anti-Activin A Receptor Type II-Like 1 (ACVRL1) Antibodies

Cow (Bovine) Activin A Receptor Type II-Like 1 (ACVRL1) interaction partners

1. Results show that ALK5 and ALK1 play antagonistic roles in TGF-beta-induced podosome formation in aortic endothelial cells.

2. ALK1 and ALK5 are both essential for correct regulation of VEGF, and that disruption of either pathway leads to disease.

Zebrafish Activin A Receptor Type II-Like 1 (ACVRL1) interaction partners

1. alk1 loss has no effect on arterial endothelial cell proliferation but alters arterial endothelial cell migration within lumenized vessels.

2. Control of Notch targets in arterial endothelium is context-dependent, with gene-specific and region-specific requirements for Notch and Alk1

3. Blood flow is required not only for alk1 expression but also for Alk1 activity.

4. 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.

5. vbg encodes activin receptor-like kinase 1 (acvrl1), a TGFbeta type I receptor that is expressed predominantly in the endothelium of the vessels that become dilated in vbg mutants.

Human Activin A Receptor Type II-Like 1 (ACVRL1) interaction partners

1. Despite the difficulty of interpreting deep intronic variants, our study highlights the importance of non-coding regions in the disease mechanism of HHT, particularly the CT-rich hotspot region of ACVRL1intron 9. The addition of this region to HHT molecular diagnostic testing algorithms will improve clinical sensitivity.

2. Recurrent epistaxis is the main manifestation of hereditary hemorrhagic telangiectasia in this family. The mutation of ACVRL1 gene is the pathogenic gene of this family.

3. The SNPs of the rs6435156 and rs1048829 locus in the BMPR2 gene, the rs121909287 loci in the ACVRL1 gene, and the rs397514716 locus in the SMAD9 gene were associated with a risk of essential hypertension (EH) in Han Chinese.

4. Loss of ALK1 function in endothelial cells results in increased activity of the PI3K pathway and vascular hyperplasia.

5. ACVRL1 expression could serve as a prognostic biomarker in metastatic colorectal cancer patients receiving chemotherapy and bevacizumab.

6. Heterozygous SNP, rs372023206, was found in all tested patients with idiopathic pulmonary hypertension (heterozygosity).

7. ENG, ACVRL1, and SMAD4 mutations result in different phenotypes in hereditary hemorrhagic telangiectasia

8. ENG mutation carriers were more likely than ACVRL1 mutation carriers to have pAVMs (P < 0.001) or multiple lesions (P = 0.03), and to undergo procedural intervention (P = 0.02). The HHT severity score was significantly higher in ENG than in ACVRL1 (P = 0.02).

9. These studies identified pathways mediating LDLR-independent uptake of LDL may provide unique opportunities to block the initiation of LDL accumulation in the vessel wall or augment hepatic LDLR-dependent clearance of LDL.

10. We have identified a novel role for ALK1 in cardiac remodeling

11. The present study showed that deletion-duplication mutations in the BMPR2 or ACVRL1 genes may not be associated with non-regression of Pulmonary arterial hypertension.

12. Study identified 2 non-synonymous missense mutations: c.C652T, p.R218W in ACVRL1, c.C717G, p.D239E in SGCD in Chinese population with total anomalous pulmonary venous return.

13. Mutations in ACVRL1 gene encoding for transforming growth factor (TGF)-[beta] superfamily have been identified in Pulmonary Arterial Hypertension.

14. Treatment-related telangiectasia was noted in 7% of patients, suggesting in vivo inhibition of the ALK-1 pathway.

15. 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).

16. Study showed that rs706819, rs2293094, and rs11169953 polymorphisms in the ACVRL1 gene are associated with higher susceptibility to brain arteriovenous malformations.

17. c.1027C > T(p.Gln343) mutation within the ACVRL1 gene in family with hereditary hemorrhagic telangiectasia

18. Bone morphogenetic protein (BMP)9 and BMP10 are high affinity ligands for activin receptor-like kinase 1 (ALK1).

19. Activin receptor-like kinase (ALK)1 is a transforming growth factor beta (TGF-beta) type I receptor predominantly expressed in actively proliferating endothelial cells (ECs).

20. Two novel missense mutations and two recurrent mutations in the ACVRL1 gene are associated with pulmonary arterial hypertension in in Chinese families.

Mouse (Murine) Activin A Receptor Type II-Like 1 (ACVRL1) interaction partners

1. Loss of ALK1 function in endothelial cells results in increased activity of the PI3K pathway and vascular hyperplasia.

2. our data show that in a tumor environment BMP9 and BMP10 play different roles and thus blocking their shared receptor ALK1 is maybe not appropriate. Indeed, BMP9, but not BMP10, acts as a quiescence factor on tumor growth, lung metastasis and vessel normalization.

3. These studies identified pathways mediating LDLR-independent uptake of LDL may provide unique opportunities to block the initiation of LDL accumulation in the vessel wall or augment hepatic LDLR-dependent clearance of LDL.

4. We have identified a novel role for ALK1 in cardiac remodeling

5. Data show that concomitant activin receptor-like kinase 1 (Acvrl1) and endoglin (Eng) deficiency synergistically decreases pancreatic neuroendocrine tumor volume.

6. Global deletion of AlK-1 is associated with the development of high output heart failure without maladaptive remodeling.

7. These data indicate that both Itgb8 and Alk1 are important in maintaining normal cerebral angiogenesis in response to VEGF. Itgb8 deficiency enhances the formation of dysplastic vessels and hemorrhage in Alk1 (+/-) mice.

8. these studies characterize an accessory TGF-beta-stimulated BMP R-Smad signaling mechanism in interstitial cells of the developing lung.

9. 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.

10. CD109 differentially regulates TGF-beta-induced ALK1-Smad1/5 versus ALK5-Smad2/3 pathways, leading to decreased extracellular matrix production in the skin; epidermal CD109 expression regulates dermal function through a paracrine mechanism

11. he results of the present study demonstrated that BMP9 promoted the osteoclast differentiation of osteoclast precursors via binding to the ALK1 receptor on the cell surface, and inhibiting the ERK1/2 signaling pathways in the cell

12. 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.

13. Report interaction between ALK1 signaling and connexin40 in the development of arteriovenous malformations.

14. In vascular sprouting, neuropilin-1 suppresses the stalk-cell phenotype by limiting Smad2/3 activation through Alk1 and Alk5. Notch downregulates Nrp1, thus relieving the inhibition of Alk1 and Alk5, thereby driving stalk-cell behaviour.

15. BMP9/ALK1 augmented vasculogenesis and angiogenesis, and thereby enhanced neovascularization. Thus, we suggest that BMP9/ALK1 may improve the efficacy of EPC-based therapies for treating ischemic diseases.

16. BMP-9 induces vascular smooth muscle cell osteogenic differentiation and calcification via ALK1, Smad and ALP dependent mechanisms.

17. 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.

18. Results show that ALK5 and ALK1 play antagonistic roles in TGF-beta-induced podosome formation in aortic endothelial cells.

19. ALK1 modulates obstruction-induced renal fibrosis by increased extracellular matrix synthesis in myofibroblasts, but without differences in myofibroblast number.

20. the mechanisms responsible for the angiogenic imbalance and the response to anti-VEGF therapy differ between Eng and Alk1 heterozygous mice and raise the need for systemic monitoring of anti-angiogenic therapy effects in HHT patients.