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Cyclic AMP (cAMP), a secondary messenger responsible for various physiological processes regulates cell metabolism by activating Protein kinase A (PKA) and by targeting exchange protein directly activated by cAMP (EPAC). EPAC is present in two isoforms EPAC1 and EPAC2, which exhibit different tissue distribution and is involved in GDP/GTP exchange along with activating Rap1- and Rap2-mediated signaling pathways.
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Study identifies Epac2-Rap1 signaling as a novel feedback mechanism in the heart, which controls mitochondrial reactive oxygen species production.
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rs17746510, one of the three single-nucleotide polymorphisms (SNPs) in RAPGEF4 associated with cognitive decline in Chinese Alzheimer's disease (AD) patients, was significantly correlated with apathy and mood disturbance
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This review focus is on the function of Epac in the heart. Accumulating evidence has revealed that both Epac1 and Epac2 play important roles in the structure and function of the heart under physiological and pathological conditions. [review]
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Data show that Epac2 is activated by cAMP and changes its structure. It is involved in cAMP-mediated signal transduction through activation of the Ras-like small GTPase and is expressed mainly in brain, neuroendocrine and endocrine tissues. [review]
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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, display distinct subcellular distributions.
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CALR regulated by EPAC2 in endometrial glandular epithelial cells is critical for the expression of LIF and PTGS2-mediated production of PGE2 through cAMP signaling.
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Follow-up replication analyses in up to an additional 21,345 participants identified three new fasting plasma glucose loci reaching genome-wide significance in or near PDK1-RAPGEF4, KANK1, and IGF1R.
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EPAC1 and EPAC2 are critical signaling intermediates in osteoclast differentiation that permit RANKL-stimulated NFkB nuclear translocation and actin rearrangements
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data show the expression of EPAC is blunted in HPRT-deficient neuron-like cell lines and fibroblast cells from Lesch-Nyhan syndrome (LNS) patients; propose that the alterations in EPAC/RAP1 signaling and cell migration in HPRT deficiency are crucial for neuro-developmental events that may contribute to neurological dysfunctions in LNS
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EPAC2-mediated CRT expression is essential for the functional and morphological differentiation of endometrial stromal cells into decidual cells
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Cigarette smoke extract decreased Epac1 expression, but did not affect Epac2 and PKA expression.
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Mechanism of intracellular cAMP sensor Epac2 activation: cAMP-induced conformational changes identified by amide hydrogen/deuterium exchange mass spectrometry
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An important time-limited role is identified for hippocampal Epac2 signaling in cognition, opening new avenues to investigate the molecular mechanisms underlying memory retrieval.
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Epac2 & Epac1 signaling pathways may be associated with cAMP-mediated functional differentiation and syncytialization of trophoblasts. Expression of Epac2 & Epac 1 in placenta at different stages was investigated.
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Studies demonstrate the occurrence of the EPAC2 splicing variant EPAC2B in adrenocortical cancer cells and reveal the involvement of EPAC2B in cAMP-induced effects on cytoskeleton integrity and cell migration.
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Mutations in the hinge of Epac can uncouple cAMP binding from its exchange activity.
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variants were present in five families, where they segregate with the autistic phenotype.
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a novel protein-binding partner for EPAC1 and EPAC2, light chain 2 of MAP1A (microtubule-associated protein 1A)
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Epac1 and Epac2 induce a potent activation of the Ca2+-sensitive big K+ channel, slight membrane hyperpolarization, and increased after-hyperpolarization in cultured cerebellar granule cells. These effects involve activation of Rap and p38 MAPK.
