anti-Activin A Receptor, Type IB (ACVR1B) Antibodies

Mouse (Murine) Activin A Receptor, Type IB (ACVR1B) interaction partners

1. Our study provided experimental and clinical evidence for the involvement of activin A and ALK4 in the pathophysiology of atrial fibrosis and atrial fibrillation

2. Our results demonstrate that ALK4 haploinsufficiency ameliorates cardiac fibrosis and dysfunction in a mouse pressure-overload model associated with inhibition of cardiac fibroblast activation and cardiomyocyte apoptosis through the suppression of Smad2/3 activity.

3. ALK4 is an important profibrotic signaling molecule in the post-MI CF. Haplodeficiency of ALK4 significantly improved LV function and survival rate by attenuating CF in vivo, ameliorated

4. Uterine Activin-Like Kinase 4 Regulates Trophoblast Development During Mouse Placentation

5. These results indicate that an appropriate level of activin signaling may be required for GSIS in pancreatic beta cells, and that activin signaling involves modulation of KATP channel activity.

6. Signaling through the TGF beta-activin receptors ALK4/5/7 regulates testis formation and male germ cell development.

7. identified ACVRIB as a direct target of miR-145. The ectopic expression of miR-145 reduced the levels of both ACVRIB mRNA and protein and also interfered with activin-induced Smad2 phosphorylation.

8. Results identify a molecular mechanism that explains the cell-type specific aspects of signaling by myostatin, ALK4, ALK5, and other TGF-beta family members.

9. Inhibin alpha-subunit N terminus interacts with activin type IB receptor to disrupt activin signaling.

10. Knockdown or pharmacological inhibition of the Nodal/Activin receptor Alk4/7 in cancer stem cells virtually abrogated their self-renewal capacity and in vivo tumorigenicity

11. Our analysis of this Acvr1b knockout mouse line provides direct genetic evidence that Acvr1b signaling is required for both hair follicle development and cycling.

12. analysis of expression and cellular compartmentalization of the activin receptors ActRIIA, ActRIIB and ActRIB, the inhibin co-receptor (betaglycan), and activin signaling proteins Smads 2, 3 and 4, and growth regulatory role during lactation

13. Alk4 is expressed in the early development of thymocytes.

14. activin receptor signaling is essential to optimize the performance of neuronal circuits in the mature brain under physiological conditions

15. ALK5 is required in endothelial cells and vascular smooth muscle cells for yolk sac vasculogenesis; in the absence of ALK5, ALK4 mediates SMAD2 phosphorylation and consequently SMAalpha expression.

Human Activin A Receptor, Type IB (ACVR1B) interaction partners

1. Overexpression of ALK4 suppressed glioma cell proliferation, migration and invasion through the inactivation of JAK/STAT3 signaling pathway.

2. Results showed that ACVR1B expression is upregulated during latent infection with a miR-UL148D deletion virus. Data indicates miR-UL148D inhibits ACVR1B expression in latently infected cells to limit proinflammatory cytokine secretion.

3. Our study provided experimental and clinical evidence for the involvement of activin A and ALK4 in the pathophysiology of atrial fibrosis and atrial fibrillation

4. It was concluded that ALK4 inhibition increases myogenesis but also regulates the tight balance of protein synthesis and degradation.

5. in a relatively large cohort of athletes from Europe and South America we have shown that the ACVR1B rs2854464 A allele is associated with sprint/power performance in Caucasians but not in Brazilian athletes.

6. ALK4 is an important profibrotic signaling molecule in the post-MI CF. Haplodeficiency of ALK4 significantly improved LV function and survival rate by attenuating CF in vivo, ameliorated

7. ALK4 is expressed in male germ cells and Sertoli cells.

8. This study demonstrated positive regulation of monocyte/macrophage differentiation by lnc-MC and uncovered an elaborate regulation mechanism composed of PU.1, lnc-MC, miR-199a-5p, and ACVR1B.

9. Data suggest that activin A up-regulates SNAIL expression via ALK4/ACVR1B-induced SMAD signaling in trophoblast cells; elevated SNAIL contributes to up-regulation of MMP2 expression which plays key role in promoting trophoblast cell invasion.

10. ACVR1B functions as a positive regulator of monocyte/macrophage differentiation. ACVR1B knockdown promoted THP-1 proliferation by increasing Rb phosphorylation. Down-regulation reduced p-Smad2/3 and C/EBPalpha, inhibiting monocyte/macrophage differentiation.

11. The deletion of the ACVR1B gene may mediate an aggressive cancer phenotype in pancreatic cancer.

12. Findings define a regulatory role of miR-98 in tumor angiogenesis and invasion through repressed ALK4 and MMP11 expression.

13. ActRIBCA signaling can promote cell migration in prostate cancer cells via a network of signaling molecules that work together to trigger the process of EMT, and thereby aid in the aggressiveness and progression of prostate cancers.

14. Act A protein levels were significantly higher in NTM tissues compared to GTM tissues.

15. Inhibin alpha-subunit N terminus interacts with activin type IB receptor to disrupt activin signaling.

16. Activin A-ACVRIB/ALK4-Smad-dependent collagen production was augmented in SSc fibroblasts, suggesting the involvement of this signaling mechanism in systemic sclerosis.

17. We applied a two-stage fine mapping approach, and are the first to identify and partially replicate genetic variants in the ACVR1B gene that account for genetic variation in human muscle strength.

18. activin A signal is transduced through the activin A type 1 receptor, ALK4, and transactivates several TGF-beta target genes in a SMAD-independent manner.

19. distribution in gestational tissues across human pregnancy and during labour

20. data indicate that truncated Alk4 isoforms interfere with activin signaling pathways and thereby may contribute to uncontrolled cell growth