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Validated All-in-One™ qPCR Primer for PPP1R15A(NM_014330.3) Search again
Powered by BiozBy default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Summary
This gene is a member of a group of genes whose transcript levels are increased following stressful growth arrest conditions and treatment with DNA-damaging agents. The induction of this gene by ionizing radiation occurs in certain cell lines regardless of p53 status, and its protein response is correlated with apoptosis following ionizing radiation. [provided by RefSeq].
Gene References into function
- SNF5/INI1 protein facilitates the function of the growth arrest and DNA damage-inducible protein and modulated protein phosphatase-1 activity
- GADD 34 may play an important role in melanoma progression
- the GADD34-mediated cellular stress response is suppressed by BAG-1
- Human Gadd34 lacking the viral homology domain does not interfere with normal Gadd34-induced apoptosis in cultured cells. This suggests that viral similarity sequences may be required for Gadd34-mediated functions other than apoptosis.
- These findings suggest that phenethylisothiocyanate creates an oxidative cellular environment that induces DNA damage and GADD153, 34 and 45 gene activation, which in turn helps trigger apoptosis
- GADD34-PP1c recruited by Smad7 inhibits TGFbeta-induced cell cycle arrest.
- the up-regulation of GADD34 in response to global ischaemia in the human brain plus its influence on protein synthesis and DNA repair suggests that this protein may have the potential to influence cell survival
- GADD34 may perform important functions in cardiac tissue in response to ischaemia.
- During conditions of cell stress, GADD34 forms a stable complex with tuberous sclerosis complex (TSC) 1/2, causes TSC2 dephosphorylation, and inhibits signaling by mammalian target of the rapamycin (mTOR).
- mechanisms that control GADD34 levels in human cells