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ACVRL1 encodes a type I cell-surface receptor for the TGF-beta superfamily of ligands. Zusätzlich bieten wir Ihnen ACVRL1 Kits (26) und ACVRL1 Proteine (23) und viele weitere Produktgruppen zu diesem Protein an.
Showing 10 out of 159 products:
Human Polyclonal ACVRL1 Primary Antibody für 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
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Human Polyclonal ACVRL1 Primary Antibody für ELISA, WB - ABIN250173
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 für IHC, IHC (p) - ABIN4279393
Cunha, Pardali, Thorikay, Anderberg, Hawinkels, Goumans, Seehra, Heldin, ten Dijke, Pietras: Genetic and pharmacological targeting of activin receptor-like kinase 1 impairs tumor growth and angiogenesis. in The Journal of experimental medicine 2010
Human Polyclonal ACVRL1 Primary Antibody für WB - ABIN1944774
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
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Results show that ALK5 (zeige TGFBR1 Antikörper) and ALK1 play antagonistic roles in TGF-beta (zeige TGFB1 Antikörper)-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.
alk1 loss has no effect on arterial endothelial cell proliferation but alters arterial endothelial cell migration within lumenized vessels.
Control of Notch (zeige NOTCH1 Antikörper) targets in arterial endothelium is context-dependent, with gene-specific and region-specific requirements for Notch (zeige NOTCH1 Antikörper) 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 (zeige TGFB1 Antikörper) type I receptor that is expressed predominantly in the endothelium of the vessels that become dilated in vbg mutants.
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 (zeige GDF2 Antikörper) and BMP10 (zeige BMP10 Antikörper) 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 (zeige TGFBR1 Antikörper) predominantly expressed in actively proliferating endothelial cells (ECs).
Two novel missense mutations and two recurrent mutations in the ACVRL1 gene are associated with pulmonary arterial hypertension in in Chinese families.
ALK1 expression and microvessel density are increased in oral lichen planus , particularly in atrophic/erosive OLP type.
The genetic-interactions among BMPR-2 (zeige BMPR2 Antikörper), ALK-1, and 5-HTT (zeige SLC6A4 Antikörper) polymorphisms, elevated BMP-2 (zeige BMP2 Antikörper) and 5-HT (zeige DDC Antikörper) 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 (zeige BMPR2 Antikörper), ACVRL1 and ENG (zeige ENG Antikörper) 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.
These data indicate that both Itgb8 and Alk1 are important in maintaining normal cerebral angiogenesis in response to VEGF (zeige VEGFA Antikörper). Itgb8 deficiency enhances the formation of dysplastic vessels and hemorrhage in Alk1 (+/-) mice.
these studies characterize an accessory TGF-beta (zeige TGFB1 Antikörper)-stimulated BMP R-Smad (zeige SMAD1 Antikörper) 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 (zeige CD109 Antikörper) differentially regulates TGF-beta (zeige TGFB1 Antikörper)-induced ALK1-Smad1 (zeige SMAD1 Antikörper)/5 versus ALK5 (zeige TGFBR1 Antikörper)-Smad2 (zeige SMAD2 Antikörper)/3 pathways, leading to decreased extracellular matrix production in the skin; epidermal CD109 (zeige CD109 Antikörper) expression regulates dermal function through a paracrine mechanism
he results of the present study demonstrated that BMP9 (zeige GDF2 Antikörper) promoted the osteoclast differentiation of osteoclast precursors via binding to the ALK1 receptor on the cell surface, and inhibiting the ERK1/2 (zeige MAPK1/3 Antikörper) 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.
In vascular sprouting, neuropilin-1 (zeige NRP1 Antikörper) suppresses the stalk-cell phenotype by limiting Smad2 (zeige SMAD2 Antikörper)/3 activation through Alk1 and Alk5 (zeige TGFBR1 Antikörper). Notch (zeige NOTCH1 Antikörper) downregulates Nrp1 (zeige NRP1 Antikörper), thus relieving the inhibition of Alk1 and Alk5 (zeige TGFBR1 Antikörper), thereby driving stalk-cell behaviour.
BMP9 (zeige GDF2 Antikörper)/ALK1 augmented vasculogenesis and angiogenesis, and thereby enhanced neovascularization. Thus, we suggest that BMP9 (zeige GDF2 Antikörper)/ALK1 may improve the efficacy of EPC (zeige TCF21 Antikörper)-based therapies for treating ischemic diseases.
BMP-9 (zeige GDF2 Antikörper) induces vascular smooth muscle cell osteogenic differentiation and calcification via ALK1, Smad (zeige SMAD1 Antikörper) and ALP (zeige CCL21A Antikörper) dependent mechanisms.
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