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ACVRL1 encodes a type I cell-surface receptor for the TGF-beta superfamily of ligands. Additionally we are shipping ACVRL1 Kits (22) and ACVRL1 Proteins (20) and many more products for this protein.
Showing 10 out of 130 products:
Human Polyclonal ACVRL1 Primary Antibody for EIA, IHC (p) - ABIN360125
Berg, Gallione, Stenzel, Johnson, Allen, Schwartz, Jackson, Porteous, Marchuk: The activin receptor-like kinase 1 gene: genomic structure and mutations in hereditary hemorrhagic telangiectasia type 2. in American journal of human genetics 1997
Show all 5 references for ABIN360125
Human Polyclonal ACVRL1 Primary Antibody for FACS, IHC (p) - ABIN392241
Strausberg, Feingold, Grouse, Derge, Klausner, Collins, Wagner, Shenmen, Schuler, Altschul, Zeeberg, Buetow, Schaefer, Bhat, Hopkins, Jordan, Moore, Max, Wang, Hsieh, Diatchenko, Marusina, Farmer et al.: Generation and initial analysis of more than 15,000 full-length human and mouse cDNA sequences. ... in Proceedings of the National Academy of Sciences of the United States of America 2002
Show all 5 references for ABIN392241
Human Polyclonal ACVRL1 Primary Antibody for WB - ABIN1944774
Attisano, Cárcamo, Ventura, Weis, Massagué, Wrana: Identification of human activin and TGF beta type I receptors that form heteromeric kinase complexes with type II receptors. in Cell 1993
Show all 3 references for ABIN1944774
Human Polyclonal ACVRL1 Primary Antibody for ELISA, WB - ABIN185181
Johnson, Berg, Baldwin, Gallione, Marondel, Yoon, Stenzel, Speer, Pericak-Vance, Diamond, Guttmacher, Jackson, Attisano, Kucherlapati, Porteous, Marchuk: Mutations in the activin receptor-like kinase 1 gene in hereditary haemorrhagic telangiectasia type 2. in Nature genetics 1996
Human Polyclonal ACVRL1 Primary Antibody for EIA, IF - ABIN360124
Yu, Pisitkun, Wang, Shen, Knepper: LC-MS/MS analysis of apical and basolateral plasma membranes of rat renal collecting duct cells. in Molecular & cellular proteomics : MCP 2006
Results show that ALK5 (show TGFBR1 Antibodies) and ALK1 play antagonistic roles in TGF-beta (show TGFB1 Antibodies)-induced podosome formation in aortic endothelial cells.
ALK1 and ALK5 are both essential for correct regulation of VEGF, and that disruption of either pathway leads to disease.
Control of Notch (show NOTCH1 Antibodies) targets in arterial endothelium is context-dependent, with gene-specific and region-specific requirements for Notch (show NOTCH1 Antibodies) 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 (show TGFB1 Antibodies) type I receptor that is expressed predominantly in the endothelium of the vessels that become dilated in vbg mutants.
The genetic-interactions among BMPR-2 (show BMPR2 Antibodies), ALK-1, and 5-HTT (show SLC6A4 Antibodies) polymorphisms, elevated BMP-2 (show BMP2 Antibodies) and 5-HT (show DDC Antibodies) levels and differential gene expression substantiated the strong genetic contribution in high altitude pulmonary edema pathophysiology.
Study of four patients with pulmonary arterial hypertension associated with human immunodeficiency virus infection found predisposing mutations in the BMPR2 (show BMPR2 Antibodies), ACVRL1 and ENG (show ENG Antibodies) genes.
The preponderance of ACVRL1 mutations was due to founder mutations, specifically, c.830C>A (p.Thr277Lys), which was found in 24 families from the same geographical area of Norway.
Report interaction between ALK1 signaling and connexin40 in the development of arteriovenous malformations.
Data suggest ALK1 and ACVR2A (show ACVR2A Antibodies)/ACVR2B (show ACVR2B Antibodies), acting as BMP9 (show GDF2 Antibodies) co-receptors, rearrange pro-domains of BMP9 (show GDF2 Antibodies)--pro-domain dimer complex leading to displacement of pro-domains after receptor binding, release of mature non-dimer BPM9, and activation of signaling.
Short hairpin-mediated downregulation of either ALK5 (show TGFBR1 Antibodies) or ALK1 resulted in a strong inhibition of TGFbeta (show TGFB1 Antibodies)-induced chondrogenesis.
This work was designed to examine the pathogenicity of 23 nucleotide variations in ACVRL1 gene detected in more than 400 Hereditary Hemorrhagic Telangiectasia syndrome patients.
The ACVRL1 c.314-35A>G polymorphism is associated with organ vascular malformations in hereditary hemorrhagic telangiectasia patients with ENG (show ENG Antibodies) mutations, but not in patients with ACVRL1 mutations.
bone morphogenic proteins within the serum of cell culture medium are potent inducers of endothelial Hey1 (show HEY1 Antibodies) and Hey2 (show HEY2 Antibodies) gene expression within the first few hours after medium change
endoglin (show ENG Antibodies) and ALK1 have been identified as potential therapeutic targets for antibody treatment in various cancers.
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.
In vascular sprouting, neuropilin-1 (show NRP1 Antibodies) suppresses the stalk-cell phenotype by limiting Smad2 (show SMAD2 Antibodies)/3 activation through Alk1 and Alk5 (show TGFBR1 Antibodies). Notch (show NOTCH1 Antibodies) downregulates Nrp1 (show NRP1 Antibodies), thus relieving the inhibition of Alk1 and Alk5 (show TGFBR1 Antibodies), thereby driving stalk-cell behaviour.
BMP9 (show GDF2 Antibodies)/ALK1 augmented vasculogenesis and angiogenesis, and thereby enhanced neovascularization. Thus, we suggest that BMP9 (show GDF2 Antibodies)/ALK1 may improve the efficacy of EPC (show TCF21 Antibodies)-based therapies for treating ischemic diseases.
BMP-9 (show GDF2 Antibodies) induces vascular smooth muscle cell osteogenic differentiation and calcification via ALK1, Smad (show SMAD1 Antibodies) and ALP (show CCL21A Antibodies) dependent mechanisms.
during development, endothelial Acvrl1 plays an essential role to regulate endothelial cell proliferation and arterial identity during angiogenesis, whilst in adult life endothelial Acvrl1 is required to maintain vascular integrity.
ALK1 modulates obstruction-induced renal fibrosis by increased extracellular matrix synthesis in myofibroblasts, but without differences in myofibroblast number.
the mechanisms responsible for the angiogenic imbalance and the response to anti-VEGF (show VEGFA Antibodies) therapy differ between Eng (show ENG Antibodies) and Alk1 heterozygous mice and raise the need for systemic monitoring of anti-angiogenic therapy effects in HHT patients.
Deletion of Alk1 in endothelial cells in adult mice leads to an increased local endothelial cell proliferation during brain angiogenesis
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