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MAPK1 — PRKAB1

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

Studies that report less than 10 interactions are marked with *

• Gene Ontology Complexes protein complex: protein complex complex (HSF1-TRMT112-HIST1H4A-UBQLN1-CDX2-USP28-HDAC5-CAV3-CANX-LHX1-TUBA3C-TUBA3E-PI4K2A-NR0B2-RYR2-NTRK1-MPP5-N6AMT1-STAP1-ZFP42-FADD-ATP6V0D1-PRKCDBP-AQP2-FNTB-PRPSAP2-WIPI2-CRB3-CRB2-PEX11A-LDB1-RBP4-TMEM102-GATA2-ADCY2-DZIP1-SYK-TUBB4B-PTPN11-KAT5-CEP290-SYP-ASF1B-PLEKHA2-KIF24-MYO5B-RGP1-CFTR-SPTBN5-VPS72-ACTA2-PRKCI-CNST-SNX4-GNAO1-NFKBIA-UBE2D2-EPB41-RAB5A-GLUL-BSND-GSK3B-SKI-XRCC6-PPM1E-TTR-TUBA1A-SUCLG1-TRIAP1-AKT1S1-MYD88-NPPB-GDF11-INCENP-PLCB3-BECN1-PRKAB1-SOD1-TUBB1-NPHS2-NPHS1-EPS8L1-GDI1-TUBB2A-TUBB2B-SUCLG2-PEX3-TUBAL3-ERLIN1-MAGED1-GCH1-TUBB-CPS1-MEF2C-ZNF703-SLC22A6-CPLX1-EIF4EBP1-TUBE1-FLNA-CD19-STX1A-HDAC2-TOMM40L-HDAC6-SMAD6-SMAD7-TLE6-SMAD2-PARD6B-STXBP1-ACR-TRPC1-PARD6A-TRPC4-PANX1-DCTN1-SOX9-PXMP2-BCR-SET-MALT1-BHMT-RILP-TRADD-HIST1H3A-MAPK1-PVALB-NFKB1-NUFIP1-ACVR2B-TAL1-FOXP3-SSX2IP-GNB2-SLC27A5-GOPC-PAX2-CXADR-AIF1L-APBA1-MYL12A-LMO2-ID2-CCDC113-DDOST-SPP2-GATAD2B-PLN-ERCC8-BIRC8-ASF1A-CAB39-BIRC3-BIRC2-CTNNB1-CORO1A-PRELID1-HAND2-CHAF1B-SCAP-GNAT3-CDC20-SMARCA4-IQGAP1-YWHAZ-CEBPA-PRPS2-AXIN1-XRCC5-YWHAQ-UVRAG-SLC51B-RGS4-RGS6-HTT-YWHAB-APCS-CDCA8-RIPK1-MTA2-SIN3A-ANXA1-NOS1-SNTA1-TRAF6-KPNB1-VCL-VCP-PTRF-PRKCZ-SKIL-RAB3A-KRIT1-SSBP3-PRPSAP1-PPP1CC-TAB1-MYO6-ACTL7A-TUBG2-MBD2-COL6A1-COL6A2-BCL3) Helps et al., Biochem J 2000, Lauderdale et al., Proc Natl Acad Sci U S A 2000, Didichenko et al., FEBS Lett 2000, Koh et al., Curr Biol 2002, Fan et al., Mol Cell Biol 2002, Groisman et al., Cell 2003, Offenhäuser et al., Mol Biol Cell 2004, Tagami et al., Cell 2004, Doyon et al., Mol Cell Biol 2004, Moore et al., Genomics 2004, Sun et al., Mol Cell 2004, Zang et al., J Cell Biochem 2004, Tian et al., Cancer Res 2005, An et al., Biochemistry 2005, Mahajan et al., Proc Natl Acad Sci U S A 2005, Vader et al., EMBO Rep 2006, Yeh et al., J Biol Chem 2006, Li et al., Immunol Rev 2006, Agbas et al., Biochem J 2007, Swiatecka-Urban et al., J Biol Chem 2007, McKeegan et al., Mol Cell Biol 2007, Shono et al., J Am Soc Nephrol 2007, Popov et al., Cell cycle (Georgetown, Tex.) 2007, Sato et al., J Biol Chem 2008, Fitzgerald et al., J Biol Chem 2008, Lyssand et al., J Biol Chem 2008, Figaro et al., FEBS Lett 2008, Ueda et al., Proc Natl Acad Sci U S A 2008, Shimojo et al., J Biol Chem 2008, Costantini et al., Blood 2009, Mitsuishi et al., J Biol Chem 2010, Masuda et al., J Biol Chem 2010, Koch et al., J Cell Sci 2010, Boëda et al., J Biol Chem 2011, Sircoulomb et al., EMBO Mol Med 2011, Hoxhaj et al., J Cell Sci 2012, Uckun et al., Proc Natl Acad Sci U S A 2012, Pusapati et al., J Biol Chem 2012, Ghai et al., Proc Natl Acad Sci U S A 2013, Kelly et al., PLoS Biol 2013, Chiang et al., PloS one 2013, Dauphinee et al., J Immunol 2013, Potting et al., Cell Metab 2013, Ludwig et al., PLoS Biol 2013, Lee et al., Proc Natl Acad Sci U S A 2013, Kobayashi et al., J Cell Biol 2014, Zheng et al., Am J Physiol 1994, Kumar et al., Biochem Biophys Res Commun 1998, Watabe-Uchida et al., J Cell Biol 1998, Haft et al., Mol Cell Biol 1998

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