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ACVRL1 encodes a type I cell-surface receptor for the TGF-beta superfamily of ligands. 再加上，我们可以发ACVRL1 抗体 (173) 和 ACVRL1 蛋白 (26)和数多这个蛋白质的别的产品。
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Results show that ALK5 (显示 TGFBR1 ELISA试剂盒) and ALK1 play antagonistic roles in TGF-beta (显示 TGFB1 ELISA试剂盒)-induced podosome formation in aortic endothelial cells.
ALK1 and ALK5 (显示 TGFBR1 ELISA试剂盒) are both essential for correct regulation of VEGF (显示 VEGFA ELISA试剂盒), and that disruption of either pathway leads to disease.
alk1 loss has no effect on arterial endothelial cell proliferation but alters arterial endothelial cell migration within lumenized vessels.
Control of Notch (显示 NOTCH1 ELISA试剂盒) targets in arterial endothelium is context-dependent, with gene-specific and region-specific requirements for Notch (显示 NOTCH1 ELISA试剂盒) and Alk1
Blood flow is required not only for alk1 expression but also for Alk1 activity.
Study demonstrate that alk1 expression requires blood flow, and despite normal levels of shear stress, some flow-responsive genes are dysregulated in alk1 mutant arterial endothelial cells.
vbg encodes activin receptor-like kinase 1 (acvrl1), a TGFbeta (显示 TGFB1 ELISA试剂盒) type I receptor that is expressed predominantly in the endothelium of the vessels that become dilated in vbg mutants.
We have identified a novel role for ALK1 in cardiac remodeling
The present study showed that deletion-duplication mutations in the BMPR2 (显示 BMPR2 ELISA试剂盒) or ACVRL1 genes may not be associated with non-regression of Pulmonary arterial hypertension.
Study identified 2 non-synonymous missense mutations: c.C652T, p.R218W in ACVRL1, c.C717G, p.D239E in SGCD (显示 SGCD ELISA试剂盒) in Chinese population with total anomalous pulmonary venous return.
Mutations in ACVRL1 gene encoding for transforming growth factor (TGF)-[beta] superfamily have been identified in Pulmonary Arterial Hypertension.
Treatment-related telangiectasia was noted in 7% of patients, suggesting in vivo inhibition of the ALK-1 pathway.
Data indicate that simultaneous targeting of molecules that control distinct phases of angiogenesis, such as ALK1 and VEGFR, is a valid strategy for treatment of metastatic renal cell carcinoma (mRCC).
Study showed that rs706819, rs2293094, and rs11169953 polymorphisms in the ACVRL1 gene are associated with higher susceptibility to brain arteriovenous malformations.
c.1027C > T(p.Gln343) mutation within the ACVRL1 gene in family with hereditary hemorrhagic telangiectasia
Bone morphogenetic protein (BMP)9 (显示 GDF2 ELISA试剂盒) and BMP10 (显示 BMP10 ELISA试剂盒) are high affinity ligands for activin receptor-like kinase 1 (ALK1).
Activin receptor-like kinase (ALK)1 is a transforming growth factor beta (TGF-beta) type I receptor (显示 TGFBR1 ELISA试剂盒) predominantly expressed in actively proliferating endothelial cells (ECs).
Data show that concomitant activin receptor-like kinase 1 (Acvrl1) and endoglin (Eng (显示 ENG ELISA试剂盒)) deficiency synergistically decreases pancreatic neuroendocrine tumor volume.
Global deletion of AlK-1 is associated with the development of high output heart failure without maladaptive remodeling.
These data indicate that both Itgb8 and Alk1 are important in maintaining normal cerebral angiogenesis in response to VEGF (显示 VEGFA ELISA试剂盒). Itgb8 deficiency enhances the formation of dysplastic vessels and hemorrhage in Alk1 (+/-) mice.
these studies characterize an accessory TGF-beta (显示 TGFB1 ELISA试剂盒)-stimulated BMP R-Smad (显示 SMAD1 ELISA试剂盒) signaling mechanism in interstitial cells of the developing lung.
this study demonstrates that ACVRL1 signaling plays a pivotal role whereby it suppresses plasmacytoid dendritic cell development while enhancing that of CD8alpha(+) dendritic cells, thus contributing to DC diversity development.
CD109 (显示 CD109 ELISA试剂盒) differentially regulates TGF-beta (显示 TGFB1 ELISA试剂盒)-induced ALK1-Smad1 (显示 SMAD1 ELISA试剂盒)/5 versus ALK5 (显示 TGFBR1 ELISA试剂盒)-Smad2 (显示 SMAD2 ELISA试剂盒)/3 pathways, leading to decreased extracellular matrix production in the skin; epidermal CD109 (显示 CD109 ELISA试剂盒) expression regulates dermal function through a paracrine mechanism
he results of the present study demonstrated that BMP9 (显示 GDF2 ELISA试剂盒) promoted the osteoclast differentiation of osteoclast precursors via binding to the ALK1 receptor on the cell surface, and inhibiting the ERK1/2 (显示 MAPK1/3 ELISA试剂盒) signaling pathways in the cell
Conclude that the ALK-1 receptor is involved in the control of arterial pressure. High AP of Alk1(+/-) mice is explained mainly by the sympathetic overactivation, which is probably related to the decreased number of cholinergic neurons.
Report interaction between ALK1 signaling and connexin40 in the development of arteriovenous malformations.
This gene encodes a type I cell-surface receptor for the TGF-beta superfamily of ligands. It shares with other type I receptors a high degree of similarity in serine-threonine kinase subdomains, a glycine- and serine-rich region (called the GS domain) preceding the kinase domain, and a short C-terminal tail. The encoded protein, sometimes termed ALK1, shares similar domain structures with other closely related ALK or activin receptor-like kinase proteins that form a subfamily of receptor serine/threonine kinases. Mutations in this gene are associated with hemorrhagic telangiectasia type 2, also known as Rendu-Osler-Weber syndrome 2.
activin A receptor type II-like 1
, serine/threonine-protein kinase receptor R3
, serine/threonine-protein kinase receptor R3-like
, activin receptor-like kinase 1
, violet beauregarde
, TGF-B superfamily receptor type I
, activin A receptor, type II-like kinase 1
, Activin receptor like kinase 1
, activin receptor-like kinase-1