catalyzed by GOT1; OAA \u2192 Mal by MDH1; Mal \u2192 pyruvate by ME1 .(30) 4-OH-proline \u2192\u2192\u2192 pyruvate, through glyoxylate formation (see pathway no. 26).(31) Cys \u2192\u2192\u2192 pyruvate through the sulfinate pathway , 2020. N(32) Cys \u2192 3-sulfino-L-alanine catalyzed by aspartate 4-decarboxylase ; 3-sulfi2S + pyruvate through the 3-mercaptopyruvate pathway ((33) Cys \u2192\u2192\u2192 H pathway . Cys can2S by 3-mercaptopyruvate sulfurtransferase (3MST) ((34) L-cysteine is isomerized to D-cysteine by cysteine racemase (2-amino-3-mercaptopropionic acid racemase) ; D-Cys ie (3MST) or thiose (3MST) . The pose (3MST) in mamma3 and pyruvate through SDS, SDSL, or SRR Ser \u2192 dehydroalanine (2-aminoacrylate) by serine dehydratase (SDS), serine dehydratase-like protein (SDSL), or serine racemase (SRR): Dehydroalanine can further hydrolyze to NH, or SRR ; sometimeaminase . Dehydroeaminase . The cru3, and pyruvate by selenocysteine lyase ((36) Se-methyl-L-selenocysteine can be deaminated to methaneselenol, NHne lyase . SeMSC cne lyase . SeMSC wne lyase and evenne lyase .(37) Val \u2192\u2192\u2192 2-methyl-3-oxopropanoate; 2-methyl-3-oxopropanoate can get transaminated with alanine by AGXT2 to D-3-amino-isobutanoate + pyruvate . The ove(38) Leu \u2192\u2192\u2192 3-methylbutanoyl-CoA; the latter compound is converted to isobutyryl-CoA through branched-chain fatty acid metabolism (many steps); isobutyryl-CoA \u2192\u2192\u2192 2-methyl-3-oxopropanoate; 2-methyl-3-oxopropanoate can get transaminated with alanine by AGXT2 to D-3-amino-isobutanoate + pyruvate . Because(39) Ile \u2192\u2192\u2192 2-methylbutanoyl-CoA; the latter compound is converted to isobutyryl-CoA through branched-chain fatty acid metabolism (many steps); isobutyryl-CoA \u2192\u2192\u2192 2-methyl-3-oxopropanoate; 2-methyl-3-oxopropanoate can get transaminated with alanine by AGXT2 to D-3-amino-isobutanoate + pyruvate . Because2 \u2192 CO2 + succinate + trans-4-hydroxy-L-proline, catalyzed by prolyl 4-hydroxylase subunit alpha ; trans-4-hydroxy-L-proline is then converted to L-1-pyrroline-3-hydroxy-5-carboxylate, also yielding NAD(P)H, by either pyrroline-5-carboxylate reductase or left\u2013right determination factor 1 (LEFTY1), a member of the TGF-\u2192 family of proteins; L-1-pyrroline-3-hydroxy-5-carboxylate can be converted to L-erythro-4-hydroxyglutamate, also yielding NAD(P)H, by aldehyde dehydrogenase 4 family member A1; in turn, L-erythro-4-hydroxyglutamate is transaminated with either OAA by GOT2, yielding 4-hydroxy-2-oxoglutarate + aspartate, or \u2192Kg by GOT1 or GOT2, yielding 4-hydroxy-2-oxoglutarate + glutamate; finally, 4-hydroxy-2-oxoglutarate is converted to glyoxylate and pyruvate by 4-hydroxy-2-oxoglutarate glyoxylate-lyase. It is relevant that increased proline catabolism has been recently reported to support metastasis ((40) Pro + \u03b1Kg + Otastasis . Arg, thThese pathways are shown in (41) Thr \u2192\u2192\u2192 acetyl-CoA; acetyl-CoA + OAA \u2192 citrate, catalyzed by CS; citrate exits the mitochondria through the dicarboxylate carrier; citrate + ATP + CoASH \u2192 Acetyl-coA + ADP + Pi + OAA by ACLY ; OAA \u2192 M(42) Thr \u2192\u2192\u2192 acetyl-CoA; acetyl-CoA + OAA \u2192 citrate, catalyzed by CS; citrate \u2192 cis-aconitate, intermediate of ACO2 reaction; cis-aconitate \u2192 itaconate by cADC; itaconate + CoASH + ATP (or GTP) \u2192 itaconyl-CoA + Pi + ADP (or GDP) by SUCL; itaconyl-CoA \u2192 citramalyl-CoA by MGTK; citramalyl-coA \u2192 acetyl-CoA + pyruvate by CLYBL. Pyruvate may exit the mitochondria through the MPC .(43) Asn \u2192\u2192\u2192 Asp; Asp + \u03b1Kg \u2192 Glu + OAA by GOT2; OAA by PCK2; OAA \u2192 pyruvate by reverse operation of PC. However, this is expected to be a path of a very minor flux. Pyruvate may exit the mitochondria through the MPC. The crucial role of asparagine availability in cancer is explored in (44) Asn \u2192\u2192\u2192 Asp; Asp + \u03b1Kg \u2192 Glu + OAA by GOT2; OAA \u2192 pyruvate by acylpyruvase (FAHD1). Pyruvate may exit the mitochondria through the MPC .(45) Asn \u2192\u2192\u2192 Asp; Asp + \u03b1Kg \u2192 Glu + OAA by GOT2; OAA \u2192 Mal by MDH2; Mal \u2192 pyruvate by ME2,3. Pyruvate may exit the mitochondria through the MPC .(46) Asn \u2192\u2192\u2192 Asp; Asp + \u03b1Kg \u2192 Glu + OAA by GOT2; OAA \u2192 Mal by MDH2; Mal exits the mitochondria; Mal \u2192 pyruvate by ME1 .(47) Tyr, Phe \u2192\u2192\u2192 Fum; Fum \u2192 Mal by FH; Mal \u2192 pyruvate by ME2,3 .(48) Tyr, Phe \u2192\u2192\u2192 Fum; Fum \u2192 Mal by FH; Mal exits the mitochondria; Mal \u2192 pyruvate by ME1 .(49) Tyr, Phe \u2192\u2192\u2192 Fum; Fum \u2192 Mal by FH; Mal \u2192 OAA by MDH2; OAA \u2192 pyruvate by acylpyruvase (FAHD1). Pyruvate may exit the mitochondria through the MPC .(50) Thr \u2192\u2192\u2192 acetyl-CoA; acetyl-CoA + OAA \u2192 citrate, catalyzed by CS; citrate exits the mitochondria through the dicarboxylate carrier; citrate + ATP + CoASH \u2192 acetyl-coA + ADP + Pi + OAA by ACLY; OAA \u2192 PEP by PCK1; PEP enters the mitochondria; PEP \u2192 OAA by PCK2; OAA \u2192 pyruvate by acylpyruvase (FAHD1). Pyruvate may exit the mitochondria through the MPC .(51) Thr \u2192\u2192\u2192 acetyl-CoA; acetyl-CoA + OAA \u2192 citrate, catalyzed by CS; citrate exits the mitochondria through the dicarboxylate carrier; citrate + ATP + CoASH \u2192 acetyl-coA + ADP + Pi + OAA by ACLY; OAA \u2192 PEP by PCK1; PEP enters mitochondria; PEP \u2192 OAA by PCK2; OAA \u2192 Mal by MDH2; Mal \u2192 pyruvate by ME2,3. Pyruvate may exit the mitochondria through the MPC .(52) Thr \u2192\u2192\u2192 acetyl-CoA; acetyl-CoA + OAA \u2192 citrate, catalyzed by CS; citrate exits the mitochondria through the dicarboxylate carrier; citrate + ATP + CoASH \u2192 acetyl-CoA + ADP + Pi + OAA by ACLY; OAA \u2192 PEP by PCK1; PEP enters the mitochondria; PEP \u2192 OAA by PCK2; OAA \u2192 Mal by MDH2; Mal exits the mitochondria; Mal \u2192 pyruvate by ME1 .(53) Thr \u2192\u2192\u2192 acetyl-CoA; acetyl-CoA + OAA \u2192 citrate, catalyzed by CS; citrate exits the mitochondria through the dicarboxylate carrier; citrate + ATP + CoASH \u2192 Acetyl-coA + ADP + Pi + OAA by ACLY; OAA \u2192 PEP by PCK1; PEP + GalNAc \u2192 GalNAc-1P + pyruvate. Terminal reaction catalyzed by N-acetylgalactosamine kinase isoforms 1 or 2 .(54) Thr \u2192\u2192\u2192 acetyl-CoA; acetyl-CoA + OAA \u2192 citrate, catalyzed by CS; citrate exits the mitochondria through the dicarboxylate carrier; citrate + ATP + CoASH \u2192 acetyl-coA + ADP + Pi + OAA by ACLY; OAA \u2192 PEP by PCK1; PEP \u2192 pyruvate; the terminal reaction is catalyzed by tartrate-resistant acid phosphatases .In the literature, some reactions have been described to produce pyruvate but are incompletely characterized. These are collectively listed below:2O \u2192 pyruvate + 2 NH3, catalyzed by carbamoyl-serine ammonia lyase ((55) O-carbamoyl-L-serine + Hia lyase . O-Carbaia lyase ; mindful2O \u2192 a thiol + NH3 + pyruvate, catalyzed by cysteine S-conjugate \u2192-lyases ((56) L-Cysteine-S-conjugate + H\u2192-lyases . The pos2O \u2192 L-homocysteine + pyruvate + NH3 or cysteine + H2O \u2192 sulfide + NH3 + pyruvate or cystine \u2192 thiocysteine + pyruvate + NH3, all catalyzed by cystathionine gamma-lyase ((57) cystathionine + Hma-lyase . Cystathma-lyase . In the ma-lyase .2O \u2192 pyruvate + NH3 + sulfate catalyzed by serine-sulfate ammonia-lyase ((58) L-Serine O-sulfate + Hia-lyase . I was u(59) N-Acetylneuraminate \u2192 N-acetyl-D-mannosamine + pyruvate catalyzed by N-acetylneuraminate lyase ; relevan2O + O2 \u2192 pyruvate + NH3 + H2O2 catalyzed by DAAO ((60) D-Alanine + H by DAAO . The int3 catalyzed by glutamate dehydrogenase; this reaction exhibits a weak activity ((61) L-Alanine \u2192 pyruvate + NHactivity . The rol(62) 2-Oxosuccinamic acid + Ala \u2192 Asn + pyruvate, catalyzed by asparagine aminotransferase . The ori(63) Pyruvate oxime + acetone \u2192 pyruvate + acetone oxime, catalyzed by oximinotransferase . Due to (64) Methylmalonyl-CoA + pyruvate \u2192 propionyl-CoA + oxaloacetate catalyzed by methylmalonyl-CoA carboxytransferase . This re(65) L-Alanine + 3-oxopropanoate \u2192 pyruvate + \u2192-alanine, catalyzed by either \u2192-alanine-pyruvate transaminase or alani(66) Phenylpyruvate + L-alanine \u2192 L-phenylalanine + pyruvate catalyzed by phenylalanine (histidine) transaminase . Phenylp(67) 2-Oxoisohexanoate + L-alanine \u2192 L-leucine + pyruvate, catalyzed by the mitochondrial branched-chain L-amino acid aminotransferase . The rol2 and pyruvate ((68) PCK1, ME1, and ME2,3 may also convert OAA to COpyruvate (for con(69) Salsolinol can be converted to salsolinol-1-carboxylate by salsolinol synthetase which can then be catabolized to dopamine and pyruvate (by an unknown enzyme); salsolinol is an endogenous catechol isoquinoline detected in humans derived from dopamine metabolism . SalsoliThese pathways are shown in Lactate\u2014unlike pyruvate\u2014exhibits chirality; thus, it exists in L- or D- configuration. In humans, a putative D-lactate dehydrogenase is known to exist . In meta(70) D-lactate formation by methylglyoxal and intestinal flora Pyruvate + QHl matrix , 1970. Ml matrix ; thus, i+ + pyruvate, catalyzed by D-lactate dehydrogenase; this reaction is mentioned in several databases, but no reference is given.(72) D- (or L-) Lactate + 2 ferricytochrome \u2192 2 ferrocytochrome C + 2 H+ + pyruvate, catalyzed by cytochrome B5 domain-containing protein 1; this reaction is mentioned in several databases, but no reference is given.(73) D- (or L-) Lactate + 2 ferricytochrome \u2192 2 ferrocytochrome C + 2 H+ + L-lactate, catalyzed by ADH ((74) Pyruvate + NADPH \u2192 NADPd by ADH . The man2O2 \u2192 L-lactate + O2, catalyzed by hydroxyacid oxidases ((75) Pyruvate + HAO1,2,3) . HoweverAO1,2,3) . HAO2 wa(76) Protein deglycase (E.C. 3.5.1.124) may form D-lactate from proteins . Relevan(77) Methylglyoxal spontaneously forms a hemithioacetal adduct with GSH; subsequently, glyoxalase I produces S-D-lactoylglutathione from this adduct , and gly+ to oxalate + NADH or \u03b1-ketobutyrate to \u2192-hydroxybutyrate or L-glycerate to hydroxypyruvate \u2192 pyruvate , several other routes may also contribute Gln \u2192 Glu \u2192 aKg \u2192 isocitrate \u2192 cis-aconitate \u2192 itaconate by cADC; itaconate + CoASH + ATP (or GTP) \u2192 itaconyl-CoA + Pi + ADP (or GDP) by SUCL ; itacony(80) Gln \u2192 Glu \u2192 aKg \u2192 isocitrate \u2192 cis-aconitate \u2192 citrate, exiting the mitochondria \u2192 citrate + ATP + CoASH \u2192 acetyl-coA + ADP + Pi + OAA by ACLY ; OAA \u2192 M(81) Gln \u2192 Glu \u2192 aKg \u2192 isocitrate \u2192 cis-aconitate \u2192 citrate, exiting the mitochondria \u2192 citrate + ATP + CoASH \u2192 acetyl-coA + ADP + Pi + OAA by ACLY; OAA \u2192 PEP by PCK1; PEP + GalNAc \u2192 GalNAc-1P + pyruvate. The terminal reaction is catalyzed by N-acetylgalactosamine kinase isoforms 1 or 2.(82) Gln \u2192 Glu \u2192 aKg \u2192 isocitrate \u2192 cis-aconitate \u2192 citrate, exiting the mitochondria \u2192 citrate + ATP + CoASH \u2192 acetyl-coA + ADP + Pi + OAA by ACLY; OAA \u2192 PEP by PCK1; PEP \u2192 pyruvate; the terminal reaction is catalyzed by tartrate-resistant acid phosphatases.(83) Gln \u2192 Glu \u2192 aKg \u2192 succinyl-CoA \u2192 succinate \u2192 fumarate \u2192 malate \u2192 pyruvate by ME2,3; pyruvate may exit the mitochondria through the MPC.(84) Gln \u2192 Glu \u2192 aKg; aKg transaminates with Asp forming Glu and OAA, by GOT2; OAA \u2192 pyruvate by FAHD1 , 2015; p(85) Gln \u2192 Glu \u2192 aKg; aKg transaminates with Asp forming Glu and OAA, by GOT2; OAA \u2192 Mal by MDH2; Mal exits the mitochondria; Mal \u2192 pyruvate by ME1 .(86) Gln \u2192 Glu \u2192 aKg; aKg transaminates with Asp forming Glu and OAA, by GOT2; OAA \u2192 Mal by MDH2; malate \u2192 pyruvate by ME2,3; pyruvate may exit the mitochondria through the MPC.+/K+ ATPase), 125 of them occur in the cytosol. Clearly, while it is imperative to prevent phosphofructokinase and hexokinase from ATP-dependent feedback inhibition and allow a high flux of glycolysis for the sake of generating intermediates shuttled toward other pathways, ATP is still needed for many other reactions. Crunching the numbers regarding cytosolic energetics is a daunting task, but what is definite is that a cell with nearly zero ATP production from glycolysis may not harbor ATP-consuming mitochondria, for whatever reason . This can be solved by maintaining the adenine nucleotide translocase in \u201cforward\u201d mode, i.e., providing ATP to the cytosol which is made by SUCL supported by glutaminolysis highlight that L-lactate can still be produced from pyruvate using carbon atoms originating from glucose or other substrates in cells with kinetically impaired pyruvate kinase and (ii) show that the mitochondria may contribute to cancer metabolism irrespective of oxidative phosphorylation by providing means of contributing to pyruvate production. Having said that, it is important to emphasize that none of the aforementioned reactions take into account the potential regulatory effects of metabolites on other reactions such as those occurring on PK by amino acids . In addiCC wrote and edited the manuscript.The author declares that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest."} +{"text": "Nature Communications 10.1038/s41467-020-17123-6, published online 3 July 2020.Correction to: W\u201d should be corrected as \u201cl2 regularization of W\u201d; \u201cThe original version of this Article contained a typo in Eq. (1), in which the subscript of"} +{"text": "Scientific Reports 10.1038/s41598-017-06835-3, published online 25 July 2017Correction to: This Article contains an error in Figure 4a and Figure 4b, where the units for \u2018Evans Blue exudation\u2019 were incorrectly given as \u2018mg/ml\u2019. The correct Figure 4 appears below as Figure"} +{"text": "In the article titled \u201cMicrowave Tunneling and Robust Information Transfer Based on Parity-Time-Symmetric Absorber-Emitter Pairs\u201d , there w"} +{"text": "Correction to: CVIR Endovasc (2019) 2:9https://doi.org/10.1186/s42155-019-0052-6\u2018In the published article (Salaskar et al. \u201cIRB approval not needed for this type of submission at our institution.\u201dshould read:\u201cInformed consent for publication of this case report and its accompanying images has been obtained from the patient\u201d"} +{"text": "Scientific Reports 10.1038/s41598-020-74227-1, published online 14 October 2020Correction to: This Article contains errors.In Table 3, the Manufacturer for \u2018Elutax 3\u2019,\u201cAachen Resonance GmbH\u201dshould read:\u201cAR Baltic Medical UAB\u201d"} +{"text": "Nature Communications 10.1038/s41467-020-18086-4, published online 26 August 2020.Correction to: The original version of this Article contained an error in Fig. 1j, where the correct Y-axis unit is \u201c\u03bcC\u201d instead of \u201cmC\u201d.This has been corrected in both the PDF and HTML versions of the Article."} +{"text": "In the article titled \u201cEel's Head Powder Reduces Mild-Moderate Depression in Geriatric Individual: Result from Randomized Controlled Trial Study\u201d , there w"} +{"text": "Cell Death & DiseaseCorrection to: 10.1038/s41419-019-2196-7 published online 06 January 2020This Article was originally published with the incorrect copyright line \u201cThe Authors\u201d. The correct copyright is \u201cUS Govt\u201d.The PDF and HTML versions of the Article have been modified accordingly."} +{"text": "Scientific Reports 10.1038/s41598-020-78102-x, published online 03 December 2020Correction to: This Article contains an error. A Data Availability section was originally not included\u2014it should appear as below:"} +{"text": "Scientific Reports 10.1038/s41598-019-40996-7, published online 14 March 2019Correction to: This Article contains a typographical error in the Methods section under subheading \u2018Nauplii production\u2019 where,\u201cThe content was then filtered (mesh size = 25 m) and fixed in Lugol (4%).\u201dshould read:\u201cThe content was then filtered (mesh size = 25 \u00b5m) and fixed in Lugol (4%).\u201d"} +{"text": "Nature 10.1038/s41586-020-2561-9 Published online 05 August 2020Correction to: Ne between 500 thousand million years ago and 1 million years ago.\u201d, should have read: \u201ca rapid increase in Ne between 500 thousand years ago and 1\u00a0million years ago.\u201d. The original Article has been corrected online.In this Article, owing to an error during the production process, the text: \u201ca rapid increase in"} +{"text": "Due to a production error, the funder \u201cPortuguese Foundation for Science and Technology (FCT),\u201d \u201cFCT-NSFC/0002/2016, PTDC/BIAANM/3484/2014, and CCMAR/Multi/04326/2019,\u201d and a PhD fellowship \u201cSFRH/BD/120040/2016\u201d to \u201cCarmen Sousa\u201d was erroneously omitted.The publisher apologizes for this mistake. The original article has been updated."} +{"text": "The following sentence should read: \u201cUstekinumab exhibits a generally favourable treatment persistency profile in both biologic-na\u00efve and experienced patients, while SEC exhibits favourable persistency in biologic-naive but not in biologic-experienced patients compared with ADA\u201d instead of \u201cUstekinumab exhibits a generally favourable treatment persistency profile in both biologic-na\u00efve and experienced patients, while SEC exhibits favourable persistency in biologic-experienced but not in biologic-na\u00efve patients compared with ADA\u201d.This error has now been corrected online."} +{"text": "Correction to: Antimicrob Resist Infect Control 9, 128 (2020)https://doi.org/10.1186/s13756-020-00782-xAfter publication of this article , it is r\u2018Torsten Feld\u2019 should be corrected to \u2018Torsten Feldt\u2019. The author name has thus been updated in this Correction.The original article has also been updated."} +{"text": "In the article titled \u201cCorrigendum to \u201cAssociation between Serum Matrix Metalloproteinase- (MMP-) 3 Levels and Systemic Lupus Erythematosus: A Meta-analysis\u201d\u201d , an acknThe experiments for MMP-3 were supported by a grant from the Korean Society of Pediatric Nephrology."} +{"text": "Correction to: J Exp Clin Cancer Res (2020) 39:8.https://doi.org/10.1186/s13046-019-1517-02-dependent mechanisms.\u201d, and the caption should refer to 25\u2009years and not 15\u2009years. Figure\u00a0In the original publication of this manuscript , Fig. 1 In addition, the following sentences have been adjusted to remove ambiguity and correct the record:\u2018Background\u2019 section, \u201cHypoxia Inducible Factor-1 (HIF-1), is an \u03b1/\u03b2 heterodimeric transcription factor that controls multiple oxygen-sensitive genes. In 1995 Semenza identified HIF-1\u03b1 as a basic-helix-loop-helix-PAS heterodimer regulated by cellular oxygen tension\u201d has been corrected to \u201cIn 1995, Semenza identified the Hypoxia Inducible Factor-1 (HIF-1) as a basic-helix-loop-helix-PAS \u03b1/\u03b2 heterodimeric transcription factor regulated by cellular oxygen tension.\u201d\u2018Background\u2019 section, \u201c\u2026 as evidenced by the increased number of papers published on this topic in the last 15\u2009years\u201d has been corrected to \u201c\u2026 as evidenced by the increased number of papers published on this topic in the last 25\u2009years.\u201dThe authors sincerely apologize for the inconvenience caused to the readers. The original article has been updated."} +{"text": "December 2019 Issue, vol.113 (6), page 1138In Short Editrorial \u201cAdmission NT-ProBNP in Myocardial Infarction: an Alert Sign?\u201d, consider Lu\u00eds Beck-da-Silva as the correct form for the name of the author Lu\u00eds Beck da Silva."} +{"text": "Correction to: BMC Anesthesiol 21, 60 (2021)https://doi.org/10.1186/s12871-021-01280-2non-emergent\u201d was changed to \u201cnon-emergency\u201d and the word \u201cthat\u201d found in 1st sentence of the 5th paragraph under Discussion section was deleted.Following publication of the original article , the autThe correct figures are as follows:The original article has been corrected."} +{"text": "Scientific Reports 10.1038/s41598-020-68984-2, published online 22 July 2020Correction to: This Article contains an error in Table 1 in the Locus Tag column where,tonB1)\u201d.\u201cSLG_14330 (should read:tonB1)\u201d.\u201cSLG_14430 ("} +{"text": "Scientific Reports 10.1038/s41598-020-59942-z, published online 20 February 2020Correction to: The Acknowledgements section in this Article was omitted. The Acknowledgements section should read:\u201cWe acknowledge support from the German Research Foundation (DFG) and the Open Access Publication Funds of Charit\u00e9 \u2013 Universit\u00e4tsmedizin Berlin.\u201d"} +{"text": "Xrcc4 or Lig4, leads to massive neuronal apoptosis in the central nervous system (CNS) that correlates with embryonic lethality in mice. Inactivation of either Paxx, Mri or Dna-pkcs NHEJ gene results in normal CNS development due to compensatory effects of Xlf. Combined inactivation of Xlf/Paxx, Xlf/Mri and Xlf/Dna-pkcs, however, results in late embryonic lethality and high levels of apoptosis in CNS. To determine the impact of NHEJ factors on the early stages of neurodevelopment, we isolated neural stem and progenitor cells from mouse embryos and investigated proliferation, self-renewal and differentiation capacity of these cells lacking either Xlf, Paxx, Dna-pkcs, Xlf/Paxx or Xlf/Dna-pkcs. We found that XRCC4-like factor (XLF), DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and paralogue of XRCC4 and XLF (PAXX) maintain the neural stem and progenitor cell populations and neurodevelopment in mammals, which is particularly evident in the double knockout models.Non-homologous end-joining (NHEJ) is a major DNA repair pathway in mammalian cells that recognizes, processes and fixes DNA damage throughout the cell cycle and is specifically important for homeostasis of post-mitotic neurons and developing lymphocytes. Neuronal apoptosis increases in the mice lacking NHEJ factors Ku70 and Ku80. Inactivation of other NHEJ genes, either Double-strand DNA breaks (DSBs) are common DNA damage events that threaten the stability of our genome. DSBs can be repaired by homologous recombination (HR), classical non-homologous end-joining and alternative end-joining ,2,3,4. HC-NHEJ involves recognition of the DSBs by Ku70/Ku80 heterodimer (Ku), which in turn recruits DNA-dependent protein kinase catalytic subunit (DNA-PKcs) to form a DNA-PK holoenzyme complex that protects free DNA ends. Assembly of DNA-PK triggers the autophosphorylation of DNA-PKcs, as well as DNA-PKcs-dependent phosphorylation of multiple other DNA repair factors . Ku faciXrcc4 [Lig4 [Ku70\u2212/\u2212 and Ku80\u2212/\u2212 knockout mice are viable, they present high levels of apoptosis in CNS and remarkable growth retardation [Genetic inactivation of Xrcc4 or Lig4 c4 [Lig4 in mice c4 [Lig4 ,10. Althardation ,12.Dna-pkcs\u2212/\u2212 [Xlf\u2212/\u2212 [Paxx\u2212/\u2212 [Mri\u2212/\u2212 [Dna-pkcsKD/KD) leads to Ku- and p53-dependent embryonic lethality, which correlates with high levels of apoptosis in the CNS [Dna-pkcs gene affects post-mitotic neurons. The apoptotic neurons were relatively rare in the proliferating ventricular zone [Dna-pkcs resulted in a neurological phenotype similar to observed earlier for mice lacking XRCC4 or LIG4 [Mice lacking NHEJ factors possess various phenotypes ,2,3,4. I-pkcs\u2212/\u2212 , Xlf\u2212/\u2212 [Xlf\u2212/\u2212 ,15, Paxx[Paxx\u2212/\u2212 ,18,19,20 [Mri\u2212/\u2212 knockout the CNS . Jiang elar zone ,23. Thus or LIG4 ,24, sugg or LIG4 . An impa or LIG4 . While pXlf and Dna-pkcs [Xlf and Paxx [Xlf and Mri [More recently, genetic interaction studies uncovered the importance of the NHEJ factors XLF, DNA-PKcs, PAXX and MRI in the development of immune and nervous systems and mouse development in general. Synthetic lethality was reported between Dna-pkcs ,27,28, tand Paxx ,17,19,20 and Mri . These s and Mri , no simiHere, using single and double knockout mouse models, we found that XLF, DNA-PKcs and PAXX are required to maintain pluripotency of neural stem cells, including aspects of self-renewal, proliferation, and differentiation to neurons and astrocytes.Dna-pkcs+/\u2212 [Xlf+/\u2212 [Paxx+/\u2212 [Dna-pkcs+/\u2212 and Xlf+/\u2212 mice were imported from Professor Frederick Alt lab . Paxx+/\u2212 mice were generated by Oksenych group .All experimental procedures involving mice were performed according to the protocols approved by the Comparative Medicine Core Facility at Norwegian University of Science and Technology . -pkcs+/\u2212 , Xlf+/\u2212 [Xlf+/\u2212 , and Pax[Paxx+/\u2212 mouse mo\u00aeG2 Green Master Mix or Taq 2x Master Mix Kit according to the manufacturer\u2019s instructions. Each reaction contained 50 ng of DNA and 0.8 \u00b5M of indicated primers was used to determine the mouse genotypes. DNA was isolated from ear punches by incubating overnight at 56 \u00b0C with 2% proteinase K in DNA lysis solution, containing 10 mM pH = 9.0 Tris, 1 M KCl, 0.4% NP-40 and 0.1% Tween 20. Next, the samples were heat-treated for 30 min at 95 \u00b0C. The PCR reactions were performed using GoTaq primers in a fin2 and 95% humidity. The neurospheres were dissociated every seventh day using 0.25% of trypsin in ethylenediaminetetraacetic acid (EDTA), as previously described in Castaneda-Zegarra et al. (2019) and Wang et al. (2010) [NSPCs were cultured as free-floating aggregates, also known as neurospheres ,30. Brie. (2010) ,30. For 2 and 95% humidity. At day 3, PrestoBlue\u2122 was added to final concentration of 10% in proliferation medium in each well, and the cells were incubated for 2 h at 37 \u00b0C, 5% CO2 and 95% humidity before measuring the fluorescence intensity using FLUOstar Omega system , 570 nm. The fluorescence intensity indicates the proportion of live cells. The NSPC proliferation assay was carried out on 6 replicates per clone, in 3 independent experiments.NSPCs\u2019 proliferation rates were analyzed using PrestoBlue\u2122 Cell Viability Assay following the manufacturer\u2019s protocol and as described in Xing and Oksenych (2019) . BrieflyFor self-renewal assay, we followed the protocol described earlier . BrieflyDifferentiation was induced in dissociated NSPCs, as described previously ,30. BrieWestern blots were performed using antibodies against XLF, PAXX, DNA-PKcs, and \u03b2-actin ,30.Xlf, Dna-pkcs or Paxx results in viable fertile mice without detectable phenotypes in the CNS [Xlf and Dna-pkcs [Xlf and Paxx [Xlf\u2212/\u2212, Paxx\u2212/\u2212, Dna-pkcs\u2212/\u2212, Xlf\u2212/\u2212Paxx\u2212/\u2212, and Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 mouse embryos (E15.5). NSPCs aggregated themselves form neurospheres within 7 days in culture. We used these neurospheres to characterize proliferation, self-renewal, and neural differentiation capacity of the NSPCs , while we recorded Xlf\u2212/\u2212Paxx+/+ (16) and Xlf\u2212/\u2212Paxx+/\u2212 (27) live-born mice (Xlf\u2212/\u2212Paxx\u2212/\u2212 (3), Xlf\u2212/\u2212Paxx+/+ (8) and Xlf\u2212/\u2212Paxx+/\u2212 (31) mice , while there were Xlf\u2212/\u2212Dna-pkcs+/+ (35) and Xlf\u2212/\u2212Dna-pkcs+/\u2212 (54) mice at day P30. However, live-born Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 mice were detected at days P1\u20132, in line with our previous observations [To obtain eviously , no liveorn mice A. By ana31) mice B, which earlier . Brieflyrvations ,27,28. WXlf\u2212/\u2212 ; WT vs. Paxx\u2212/\u2212 ; WT vs. Dna-pkcs\u2212/\u2212 ; WT vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; WT vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Paxx\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Dna-pkcs\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Dna-pkcs\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Dna-pkcs\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 .Detailed statistical analysis for NSPC proliferation, Xlf\u2212/\u2212 ; WT vs. Paxx\u2212/\u2212 ; WT vs. Dna-pkcs\u2212/\u2212 ; WT vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; WT vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Paxx\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Dna-pkcs\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Dna-pkcs\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Dna-pkcs\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 .Detailed statistical analysis for the relative neurosphere count per well , Xlf\u2212/\u2212 ; WT vs. Paxx\u2212/\u2212 ; WT vs. Dna-pkcs\u2212/\u2212 ; WT vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; WT vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Paxx\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Dna-pkcs\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Dna-pkcs\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Dna-pkcs\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 .Detailed statistical analysis for the relative size of neurospheres , Xlf\u2212/\u2212Paxx\u2212/\u2212 and Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 double knockout neurospheres were reduced when compared to WT and single-deficient Xlf\u2212/\u2212, Dna-pkcs\u2212/\u2212 or Paxx\u2212/\u2212 neurospheres D. Inactikgrounds D. We conXlf, Paxx or Dna-pkcs, and combined inactivation of Xlf/Paxx did not affect early neuronal differentiation based on average proportions of Tuj1-positive cells were plated on pre-coated 48-well plates and cultured with differentiation medium for 5 days. Neuronal and glial lineages were identified by immunolabeling using markers for early neurons (Tuj1), and astrocytes (GFAP). Inactivation of ve cells A. Combinof NSPCs A,C. The of NSPCs B,D.Xlf\u2212/\u2212 ; WT vs. Paxx\u2212/\u2212 ; WT vs. Dna-pkcs\u2212/\u2212 ; WT vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; WT vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Paxx\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Dna-pkcs\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Dna-pkcs\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Dna-pkcs\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 .Detailed statistical analysis for the neuron differentiation, Xlf\u2212/\u2212 ; WT vs. Paxx\u2212/\u2212 ; WT vs. Dna-pkcs\u2212/\u2212 ; WT vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; WT vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Paxx\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Xlf\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Dna-pkcs\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Dna-pkcs\u2212/\u2212 vs. Xlf\u2212/\u2212Paxx\u2212/\u2212 ; Dna-pkcs\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 ; Xlf\u2212/\u2212Paxx\u2212/\u2212 vs. Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 .Detailed statistical analysis for the astrocyte differentiation, Overall, XLF possesses functional redundancy with PAXX during the NSPC self-renewal, and with DNA-PKcs during cell growth and neuronal differentiation .Xrcc4\u2212/\u2212, Lig4\u2212/\u2212, Xlf\u2212/\u2212Paxx\u2212/\u2212 and Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 mice NHEJ is ablated. Therefore, to avoid increased genomic instability during proliferation, developing neurons undergo programmed cell death via the p53-dependent pathway [Here, we demonstrated that NHEJ factors XLF, PAXX and DNA-PKcs support proliferation of NSPCs during early mammalian neurogenesis, when the proliferation rate is high and the likelihood of DNA damages arising from DNA replication machinery is increased. In pathway ,20,27,28Xlf\u2212/\u2212, Xlf\u2212/\u2212Paxx\u2212/\u2212 and Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 NSPCs is significantly lower than that in WT cells; proliferation of Xlf\u2212/\u2212Dna-pkcs\u2212/\u2212 NSPCs is lower than that in Paxx\u2212/\u2212 cells factors in cells? As one option, it was suggested that XLF can be complementary to the second factor having an alternative function . Alternatively, the proteins can be completely redundant key structural components of NHEJ machinery [An important question challenging current research is: what is the mechanism underlying genetic interaction between mutants) . Severalmutants) . More spmutants) . More remutants) .Another model suggests that there are two major structural complexes formed during the NHEJ. Ku70-Ku80-XRCC4-LIG4 form the flexible synaptic complex (FS). Next, DSBs are brought together through interaction of XRCC4, giving rise to two Ku-XRCC4-Lig4-DNA complexes. Both XLF and PAXX are required for transition from the flexible synaptic to the second synaptic complex, or close synapsis (CS). Here, XLF stabilizes the close synapsis to a greater extent. In this model, it was suggested that DNA-PKcs is not involved in the FS and CS formation ,50. MoreXLF is functionally redundant with PAXX during the neuronal stem and progenitor cells self-renewal and proliferation, and with DNA-PKcs during cell growth and neuronal differentiation. The NHEJ factors DNA-PKcs, PAXX and XLF are required for efficient early-stage development of neuronal stem and progenitor cells in mice. Additional NHEJ factors, such as MRI/Cyren, Ku70, Ku80, XRCC4 and LIG4, as well as multiple ATM-dependent DDR factors might have similar functions in neurodevelopment. Future studies will directly address the roles of NHEJ factors, including XLF, DNA-PKcs, PAXX and MRI, in learning, memory and mood regulations."} +{"text": "In the article titled \u201cPreconditioning of Rat Bone Marrow-Derived Mesenchymal Stromal Cells with Toll-Like Receptor Agonists\u201d , there w"} +{"text": "In the article titled \u201cPartial and Transient Clinical Response to Omalizumab in IL-21-Induced Low STAT3-Phosphorylation on Hyper-IgE Syndrome\u201d [The correct affiliation of Mario Alberto Ynga-Durand is \u201cLaboratorio de Inmunidad de Mucosas, Secci\u00f3n de Investigaci\u00f3n y Posgrado, Escuela Superior de Medicina, Instituto Polit\u00e9cnico Nacional, Mexico City, Mexico.\u201d The correct affiliation for Julio C\u00e9sar Alc\u00e1ntara-Montiel is \u201cDepartment of Molecular Biomedicine, CINVESTAV-IPN, Mexico City, Mexico.\u201dThe error was introduced during the production process of the article, and Hindawi apologises for causing this error in the article.The corrected list of affiliations is shown in the authors' information above."} +{"text": "Scientific Reportshttps://doi.org/10.1038/s41598-020-63658-5, published online 24 April 2020Correction to: The original version of this Article contained an error in the title of the paper, where the expression \u201c2\u2032,3\u2032-cAMP\u201d was incorrectly given as \u201c2\u20323\u2032-cAMP\u201d.The original version of this Article also contained errors in the Abstract.\u201cIn cells lacking 2\u2032,3\u2032-cyclic nucleotide 3\u2032-phosphodiesterase , effects of IAA/DNP on exosome secretion were enhanced.\u201dnow reads:\u201cIn cells lacking 2\u2032,3\u2032-cyclic nucleotide 3\u2032-phosphodiesterase , effects of IAA/DNP on exosome secretion were enhanced.\u201dThese errors have now been corrected in the PDF and HTML versions of the Article and in the accompanying Supplementary Information file."} +{"text": "In the article titled \u201cSelf-Compassion Demonstrating a Dual Relationship with Pain Dependent on High-Frequency Heart Rate Variability\u201d , the aut\u201cFigure 1: Analysis procedure of HF-HRV. For detailed information, please refer to the Methods section (derived from [37] which has been reproduced with permission from Elsevier).\u201d"} +{"text": "Correction to: BMC Musculoskelet Disord 21, 303 (2020)https://doi.org/10.1186/s12891-020-03251-zFollowing publication of the original article , the autHealth- and work-related questions\u201cTo assess their self-rated general health, the following questions were used: How do you experience your [1] \u201cphysical health\u201d [2] \u201cmental health\u201d [3] \u201csocial environment\u201d [4] \u201cphysical environment\u201d and [5] \u201cwork ability\u201d? A seven-point scale with answers ranging from \u201cvery poor\u201d to \u201cexcellent, cannot be better\u201d was used. In the analyses, the answers were collapsed and coded into: poor (\u22643), good , or excellent (\u22656) according to Larsson et al. [16].\u201dThe original article has been"} +{"text": "In the article titled \u201cInterleukin-9 Deletion Relieves Vascular Dysfunction and Decreases Blood Pressure via the STAT3 Pathway in Angiotensin II-Treated Mice\u201d , the aut"} +{"text": "Scientific Reports 10.1038/s41598-017-08774-5, published online 16 August 2017Correction to: murG/MurG. The correct names are ypfP/YpfP.Due to an annotation error, the gene and protein name for the processive diacylglycerol beta-glucosyltransferase in this Article is listed as murG\u201d and \u201cMurG\u201d in the Article should read \u201cypfP\u201d and \u201cYpfP\u201d, respectively.Therefore, all instances of \u201c"} +{"text": "Scientific Reports 10.1038/srep45314, published online 28 March 2017Correction to: This Article contains an error in Table 5.In the first row heading, the number of male patients,\u201cMale (n\u2009=\u200970)\u201d.should read:\u201cMale (n\u2009=\u200960)\u201d."} +{"text": "In the article titled \u201cN-Acetyl Cysteine as a Novel Polymethyl Methacrylate Resin Component: Protection against Cell Apoptosis and Genotoxicity\u201d , there w"} +{"text": "Scientific Reports 10.1038/s41598-019-54461-y, published online 09 December 2019Correction to: The Article contains an error in Table 3, entitled \u201cSemi-quantitative comparisons of CNS proteins by IHC staining.\u201dIn the \u201cTyrosine Hydroxylase\u201d row under the \u201cDM-resistant, with PFB\u201d column, the value of 7+ was erroneously omitted."} +{"text": "Scientific Reports 10.1038/s41598-019-57269-y, published online 15 January 2020Correction to: The original version of this Article contained missing bar chart outlines and missing error bars in all figures.Additionally, in Figure 1 the figure key was incorrect. The individual groups for \u201cCrysophyceae\u201d, \u201cBacillariophyceae\u201d and \u201cDinophyceae\u201d are now in one group \u201cOthers\u201d.As a result, the legend of Figure 1 was incorrect.a (Chl a) concentration under full sunlight (UVR\u2009+\u2009PAR) and photosynthetically active radiation (PAR) and under ambient phosphorus (P) concentration and P-added conditions. Bars represent the mean values and error bars represent the standard deviation (SD) (n = 3).\u201d\u201cSestonic N:P ratio (on a molar basis), phytoplankton abundance (PA) and chlorophyll now reads:\u201cSestonic N:P ratio (on a molar basis), phytoplankton abundance (PA) and chlorophyll a (Chl a) concentration under full sunlight (UVR + PAR) and photosynthetically active radiation (PAR) and under ambient phosphorus (P) concentration and P-added conditions. In Fig. 1b, Others group includes Cryptophyceae, Bacillariophyceae and Dinophyceae, and represents a small proportion of the total phytoplankton abundance. Bars represent the mean values and error bars represent the standard deviation (SD) (n = 3).\u201dThis has now been corrected in the PDF and HTML versions of the original article."} +{"text": "In the article titled \u201cFrom ACTH-Dependent to ACTH-Independent Cushing's Syndrome from a Malignant Mixed Corticomedullary Adrenal Tumor: Potential Role of Embryonic Stem Cells\u201d , there w"} +{"text": "Scientific Reports 10.1038/s41598-019-41642-y, published online 05 April 2019Correction to: The Acknowledgements section in this Article is incomplete.\u201cWe acknowledge Franck Fortuna and Laurent Delbecq for access and support to the nano-focused ion beam at the CSNSM laboratory . We acknowledge support from the PETACom FET Open H2020, support from the French ministry of research through the ANR grants 2014\u201dIPEX\u201d, 2016 \u201cHELLIX\u201d, 2016 \u201cBISCOT\u201d, 2017 \u201cPACHA\u201d, the DGA RAPID grant \u201cSWIM\u201d and from the C\u2019NANO research program through the NanoscopiX grant, and the LABEX \u201cPALM\u201d (ANR-10-LABX-0039-PALM) through he grants\u201dPlasmon-X\u201d, \u201cSTAMPS\u201d and \u201cHILAC\u201d. We acknowledge the financial support from the French ASTRE program through the \u201cNanoLight\u201d grant. We aknowledge support from Conseil R\u00e9gional de Nouvelle-Aquitaine grant 2017 \u201cFLOWA\u201d. Financial support by the Deutsche Forschungsgemeinschaft, grant KO 3798/4-11 and from Lower Saxony through \u201cQuanten- und Nanometrologie\u201d (QUANOMET), project NanoPhotonik are acknowledged. J.B. acknowledges financial support from the Spanish Ministry of Economy and Competitiveness (MINECO), through the \u201cSevero Ochoa\u201d Programme for Centres of Excellence in R&D (SEV-2015- 0522) and the Fundaci\u00f3 Cellex Barcelona.\u201dshould read:\u201cWe acknowledge Franck Fortuna and Laurent Delbecq for access and support to the nano-focused ion beam at the CSNSM laboratory . We acknowledge support from the PETACom FET Open H2020, support from the French ministry of research through the ANR grants 2014\u201dIPEX\u201d, 2016 \u201cHELLIX\u201d, 2016 \u201cBISCOT\u201d, 2017 \u201cPACHA\u201d, the DGA RAPID grant \u201cSWIM\u201d and from the C\u2019NANO research program through the NanoscopiX grant, and the LABEX \u201cPALM\u201d (ANR-10-LABX-0039-PALM) through the grants\u201dPlasmon-X\u201d, \u201cSTAMPS\u201d and \u201cHILAC\u201d. We acknowledge the financial support from the French ASTRE program through the \u201cNanoLight\u201d grant. We acknowledge support from Conseil R\u00e9gional de Nouvelle-Aquitaine grant 2017 \u201cFLOWA\u201d. Financial support by the Deutsche Forschungsgemeinschaft, grant KO 3798/4-11 and from Lower Saxony through \u201cQuanten- und Nanometrologie\u201d (QUANOMET), project NanoPhotonik are acknowledged. J.B. acknowledges financial support from the Spanish Ministry of Economy and Competitiveness (MINECO), through the \u201cSevero Ochoa\u201d Programme for Centres of Excellence in R&D (SEV-2015- 0522), the Fundaci\u00f3 Cellex Barcelona, ERC Advanced Grant \u201cTRANSFORMER\u201d, Agreement No. 788218 and Laserlab-Europe (EU-H2020 654148).\u201d"} +{"text": "Scientific Reports 10.1038/s41598-018-29959-6, published online 07 August 2018Correction to: This Article contains errors in Table 2 where the two columns headings have been reversed. \u2018CAD/CAM NAM\u2019 and \u2018RapidNAM\u2019 should read \u2018RapidNAM\u2019 and \u2018CAD/CAM NAM\u2019 respectively."} +{"text": "Scientific Reportshttps://doi.org/10.1038/s41598-020-63949-x, published online 24 April 2020Correction to: This Article contains errors in the Methods section under subheading \u2018Surgical procedures\u2019.\u201c\u201dshould read:\u201c\u201dAdditionally, in the Methods section, the subheading \u201cPlasma Measurements\u201d should read \u201cPlasma and Spleen Measurements\u201d."} +{"text": "Correction to: Orphanet J Rare Dis 15, 171 (2020)https://doi.org/10.1186/s13023-020-01391-ySport and Nutrition section of the manuscript whereby it was stated that:\u2018Approximately 20\u201330 g of protein equivalent from protein substitute should be ingested post exercise.\u2019The original article containe\u2026 20g of protein equivalent from protein substitute \u2026 \u2019 which has since been implemented in the original article.This sentence should instead have stated \u2018"} +{"text": "Scientific Reports 10.1038/s41598-019-45909-2, published online 02 July 2019Correction to: This Article contains typographical errors in the \u2018Results and Discussion\u2019 section under subheading \u2018Refractive index as a function of salinity\u2019, where equation (8)\u201cshould read:\u201cand equation (10)\u201cshould read:\u201c"} +{"text": "July 19, 2019,an equation appeared incorrectly because of an author error. In the \u201cInactivatingexponential integrate and fire model (iEIF)\u201d section of the Materials andMethods, Equation 1 should have stated \u201cfor V <\u03b8\u201d instead of \u201cfor V