ACVRL1 Rabbit Recombinant mAb

Catalog No.A5397

Description

Specificity	ACVRL1 Rabbit Recombinant mAb detects endogenous level of total ACVRL1.
Background	ACVRL1 (Serine/threonine-protein kinase receptor R3, activin receptor-like kinase 1 and ALK1) is a receptor in the TGF beta signaling pathway. Activation of ALK1 results from the binding of several different ligands of the TGF-β family, including bone morphogenetic protein (BMP) 9, BMP10, and TGF-β. ALK1 is predominantly expressed in endothelial cells and at specific sites of epithelial-mesenchymal interactions, stimulates Smad1 and Smad5 phosphorylation. The TGFβ/ALK5 and TGFβ/ALK1 pathways have opposite effects on endothelial cells (ECs) behavior; ALK5 inhibits EC migration and proliferation while ALK1 stimulates both processes. ALK1 is a negative mediator of lateral TGFβ/ALK5 signaling and its optimal activation requires ALK5 kinase activity. TGFβ regulates cellular processes by binding to a heteromeric complex of type I and type II serine/threonine kinase receptors. In most cell types, TGFβ initially binds TβRII and subsequently recruits and phosphorylates ALK5. Activated ALK5 propagates the signal into the nucleus by inducing the phosphorylation of Smad2 and Smad3. In endothelial cells, however, TGFβ can signal via two distinct type I receptor/Smad pathways. Whereas activation of ALK5/Smad2/3 pathway by TGFβ results in inhibition of migration and proliferation, TGFβ-induced ALK1/Smad1/5 activation results in increased migration and proliferation. ALK1 not only induced biological responses opposite from those of ALK5, but also directly inhibited ALK5/Smad signaling.

Specificity

ACVRL1 Rabbit Recombinant mAb detects endogenous level of total ACVRL1.

Background

ACVRL1 (Serine/threonine-protein kinase receptor R3, activin receptor-like kinase 1 and ALK1) is a receptor in the TGF beta signaling pathway. Activation of ALK1 results from the binding of several different ligands of the TGF-β family, including bone morphogenetic protein (BMP) 9, BMP10, and TGF-β. ALK1 is predominantly expressed in endothelial cells and at specific sites of epithelial-mesenchymal interactions, stimulates Smad1 and Smad5 phosphorylation. The TGFβ/ALK5 and TGFβ/ALK1 pathways have opposite effects on endothelial cells (ECs) behavior; ALK5 inhibits EC migration and proliferation while ALK1 stimulates both processes. ALK1 is a negative mediator of lateral TGFβ/ALK5 signaling and its optimal activation requires ALK5 kinase activity. TGFβ regulates cellular processes by binding to a heteromeric complex of type I and type II serine/threonine kinase receptors. In most cell types, TGFβ initially binds TβRII and subsequently recruits and phosphorylates ALK5. Activated ALK5 propagates the signal into the nucleus by inducing the phosphorylation of Smad2 and Smad3. In endothelial cells, however, TGFβ can signal via two distinct type I receptor/Smad pathways. Whereas activation of ALK5/Smad2/3 pathway by TGFβ results in inhibition of migration and proliferation, TGFβ-induced ALK1/Smad1/5 activation results in increased migration and proliferation. ALK1 not only induced biological responses opposite from those of ALK5, but also directly inhibited ALK5/Smad signaling.

Usage Information

Application

WB, IHC,ELISA

Dilution

WB	IHC
1:1000	1:50

Reactivity

Human Mouse Rat

MW (kDa)

56kDa

Source

Rabbit

Concentration

1mg/ml

Storage buffer

10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA, 50% glycerol and less than 0.02% sodium azide.

Storage
(From the date of receipt)

Store at –20°C.

References

Application Data

Validated by Selleck

IHC