Protein Variants | Comment | Organism |
---|---|---|
D234A | site-directed mutagenesis | Homo sapiens |
H179A | site-directed mutagenesis, the KD value of cADPR to GAPDHHis179Ala mutant protein is markedly increased compared to wild-type GAPDH enzyme | Homo sapiens |
Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
---|---|---|---|---|---|---|
D-glyceraldehyde 3-phosphate + phosphate + NAD+ | Homo sapiens | - |
3-phospho-D-glyceroyl phosphate + NADH + H+ | - |
? |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
coronary artery smooth muscle cell | - |
Homo sapiens | - |
HEK-293 cell | - |
Homo sapiens | - |
JURKAT cell | - |
Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
D-glyceraldehyde 3-phosphate + phosphate + NAD+ | - |
Homo sapiens | 3-phospho-D-glyceroyl phosphate + NADH + H+ | - |
? | |
additional information | GAPDH directly binds to cyclic adenosine diphosphoribose (cADPR), molecule docking and molecular dynamic simulations, overview. Arg234 and His179 in GAPDH might be the potential binding sites for cADPR | Homo sapiens | ? | - |
? |
Subunits | Comment | Organism |
---|---|---|
tetramer | - |
Homo sapiens |
Synonyms | Comment | Organism |
---|---|---|
GAPDH | - |
Homo sapiens |
glyceraldehyde-3-phosphate dehydrogenase | - |
Homo sapiens |
Temperature Optimum [°C] | Temperature Optimum Maximum [°C] | Comment | Organism |
---|---|---|---|
25 | - |
assay at | Homo sapiens |
pH Optimum Minimum | pH Optimum Maximum | Comment | Organism |
---|---|---|---|
8.5 | - |
assay at | Homo sapiens |
Cofactor | Comment | Organism | Structure |
---|---|---|---|
NAD+ | - |
Homo sapiens |
General Information | Comment | Organism |
---|---|---|
malfunction | GAPDH knockdown abolishes cADPR-induced Ca2+ release. GAPDH knockdown markedly inhibits NPE-cADPR- or PALcIDPRE-induced cytosolic Ca2+ increase in Jurkat cells, RyR3-expressing HEK-293 cells, or human coronary artery smooth muscle cells. Washing saponin-treated cells with PBS abolishes cADPR-induced colocalization of GAPDH with ryanodine receptors, RyRs | Homo sapiens |
physiological function | GAPDH plays essential role in glycolysis and gluconeogenesis as a housekeeping enzyme. Cyclic adenosine diphosphoribose (cADPR), an endogenous nucleotide derived from NAD+, mobilizes Ca2+ release from endoplasmic reticulum via ryanodine receptors (RyRs). cADPR interacts directly with enzyme GAPDH and induces the transient interaction between GAPDH and RyRs in vivo, without cADPR the interaction is weak. GAPDH is required for cADPR-mediated Ca2+ mobilization from endoplasmic reticulum via RyRs. cADPR-mediated Ca2+ signaling pathway is involved in a wide variety of cellular processes,1 e.g. abscisic acid signaling, calorie restriction in gut stem cell, circadian clock in plants, and long-term synaptic depression in hippocampus | Homo sapiens |