PMID- 36963174
OWN - NLM
STAT- MEDLINE
DCOM- 20230414
LR  - 20230414
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 657
DP  - 2023 May 21
TI  - Glyceraldehyde-3-phosphate dehydrogenase regulates activation of c-Jun N-terminal 
      kinase under oxidative stress.
PG  - 1-7
LID - S0006-291X(23)00329-7 [pii]
LID - 10.1016/j.bbrc.2023.03.044 [doi]
AB  - Glyceraldehyde-3-phosphate dehydrogenase (GAPDH) acts as a sensor under oxidative 
      stress, leading to induction of various biological responses. Given that 
      mitogen-activated protein kinase (MAPK) signaling pathways mediate cellular 
      responses to a wide variety of stimuli, including oxidative stress, here, we 
      aimed to elucidate whether a cross-talk cascade between GAPDH and MAPKs occurs 
      under oxidative stress. Of the three typical MAPKs investigated-extracellular 
      signal-regulated kinase, p38, and c-Jun N-terminal kinase (JNK)-we found that 
      hydrogen peroxide (H(2)O(2))-induced JNK activation is significantly reduced in 
      HEK293 cells treated with small-interfering (si)RNA targeting GAPDH. 
      Co-immunoprecipitation with a GAPDH antibody further revealed protein-protein 
      interactions between GAPDH and JNK in H(2)O(2)-stmulated cells. Notably, both JNK 
      activation and these interactions depend on oxidation of the active-site cysteine 
      (Cys152) in GAPDH, as demonstrated by rescue experiments with either exogenous 
      wild-type GAPDH or the cysteine-substituted mutant (C152A) in endogenous 
      GAPDH-knockdown HEK293 cells. Moreover, H(2)O(2)-induced translocation of 
      Bcl-2-associated X protein (Bax) into mitochondria, which occurs downstream of 
      JNK activation, is attenuated by endogenous GAPDH knockdown in HEK293 cells. 
      These results suggest a novel role for GAPDH in the JNK signaling pathway under 
      oxidative stress.
CI  - Copyright (c) 2023 The Authors. Published by Elsevier Inc. All rights reserved.
FAU - Itakura, Masanori
AU  - Itakura M
AD  - Laboratory of Veterinary Pharmacology, Graduate School of Life and Environmental 
      Science, Osaka Prefecture University, Izumisano, Osaka, Japan.
FAU - Kubo, Takeya
AU  - Kubo T
AD  - Laboratory of Veterinary Pharmacology, Graduate School of Life and Environmental 
      Science, Osaka Prefecture University, Izumisano, Osaka, Japan.
FAU - Kaneshige, Akihiro
AU  - Kaneshige A
AD  - Laboratory of Veterinary Pharmacology, Graduate School of Life and Environmental 
      Science, Osaka Prefecture University, Izumisano, Osaka, Japan.
FAU - Nakajima, Hidemitsu
AU  - Nakajima H
AD  - Laboratory of Veterinary Pharmacology, Graduate School of Life and Environmental 
      Science, Osaka Prefecture University, Izumisano, Osaka, Japan. Electronic 
      address: hnakajima@vet.osakafu-u.ac.jp.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20230317
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - K848JZ4886 (Cysteine)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - EC 2.7.11.24 (JNK Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinase 8)
RN  - EC 1.2.1.12 (GAPDH protein, human)
RN  - EC 1.2.1.12 (Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating))
SB  - IM
MH  - Humans
MH  - Cysteine/metabolism
MH  - HEK293 Cells
MH  - *Hydrogen Peroxide/pharmacology
MH  - *JNK Mitogen-Activated Protein Kinases/metabolism
MH  - Oxidative Stress
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
MH  - *Mitogen-Activated Protein Kinase 8/pharmacology
MH  - *Glyceraldehyde-3-Phosphate Dehydrogenase (Phosphorylating)/metabolism
OTO - NOTNLM
OT  - Glyceraldehyde-3-phosphate dehydrogenase (GAPDH)
OT  - H(2)O(2)
OT  - Mitogen-activated protein kinases (MAPKs)
OT  - Oxidative stress
OT  - c-Jun N-terminal kinase (JNK)
COIS- Declaration of competing interest The authors declare no conflict of interest.
EDAT- 2023/03/25 06:00
MHDA- 2023/04/12 06:41
CRDT- 2023/03/24 19:03
PHST- 2023/03/01 00:00 [received]
PHST- 2023/03/16 00:00 [accepted]
PHST- 2023/04/12 06:41 [medline]
PHST- 2023/03/25 06:00 [pubmed]
PHST- 2023/03/24 19:03 [entrez]
AID - S0006-291X(23)00329-7 [pii]
AID - 10.1016/j.bbrc.2023.03.044 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2023 May 21;657:1-7. doi: 10.1016/j.bbrc.2023.03.044. 
      Epub 2023 Mar 17.