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Hyperinsulinemia caused significant changes in endothelin receptor expression, which suggested that ETR antagonists might be beneficial for treatment of laminitis in horses.
both endothelin A and endothelin B receptors are involved in the net tonic response to ET-1 (show EDN1 ELISA Kits) in normal laminar veins.
Data suggest that edn1 (show EDN1 ELISA Kits)/ednraa (endothelin-1/endothelin-1 (show EDN1 ELISA Kits) receptor type A) signaling is involved in acid-base regulation and transepithelial proton secretion via vacuolar proton-translocating ATPase (show DNAH8 ELISA Kits) in zebrafish embryonic skin.
Edn1 (show EDN1 ELISA Kits) from the pharyngeal ectoderm signals through Ednra proteins to direct early dorsoventral patterning of the skeletogenic neural crest.
A new role for ednra signaling during early neural crest specification is reported.
ETA and ETB (show EDNRB ELISA Kits) receptors are present in human haemorrhoids with ETB (show EDNRB ELISA Kits) receptors predominating
ETAR stimulation acted via downstream G-protein Galphaq (show GNAQ ELISA Kits)/11 and Rho GTPase (show RACGAP1 ELISA Kits) to suppress the Hippo pathway, thus leading to YAP (show YAP1 ELISA Kits)/TAZ (show TAZ ELISA Kits) activation, which was required for ETAR-induced tumorigenesis. Overall, these results indicate a critical role of the YAP (show YAP1 ELISA Kits)/TAZ (show TAZ ELISA Kits) axis in ETAR signaling
Data show that endothelin A receptor drives invadopodia function by direct interaction of beta-arrestin-1 (show ARRB1 ELISA Kits) (beta-arr1 (show ARRB1 ELISA Kits)) with Rho guanine nucleotide exchange factor (GEF) 11 (show ARHGEF11 ELISA Kits) protein (PDZ-RhoGEF (show ARHGEF11 ELISA Kits)).
In control arteries, ETAR was expressed by vascular smooth muscle cells in the media whereas ETBR (show EDNRB ELISA Kits) was hardly detected. In giant cell arteritis, both ETAR and ETBR (show EDNRB ELISA Kits) receptors were expressed by alphaSMA (show ACTA2 ELISA Kits)-positive cells at the intima-media border. Endothelial cells and inflammatory cells also expressed both ET receptors.
Increased circulating Edn1 (show EDN1 ELISA Kits) and expression of Ednra in endothelial cells are characteristic of diabetic kidney disease.
Data suggest that TNFalpha (tumor necrosis factor-alpha (show TNF ELISA Kits)) induces proliferation of airway smooth muscle cells via ET1 (endothelin-1 (show EDN1 ELISA Kits)), GM-CSF (granulocyte-macrophage colony-stimulating factor (show CSF2 ELISA Kits)), and IL6 (interleukin 6 (show IL6 ELISA Kits)) signaling; ET1 (show EDN1 ELISA Kits) induces cell proliferation via ETAR (endothelin receptor type A); ETBR (endothelin receptor type B (show EDNRB ELISA Kits)) is up-regulated by TNFalpha (show TNF ELISA Kits) and appears to mediate ET1 (show EDN1 ELISA Kits) effects on cell proliferation.
presence of ET-1 (show EDN1 ELISA Kits) receptors in the chronic thrombus in proximal CTEPH suggests ET-1 (show EDN1 ELISA Kits) could act not only on the distal vasculopathy in the unobstructed vessels but may also stimulate smooth muscle cell proliferation within chronic clot (show TXNDC17 ELISA Kits)
Data show that auriculo-condylar syndrome (ACS (show PLA2G15 ELISA Kits))-associated mutations in G protein subunit alpha i3 (GNAI3 (show GNAI3 ELISA Kits)) produce dominant-negative Galpha (show SUCLG1 ELISA Kits)(i3) mutant proteins that couple to endothelin type A receptor (ET(A)R).
Patients with lung fibrosis and patients with high modified Rodnan skin score showed a reduced endothelin 1 (show EDN1 ELISA Kits) Type A receptor (ETAR)/ETBR (show EDNRB ELISA Kits) ratio.
High ETAR expression is associated with ovarian carcinoma.
AMPK (show PRKAA1 ELISA Kits) was sufficient to stimulate osteogenesis of MC3T3-E1 cells and inhibit adipogenesis of 3T3-L1 cells through the AMPK (show PRKAA1 ELISA Kits)-Gfi1 (show ZNF163 ELISA Kits)-OPN (show SPP1 ELISA Kits) axis.
Excess osteopontin (show SPP1 ELISA Kits) exacerbated sarcolemmal injury, and correspondingly, that loss of osteopontin (show SPP1 ELISA Kits) reduced injury extent both in isolated myofibers and in muscle.
A MMP-9 (show MMP9 ELISA Kits)-cleaved OPN (show SPP1 ELISA Kits) fragment, OPN (show SPP1 ELISA Kits)-32kDa (show TXNL1 ELISA Kits), was responsible for inducing expansion of myeloid-derived suppressor cells, which may contribute to 3LL tumor's evasion of the immune response.
OPN (show SPP1 ELISA Kits) played a critical role in activating the migration of Mesenchymal stem cells to injured sites and their differentiation into specific skin cell types during skin wound healing.
Findings demonstrate that claudin-low mammary tumor cells rely on OPN (show SPP1 ELISA Kits) for proliferation, survival and migration as knockdown of OPN (show SPP1 ELISA Kits) using siRNA inhibited proliferation and migration while increasing apoptosis.
endothelin A receptor activation on mesangial cells is a key event in initiation of Alport glomerular disease in this mouse model.
TSC1 (show TSC1 ELISA Kits)/TSC2 (show TSC2 ELISA Kits) complex upregulation of OPN (show SPP1 ELISA Kits) expression is mediated by transcription factor SOX9 (show SOX9 ELISA Kits) in an mTOR (show FRAP1 ELISA Kits)-independent manner. Moreover, ablation of OPN (show SPP1 ELISA Kits) by deficient TSC1 (show TSC1 ELISA Kits)/TSC2 (show TSC2 ELISA Kits) complex contributed to inactivation of AKT (show AKT1 ELISA Kits) in TSC (show SLC12A3 ELISA Kits) cells
Intracellular OPN (show SPP1 ELISA Kits) (iOPN) diminished the population size of myeloid progenitor cells and myeloid cells, and secreted OPN (show SPP1 ELISA Kits) (sOPN) increase the population size of lymphoid cells. The total effect of OPN (show SPP1 ELISA Kits) on skewing the leukocyte population balance was observed as host sensitivity to early systemic infection with Candida albicans and T cell-mediated colitis.
this study shows that OPN (show SPP1 ELISA Kits) promotes sepsis in Pseudomonas aeruginosa-infected mice and potentially blocks B cell-dependent immunity
observed a marked decrease of renal gene expression and urinary excretion of osteopontin in Npt2a(-/-) mice
sub-vasomotor concentration of ET-1 (show EDN1 ELISA Kits) leads to vascular dysfunction by impairing endothelium-dependent NO-mediated dilation via p38 (show MAPK14 ELISA Kits) kinase-mediated production of superoxide from NADPH oxidase (show NOX1 ELISA Kits) following ETA receptor activation
PDE5 (show PDE5A ELISA Kits) inhibition and increase in cGMP produce pulmonary vasodilation that is mediated in part through inhibition of the ET pathway, thereby precluding an additional vasodilator effect of ETA/ETB (show EDNRB ELISA Kits) receptor blockade in the presence of PDE5 (show PDE5A ELISA Kits) inhibition.
Blocking ET(A) and ET(B (show EDNRB ELISA Kits)) receptors partially protects sinusoidal circulation and tissue oxygenation against stress induced by high intra-abdominal pressure (IAP (show CD47 ELISA Kits)).
Anti-endothelin receptor A therapy accelerated the reversal of flow-induced pulmonary arterial disease after flow correction.
study suggests a possible role for endothelin-1 (show EDN1 ELISA Kits)(resulting from the actions of endothelin-converting enzyme-1 (show ECE1 ELISA Kits)) acting via endothelin receptor A in the control of luteolytic sensitivity in the pig
Endothelin-A receptor antagonist alters the expression of vasoactive genes and proinflammatory cytokines during hepatic ischemic/reperfusion.
Report that inhalation of the endothelin-A receptor antagonist LU-135252 at various doses in experimental acute lung injury improved gas exchange and hemodynamics.
ET(A) blockade had no effect on pulmonary vascular resistance at rest or during exercise.
PKC (show FYN ELISA Kits) and MAPK (show MAPK1 ELISA Kits) seem to be involved in the regulation of endothelin type A and type B receptor expression in porcine coronary arteries
Data suggest that, in Fallopian tubes, endothelins (EDN1 (show EDN1 ELISA Kits), EDN2 (show EDN2 ELISA Kits), EDN3 (show EDN3 ELISA Kits)) and EDN (show RNASE2 ELISA Kits)-converting enzymes (ECE1 (show ECE1 ELISA Kits), ECE2 (show ECE2 ELISA Kits)) are expressed in epithelial cells; EDN (show RNASE2 ELISA Kits) receptors (EDNRA, EDNRB (show EDNRB ELISA Kits)) are present in smooth-muscle. Expression of EDN1 (show EDN1 ELISA Kits), EDN2 (show EDN2 ELISA Kits), and ECE2 (show ECE2 ELISA Kits) is highest on day of ovulation. EDN (show RNASE2 ELISA Kits)/ENDR signaling appears to participate Fallopian tube function. These studies were conducted in Holstein cows.
Differential cell-specific and spatiotemporal expression of the EDN1 (show EDN1 ELISA Kits) system and NOS (show NOS ELISA Kits) in the bovine utero-placental unit may be associated with regulation of vascular and cellular functions during pregnancy.
Elevated local expression of ET-1 (show EDN1 ELISA Kits) and Ednra/Ednrb (show EDNRB ELISA Kits) during the peri (show PLIN1 ELISA Kits)-ovulatory period induces the high contractile activity of the oviduct to optimize gamete transport.
This gene encodes the receptor for endothelin-1, a peptide that plays a role in potent and long-lasting vasoconstriction. This receptor associates with guanine-nucleotide-binding (G) proteins, and this coupling activates a phosphatidylinositol-calcium second messenger system. Polymorphisms in this gene have been linked to migraine headache resistance. Alternative splicing results in multiple transcript variants.
, endothelin receptor A
, endothelin receptor type A
, endothelin type-A receptor 2
, Endothelin-1 receptor type A
, endothelin receptor type A a
, G protein-coupled receptor
, endothelin receptor subtype A
, endothelin-1-specific receptor
, endothelin A receptor
, G-protein coupled receptor 10
, 44 kDa bone phosphoprotein
, bone sialoprotein 1
, calcium oxalate crystal growth inhibitor protein
, early T-lymphocyte activation 1 protein
, osteopontin-like protein