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UCSC Genome Browser Gene Interaction Graph
Gene interactions and pathways from curated databases and text-mining

◀ Back to GSK3B

GSK3B — TP53

Pathways - manually collected, often from reviews:

  • OpenBEL Selventa BEL large corpus: TP53 → GSK3B (increases, GSK3B Activity, TP53 Activity)
    Evidence: p53-mediated regulation of mPTP might be suppressed by inhibition of GSK-3b activity. Activation of p53 by GSK-3b enhances its functional activity and translocation to the nucleus and mitochondria.52
  • OpenBEL Selventa BEL large corpus: TP53 → GSK3B (directlyIncreases, TP53 Activity)
    Evidence: In contrast, apoptosis induced by intrinsic mechanisms is facilitated by active GSK-3b. Phosphorylation of 4 GSK-3b substrates (p53, heat shock factor-1 [HSF-1], myeloid cell leukemia sequence-1 [MCL-1], Bax) is involved in the pro-apoptotic functions.
  • WikiPathways Senescence and Autophagy in Cancer: GSK3B → TP53 (unknown)

Protein-Protein interactions - manually collected from original source literature:

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Turenne et al., BMC cell biology 2001 : GSK3beta increased the transcriptional activity of the p53 protein in vivo ... However, GSK3beta kinase activity was inhibited in response to DNA damage, suggesting that GSK3beta regulation of p53 is not involved in the p53-DNA damage response
Sadot et al., Mol Cell Biol 2001 : The inhibitory effect of p53 on beta-catenin is apparently mediated by the ubiquitin-proteasome system and requires an active glycogen synthase kinase 3beta ( GSK3beta )
Watcharasit et al., J Biol Chem 2003 : GSK3beta activity was not required for p53 binding, but inhibition of GSK3beta stabilized the association, suggesting a transient interaction during which active GSK3beta promotes actions of p53 ... Besides promoting p53 mediated transcription, GSK3beta also contributed to mitochondrial p53 apoptotic signaling
Cai et al., Int J Oncol 2007 (Ovarian Neoplasms) : We demonstrated that GSK-3beta negatively regulated the expression of p53
Matsui et al., Oncogene 2008 (Neoplasms, Glandular and Epithelial) : We further demonstrated that the functional regulation of p53 by triptolide was mediated by an intranuclear association of p53 with glycogen synthase kinase-3beta ( GSK3beta ), which was inactivated by protein kinase C ( PKC )
Yao et al., J Cell Sci 2008 (Disease Progression...) : Thus, Fos synergism with Pten loss elicited a benign tumour context where GSK3beta induced p53/p21 WAF expression continually switched AKT associated proliferation into differentiation, preventing further progression
Ren et al., Crit Care Med 2008 (Cardiomyopathies) : Western blot analysis showed reduced expression of sacro ( endo ) plasmic reticulum Ca2+-ATPase2a, Bcl-2 and phosphorylated GSK-3beta , enhanced calreticulin, Bax, p53 , myosin heavy chain-beta isozyme switch, and IkappaB phosphorylation in FVB-BSO mice, all of which with the exception of p53 were nullified by MT
Thotala et al., Cancer Res 2008 (Nervous System Diseases...) : At the same time, radiation led to increased accumulation of p53, whereas inhibition of the basal level of GSK-3beta activity before radiation prevented p53 accumulation, suggesting a possible mechanism of cytoprotection by GSK-3beta inhibitors
Miura et al., J Pharmacol Sci 2009 (Myocardial Infarction...) : Although the effect of GSK-3beta phosphorylation on mPTP structure and function remains unclear, suppression of ANT-CyP-D interaction by binding of phospho-GSK-3beta to ANT and reduction in GSK-3beta mediated phosphorylation of p53 may contribute to elevation of the threshold for mPTP opening