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

◀ Back to MAPK3

MAPK3 — PRKAB1

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

Studies that report less than 10 interactions are marked with *

Text-mined interactions from Literome

Li et al., Circ Res 2005 (Myocardial Ischemia) : In isolated heart muscles, the AMPK activator 5-aminoimidazole-4-carboxy-amide-1-beta-D-ribofuranoside ( AICAR ) increased p38 MAPK activation ... p38 MAPK recruitment to TAB1/AMPK complexes required AMPK activation and was reduced in ischemic AMPK-deficient transgenic mouse hearts
Capano et al., Biochem J 2006 (Myocardial Ischemia) : Inhibition of p38 MAPK with SB203580 attenuated the phosphorylation of the downstream substrates, MAPK activated protein kinases 2 and 3, but not that of the upstream MAPK kinase 3, nor of AMPK
Cheng et al., Biochim Biophys Acta 2006 : Inhibition of AMPK reduces p38 MAPK phosphorylation, suggesting that AMPK lies upstream of p38 MAPK
Li et al., Endocrinology 2007 : We conclude that in cultured bAECs, TNF-alpha induces insulin resistance in the phosphatidylinositol 3-kinase/Akt/eNOS pathway via a p38 MAPK dependent mechanism and enhances ERK1/2 and AMPK phosphorylation independent of the p38 MAPK pathway
Ho et al., Biochem Biophys Res Commun 2007 : In conclusion, increasing AMPK activity by AICAR and AMPKgamma1 mutation does not increase p38 MAPK phosphorylation in skeletal muscle
Jacquet et al., Cardiovasc Res 2007 (Disease Models, Animal...) : Finally, pharmacological inhibition of AMPK during ischemia with compound C did not attenuate the coincident activation of p38 MAPK
Hu et al., Hepatology 2008 (Carcinoma, Hepatocellular...) : Furthermore, CNTF induced mitogen activated protein kinase ( MAPK ) activation suppresses AMPK activity in the early phase of CNTF stimulation
Han et al., J Cell Physiol 2009 : AICAR was able to activate p38 MAPK and pre-treatment with AMPK inhibitor or expression of KD-AMPK blocked this p38 MAPK activation
Liu et al., Cell cycle (Georgetown, Tex.) 2009 (Breast Neoplasms) : At the molecular level, metformin increases P-AMPK , reduces P-EGFR, EGFR, P-MAPK , P-Src, cyclin D1 and cyclin E ( but not cyclin A or B, p27 or p21 ), and induces PARP cleavage in a dose- and time dependent manner
Kim et al., J Biol Chem 2011 (MAP Kinase Signaling System) : Expression of dominant negative AMPK suppressed HCSA mediated phosphorylation of p38 MAPK , and inhibition of AMPK and p38 MAPK blocked HCSA induced glucose uptake
Jo et al., Nat Prod Res 2012 : Inhibition of AMPK activity reduced p38 MAPK phosphorylation, whereas the inhibition of p38 MAPK activity did not affect AMPK phosphorylation
Damm et al., Mol Endocrinol 2012 (MAP Kinase Signaling System) : Inhibitory effects of a-MSH on AMPK were blocked by specific inhibitors of protein kinase A (PKA) or ERK-1/2 , pointing to an important role of both kinases in this process
Shen et al., J Biomed Biotechnol 2012 : Nuclear NT-PGC-1a can be increased by activation of protein kinase A. Activation of p38 MAPK by muscle activity or of AMPK had no effect on the subcellular distribution of NT-PGC-1a
Arsikin et al., Biochim Biophys Acta 2012 (Neuroblastoma) : 6-OHDA induced phosphorylation of p38 mitogen activated protein ( MAP ) kinase in an AMPK dependent manner, and pharmacological inhibition of p38 MAP kinase reduced neurotoxicity, but not AMPK activation and autophagy triggered by 6-OHDA
Choi et al., J Cell Physiol 2013 (Neoplasms) : Furthermore, whereas Compound C ( an AMPK inhibitor ), AMPK-DN ( AMPK-dominant negative ) mutant, and SB203580 ( a p38 MAPK inhibitor ) did not block the 8-Cl-cAMP induced phosphorylation of Akt/PKB, TCN ( an Akt1/2/3 specific inhibitor ) and an Akt2/PKBß targeted siRNA inhibited the 8-Cl-cAMP- and AICAR mediated phosphorylation of AMPK and p38 MAPK
Paweł et al., Lipids 2013 (Leiomyoma...) : Additionally, in uterine leiomyomas we found relevant activation of both PTEN and MAPK(ERK1/2) signaling pathways with only a minor change in AKT activity and relatively absent HIF-1a/AMPK activation