S-nitrosylated GAPDH initiates apoptotic cell death by nuclear translocation following Siah1 binding

By M. Hara, N. Agrawal, Sangwon F. Kim, Matthew B. Cascio, M. Fujimuro, Y. Ozeki, M. Takahashi, Jaime H. Cheah, Stephanie K. Tankou, L. Hester and 4 more. Nature Cell Biology, 2005

1,079 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/af822a76464511d3fa3b41472cd2fc8b261f3f01

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Citations in the corpus

Decoding cell death signals in liver inflammation. (2013, background): “At the cellular level, excess NO and RNS resemble ROS in their capacity to impair energetic metabolism as they covalently modify a large panel of proteins including mitochondrial complex IV [70] and ANT [71] (both involved in mitochondrial respiration) as well as glyceraldehyde-3-phosphate dehydroge”
Excitotoxicity and stroke: identifying novel targets for neuroprotection. (2014, positive): “with Siah1, which promotes the nuclear translocation of GAPDH that is essential for excitotoxic neuronal injury (Hara et al., 2005).”
Genes and growth performance in crustacean species : a review of relevant genomic studies in crustaceans and other taxa (2013, background): “1991), tRNA export (Singh & Green 1993), membrane fusion and transport (Tisdale 2001), cytoskeletal dynamics (Kumagai & Sakai 1983) and cell death (Hara et al. 2005).”
Physiological implications of hydrogen sulfide: a whiff exploration that blossomed. (2012, background): “Cys150 of GAPDH can be nitrosylated (230) or sulfhydrated (420), for example.”
NAD+/NADH and NADP+/NADPH in Cellular Functions and Cell Death: Regulation and Biological Consequences (2008, neutral): “In addition to PARP-1, the other two NAD-dependent proteins—-AIF (202) and GAPDH (58, 115)—-are also important mediators of cell death.”
A review of soil NO transformation: associated processes and possible physiological significance on organisms (2015, background): “S-1451 nitrosylation is involved in gene regulation, modulates phytohormon 1452 signalling and can control programmed cell death (PCD) in opposing ways 1453 (promote or inactivate) (Hara et al., 2005; Melotto et al., 2006; Belenghi, 1454 2007; Forman et al., 2008; Tada et al., 2008).”