◀ Back to PRKAB1
CFTR — 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
Hallows et al., J Clin Invest 2000
:
Because AMPK is a metabolic sensor in cells and responds to changes in cellular ATP,
regulation of
CFTR by
AMPK may be important in inhibiting CFTR under conditions of metabolic stress, thereby linking transepithelial transport to cell metabolic state
Hallows et al., J Biol Chem 2003
(Ion Channel Gating) :
Plasma membrane expression of
CFTR , assessed by surface biotinylation, was not
affected by
AMPK activation
King et al., Am J Physiol Cell Physiol 2009
:
To further characterize the mechanism of
AMPK dependent regulation of
CFTR , whole cell patch-clamp measurements were performed with PKA activation in Calu-3 cells expressing either constitutively active or dominant negative AMPK mutants ( AMPK-CA or AMPK-DN ) ... Baseline CFTR conductance in cells expressing AMPK-DN was substantially greater than controls, suggesting that tonic
AMPK activity in these cells
inhibits CFTR under basal conditions ... Phosphorylation studies of CFTR in human embryonic kidney-293 cells using tetracycline-inducible expression of AMPK-DN demonstrated
AMPK dependent phosphorylation of
CFTR in vivo ... Thus,
AMPK dependent
CFTR phosphorylation renders the channel resistant to activation by PKA and PKC without preventing phosphorylation by these kinases ... Ser-to-Ala mutation at this site enhanced baseline CFTR activity and rendered CFTR resistant to inhibition by AMPK, suggesting that
AMPK phosphorylation at Ser768 is
required for its inhibition of
CFTR ... In summary, our findings indicate that
AMPK dependent phosphorylation of
CFTR inhibits CFTR activation by PKA, thereby tuning the PKA-responsiveness of CFTR to metabolic and other stresses in the cell
Murphy et al., Am J Physiol Cell Physiol 2009
:
Finally, inhibition of the cystic fibrosis transmembrane regulator ( CFTR ) Cl ( - ) conductance blocked depolarization of GI neurons to decreased glucose or AMPK activation, whereas decreased glucose,
AMPK activation, and 8-Br-cGMP
increased VMH
CFTR phosphorylation
King et al., J Biol Chem 2012
:
Taken together, these results suggest that NDPK-A exists in a functional cellular complex with AMPK and CFTR in airway epithelia, and NDPK-A catalytic function is required for the
AMPK dependent regulation of
CFTR