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binds cAMP and activates the Ras superfamily guanine nucleotide binding protein (Rap1A)in a PKA-independent manner. Additionally we are shipping Rap Guanine Nucleotide Exchange Factor (GEF) 3 Proteins (8) and many more products for this protein.
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Human Polyclonal RAPGEF3 Primary Antibody for EIA, WB - ABIN492970
Kerr, Costa-Pereira, Lillemeier, Strobl: Of JAKs, STATs, blind watchmakers, jeeps and trains. in FEBS letters 2003
Show all 6 references for ABIN492970
Human Polyclonal RAPGEF3 Primary Antibody for EIA, WB - ABIN492968
Magiera, Gupta, Rundell, Satish, Ernens, Yarwood: Exchange protein directly activated by cAMP (EPAC) interacts with the light chain (LC) 2 of MAP1A. in The Biochemical journal 2004
Show all 6 references for ABIN492968
Human Polyclonal RAPGEF3 Primary Antibody for ELISA, WB - ABIN1451502
Scherer, Muzny, Buhay, Chen, Cree, Ding, Dugan-Rocha, Gill, Gunaratne, Harris, Hawes, Hernandez, Hodgson, Hume, Jackson, Khan, Kovar-Smith, Lewis, Lozado, Metzker, Milosavljevic, Miner, Montgomery et al.: The finished DNA sequence of human chromosome 12. ... in Nature 2006
prostacyclin regulates bone growth via the Epac/Rap1 pathway
cAMP binds Xepac protein enabling it to activate the Ca2 (show CA2 Antibodies)+ pathway, which is necessary to start and maintain X. laevis vitellogenin (show VTG Antibodies) uptake.
These findings suggested Epac is connected to the SDF-1 (show CXCL12 Antibodies) signaling cascades. In conclusion, our study revealed that Epac plays a role in human mesenchymal stem cells (hMSCs)homing by promoting adhesion and migration. Appropriate manipulation of Epac may enhance the homing of hMSCs and facilitate their future clinical applications.
EPAC activity is increased in arterial endothelial cells exposed to laminar-fluid shear stress, activation of EPAC1, and its activation of Rap1, plays a role in promoting alignment and elongation of these cells in the direction of flow.
EPAC activation consistently reverses clinical and experimental impairment of neutrophil phagocytosis. EPAC signals through Rap-1 (show RABGEF1 Antibodies) and bypasses RhoA (show RHOA Antibodies). EPAC activation represents a novel potential means by which to reverse impaired neutrophil phagocytosis.
The cAMP exerted divergent effects on proliferation and promoted cell adhesion of different neuroendocrine cell types, these effects being mediated by both Epac and PKA and involving the same effector GTPase Rap1.
Impaired microtubule dynamics, due to reduced EPAC1 signaling, links CFTR (show CFTR Antibodies) function to cystic fibrosis (show S100A8 Antibodies) cellular events.
Identified a conserved nuclear pore localisation signal (NPLS; amino acids 764-838 of EPAC1) in the catalytic domains of the cAMP-sensors, EPAC1 and EPAC2A. EPAC1 and EPAC2 (show RAPGEF4 Antibodies), display distinct subcellular distributions.
Thyroid carcinoma cell lines showed no or very weak EPAC1 expression and exhibited no growth-promoting effect after EPAC stimulation.
findings, coupled with the development of EPAC specific small molecule modulators, validate EPAC1 as a promising target for therapeutic interventions
association of ezrin (show EZR Antibodies) with the actin cytoskeleton and phosphorylation on Thr567 are required, but not sufficient, for PKA and EPAC1 to synergistically promote cell spreading following elevations in intracellular cAMP.
These results demonstrate that glucagon (show GCG Antibodies) increases hepatic FGF21 (show FGF21 Antibodies) secretion via a posttranscriptional mechanism and provide evidence that both the PKA branch and EPAC branch of the cAMP pathway play a role in mediating this effect.
GRK2 inhibits Epac1-to-Rap1 signaling by phosphorylation of Epac1 at Ser-108 in the Disheveled/Egl-10/pleckstrin domain, inhibiting agonist-induced Epac1 translocation to the plasma membrane, reducing Rap1 activation.
DPP4i restores cardiac remodeling and apoptosis caused by the pathological decline in circulating GLP-1 in response to pressure overload. EPAC1 is essential for cardiomyocyte survival via the cAMP/Rap1 activation independently of PKA.
Epac2 (show RAPGEF4 Antibodies), but not Epac1 has a role in decreasing severity of ischemic retinopathy after retinal ischemia/reperfusion injury
Epac1 deficiency attenuates neointima formation through, at least in part, inhibition of SMC (show DYM Antibodies) migration, in which a decrease in Ca(2 (show CA2 Antibodies)+) influx and a suppression of cofilin (show CFL1 Antibodies)-mediated lamellipodia formation occur.
PDE4 (show PDE4A Antibodies) inhibition reduces neointima formation and inhibits VCAM-1 (show VCAM1 Antibodies) expression and histone methylation in an Epac-dependent manner.
Epac1 deletion protected against beta-AR-induced cardiac remodelling and prevented the induction of autophagy.
Epac1 induces beta2-AR-mediated masseter muscle hypertrophy without influencing slow-to-fast MHC isoform transition, probably via activation of Akt (show AKT1 Antibodies) and its downstream molecules and increase of CaMKII (show CAMK2G Antibodies)-mediated HDAC4 (show HDAC5 Antibodies) phosphorylation.
these data show that Treg degrade ATP to adenosine via CD39, attracting DC by activating Epac1-Rap1-dependent pathways.
EPAC1 was found to facilitate metastasis of pancreatic ductal carcinoma.
binds cAMP and activates the Ras superfamily guanine nucleotide binding protein (Rap1A)in a PKA-independent manner
Rap guanine nucleotide exchange factor (GEF) 3
, RAP guanine-nucleotide-exchange factor 3
, exchange protein directly activated by cAMP 1
, rap guanine nucleotide exchange factor 3
, Rap1 guanine-nucleotide exchange factor
, rap guanine nucleotide exchange factor 3-like
, EPAC 1
, Rap1 guanine-nucleotide-exchange factor directly activated by cAMP
, cAMP-regulated guanine nucleotide exchange factor I
, exchange factor directly activated by cAMP 1
, cAMP-regulated guanine nucleotide exchange factor I (cAMP-GEFI)
, epac 1