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KCNK2 encodes one of the members of the two-pore-domain background potassium channel protein family. De plus, nous expédions KCNK2 Protéines (4) et beaucoup plus de produits pour cette protéine.
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Cow (Bovine) Polyclonal KCNK2 Primary Antibody pour WB - ABIN188929
Zhang, Yin, Wang, Li, Wang: Over-expressed human TREK-1 inhibits CHO cell proliferation via inhibiting PKA and p38 MAPK pathways and subsequently inducing G1 arrest. dans Acta pharmacologica Sinica 2016
ANG II inhibits bTREK-1 K(+) channels by a Ca(2+)-dependent mechanism that does not require the depletion of membrane-associated PIP(2).
Metabolites of cAMP stimulate TREK-1 expression in adrenal cortex cells by activation of a novel cAMP-independent mechanism.
TREK-1 channels may function as sensors that couple the metabolic state of the cell to membrane potential, perhaps through an associated ATP-binding protein
These results identify bTREK-1 K(+) channels as a pivotal control point where ANG II (Montrer AGT Anticorps) receptor activation is transduced to depolarization-dependent Ca(2 (Montrer CA2 Anticorps)+) entry and aldosterone secretion.
Data show that angiotensin II and paracrine factors that act through phospholipase C (Montrer PLC Anticorps) inhibit bTREK-1 in adrenocortical cells through simultaneous activation of separate Ca2 (Montrer CA2 Anticorps)+- and ATP hydrolysis-dependent signaling pathways.
Angiotensin II (ANGII) inhibits adrenocortical cell KCNK2 in an ATP dependent, PLC/PKC independent manner.
These findings demonstrate that, in addition to the well-described PKA-dependent TREK-1 inhibition, ACTH (Montrer POMC Anticorps), NPS (Montrer NPS Anticorps)-ACTH (Montrer POMC Anticorps), forskolin, and 8-pCPT-2'-O-Me-cAMP also inhibit these K(+) channels by a PKA-independent signaling pathway.
data reveal a druggable K2P site that stabilizes the C-type gate 'leak mode' and provide direct evidence for K2P selectivity filter gating
decreased TREK-1 expression in the aganglionic and ganglionic bowel observed in Hirschsprung's disease may alter intestinal epithelial barrier function leading to the development of enterocolitis
Atrial TREK-1 expression was reduced in atrial fibrillation patients with concomitant severe heart failure
The authors identified a heterozygous point mutation in the selectivity filter of the stretch-activated K2P potassium channel (Montrer KCNAB2 Anticorps) TREK-1 (KCNK2 or K2P2.1). This mutation introduces abnormal sodium permeability and stretch-activation hypersensitivity to TREK-1.
The M2-glycine hinge controls the macroscopic currents of TREK1 channels.
TREK-1 overexpression suppresses CHO (Montrer COL11A1 Anticorps) cell proliferation by inhibiting the activity of PKA and p38/MAPK (Montrer MAPK14 Anticorps) signaling pathways and subsequently inducing G1 phase cell arrest.
Trek1 expression facilitates the restoration of intestinal epithelial barrier functions in an allergic environment.
presence of TREK-1 variants correlated to reduced TREK-1 activity, suggesting a pathological role for TREK-1 variants in preterm labor
Data suggest that potassium channel protein (Montrer KCNQ5 Anticorps) TREK-1 (TREK-1) might be a biomarker in castration resistance free survival (CRFS) judgment of prostate cancer (PCa (Montrer FLVCR1 Anticorps)), as well as a potential therapeutic target.
During conductance simulation experiments, both TASK-3 (Montrer KCNK9 Anticorps) and TREK-1 channels were able to repolarise the membrane once AP threshold was reached
Data demonstrate that inhibition of TWIK (Montrer KCNK1 Anticorps)-related K(+) channel (Montrer KCNC4 Anticorps)-1 (TREK-1) protects mice from cognitive impairment induced by anesthesia and TREK-1 is a potential therapeutic target against memory impairment induced by volatile anesthetics.
Hyperoxia treatment of TREK-1/TREK-2 (Montrer KCNK10 Anticorps)/TRAAK (Montrer KCNK4 Anticorps)-deficient mice is associated with a reduction in surfactant proteins
TREK-1 deficiency promoted neurons and oligodendrocytes apoptosis, aggravated demyelination and retarded motor recovery following spinal cord injury.
Formation of TREK-1/TREK-2 (Montrer KCNK10 Anticorps) channels was also demonstrated in native dorsal root ganglion neurons indicating that heterodimerization may provide greater diversity of leak K(+) conductances also in native tissues.
Data suggest that porosome-associated proteins SNAP25 (Montrer SNAP25 Anticorps), TREK-1, syntaxin-1A (Montrer STX1A Anticorps), and Gai3 exhibit stability and functionality such that isolated proteins can be reconstituted as insulin (Montrer INS Anticorps)-secreting porosomes in cell membrane of live cells.
Data indicate that arginine vasopressin (AVP (Montrer AVP Anticorps)) and corticotropin-releasing hormone (CRH (Montrer CRH Anticorps)) show additive effects on the suppression of the potassium channel subfamily K member 2 TREK-1 current via protein kinase C (Montrer PKC Anticorps).
TWIK-1 (Montrer KCNK1 Anticorps)/TREK-1 heterodimers mediate astrocytic passive conductance and cannabinoid-induced glutamate (Montrer GRIN1 Anticorps) release from astrocytes.
In TREK1-deficient mice, brain endothelial cells displayed an inflammatory phenotype.
This gene encodes one of the members of the two-pore-domain background potassium channel protein family. This type of potassium channel is formed by two homodimers that create a channel that leaks potassium out of the cell to control resting membrane potential. The channel can be opened, however, by certain anesthetics, membrane stretching, intracellular acidosis, and heat. Three transcript variants encoding different isoforms have been found for this gene.
potassium channel subfamily K member 2
, potassium channel, subfamily K, member 2
, potassium channel subfamily K member 2-like
, K2P2.1 potassium channel
, TREK-1 K(+) channel subunit
, TWIK-related potassium channel 1
, outward rectifying potassium channel protein TREK-1
, potassium inwardly-rectifying channel, subfamily K, member 2
, tandem-pore-domain potassium channel TREK-1
, two pore domain potassium channel TREK-1
, two pore potassium channel TPKC1
, two-pore potassium channel 1
, arachidonic acid sensitive tandem pore domain potassium channel
, ion transport membrane protein