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Title:
Gadd45 in stress signaling | Journal of Molecular Signaling
Description:
Gadd45 genes have been implicated in stress signaling in response to physiological or environmental stressors, which results in cell cycle arrest, DNA repair, cell survival and senescence, or apoptosis. Evidence accumulated implies that Gadd45 proteins function as stress sensors is mediated by a complex interplay of physical interactions with other cellular proteins that are implicated in cell cycle regulation and the response of cells to stress. These include PCNA, p21, cdc2/cyclinB1, and the p38 and JNK stress response kinases. What deterministic factors dictate whether Gadd45 and partner proteins function in either cell survival or apoptosis remains to be determined. An attractive working model to consider is that the extent of cellular/DNA damage, in a given cell type, dictates the association of different Gadd45 proteins with particular partner proteins, which determines the outcome.
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Keywords {π}
cell, google, scholar, gadd, pubmed, cas, article, stress, cells, proteins, dna, gadda, apoptosis, genes, cycle, arrest, repair, liebermann, gaddb, response, activation, hoffman, growth, fornace, role, oncogene, pathways, biol, induced, expression, function, kinase, senescence, survival, damage, genotoxic, cancer, gaddg, gene, signaling, agents, mammalian, interaction, molecular, implicated, mediated, jnk, tumor, myd, evidence,
Topics {βοΈ}
tnfa-nf-kb mediated induction stress-responsive mtk1/mekk4/mapkkk c-jun n-terminal kinase myd118/gadd4/cr6 gene gamily nf-kb-mediated repression ras-driven tumor formation el-deiry ws ras-driven breast carcinogenesis article download pdf stress-activated map kinases p53-mediated growth arrest cdc2/cyclinb1 kinase inhibitors repair-mediated dna demethylation iptg-induced ectopic expression gadd45/pcna interaction impedes anti-cancer genotoxic drugs jnk/sapk-dependent apoptosis base-excision repair mechanisms stress-induced jnk activation future work addressing tgf-beta-induced apoptosis p53-regulated protein gadd45 iptg-inducible ectopic expression dna base-damaging agents gadd45-mediated growth suppression dna-damage inducing agents negative growth control o'connor pm p19arf/p53 pathways remains modulate tumor formation c-jun kinase activate p38 kinase genotoxic stress-induced apoptosis genotoxic-stress induced apoptosis privacy choices/manage cookies tgfb-induced apoptosis [68 tgfb-induced apoptosis cdk/cyclin complexes open access license genotoxic-stress-response genes terminal hematopoietic differentiation myeloid leukemia cells murine gadd45g/cr6 gene pro-apoptotic function ras-induced senescence distinct apoptotic pathways hela cell growth cyclin dependent kinases epigenetic gene activation p53-regulated protein
Questions {β}
- Kelman Z, Hurwitz J: Protein-PCNA interactions: a DNA-scanning mechanism?
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WebPage:
mainEntity:
headline:Gadd45 in stress signaling
description:Gadd45 genes have been implicated in stress signaling in response to physiological or environmental stressors, which results in cell cycle arrest, DNA repair, cell survival and senescence, or apoptosis. Evidence accumulated implies that Gadd45 proteins function as stress sensors is mediated by a complex interplay of physical interactions with other cellular proteins that are implicated in cell cycle regulation and the response of cells to stress. These include PCNA, p21, cdc2/cyclinB1, and the p38 and JNK stress response kinases. What deterministic factors dictate whether Gadd45 and partner proteins function in either cell survival or apoptosis remains to be determined. An attractive working model to consider is that the extent of cellular/DNA damage, in a given cell type, dictates the association of different Gadd45 proteins with particular partner proteins, which determines the outcome.
datePublished:2008-09-12T00:00:00Z
dateModified:2008-09-12T00:00:00Z
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pageEnd:8
sameAs:https://doi.org/10.1186/1750-2187-3-15
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Cytokines and Growth Factors
Receptors
Protein-Ligand Interactions
Cell Biology
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ScholarlyArticle:
headline:Gadd45 in stress signaling
description:Gadd45 genes have been implicated in stress signaling in response to physiological or environmental stressors, which results in cell cycle arrest, DNA repair, cell survival and senescence, or apoptosis. Evidence accumulated implies that Gadd45 proteins function as stress sensors is mediated by a complex interplay of physical interactions with other cellular proteins that are implicated in cell cycle regulation and the response of cells to stress. These include PCNA, p21, cdc2/cyclinB1, and the p38 and JNK stress response kinases. What deterministic factors dictate whether Gadd45 and partner proteins function in either cell survival or apoptosis remains to be determined. An attractive working model to consider is that the extent of cellular/DNA damage, in a given cell type, dictates the association of different Gadd45 proteins with particular partner proteins, which determines the outcome.
datePublished:2008-09-12T00:00:00Z
dateModified:2008-09-12T00:00:00Z
pageStart:1
pageEnd:8
sameAs:https://doi.org/10.1186/1750-2187-3-15
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Cytokines and Growth Factors
Receptors
Protein-Ligand Interactions
Cell Biology
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