ALK-7 Protein, Rhesus Macaque (HEK293, Fc)

ALK-7 is a type I receptor serine-threonine kinase mediate inhibitory as well as stimulatory signals for growth and differentiation by binding to members of the TGF-β superfamily. ALK-7 combined with specific ligands, such as Nodal, activin B and growth differentiation factor (GDF), can activate Smads and other signaling pathways, thereby regulating cell proliferation, differentiation and apoptosis in various cells^[1][2][3]. ALK-7 Protein, Rhesus Macaque (HEK293, Fc) is produced in HEK293 cells with a C-Terminal Fc-tag. It consists of 89 amino acids (G25-E113).

ALK-7, also known as ACVR1C, is a serine/threonine kinase consistent with the characteristics of a type-I receptor. ALK-7 is predominantly expressed in central nervous system. ALK-7 can form complexes with type II receptor serine-threonine kinases for TGF-β and activin in a ligand-dependent manner^[1].
The ALK-7 gene encodes a 55-kDa cell-surface protein that exhibits up to 78% amino acid sequence identity in the kinase domain to previously isolated type I receptors for TGF-β and activin. In the extracellular domain, however, ALK-7 is more divergent, displaying comparable similarities with all members of the ALK subfamily. Originally identified and cloned from rat brain, ALK-7 mRNA is present throughout the digestive and central nervous system of rats. The function of ALK-7 as a type I receptor was confirmed with a constitutively activemutant form that activated a TGF-β/activin response reporter. ALK-7 has also been found to activate some components of the Smad pathway, such as Smad2 and Smad3, in fetal and adult rat pancreas. In the rat pheochromocytoma PC12 cell line, ALK-7 not only activated both Smad2, Smad3, and the MAPK of extracellular signal-regulated kinase and JNK, but it inhibits cell proliferation as well. The human gene for ALK-7 has been mapped to the genetic location of 2q24.1-q3, with most of the mRNA located in the brain, pancreas, and colon. ALK-7 mediates high-ambient glucose-induced cardiomyoblasts apoptosis through the activation of Smad2/3^[1][2][3].
ALK-7 combined with specific ligands, such as Nodal, activin B and growth differentiation factor (GDF), can activate Smads and other signaling pathways, thereby regulating cell proliferation, differentiation and apoptosis in various cells. Besides that, ALK-7, along with ALK-5 and ALK-6, participated in renal interstitial fibrosis^[1][2][3].

Activin AB binds ActRIIA-Fc with a high affinity, whereas activin AB shows little binding to ALK7-Fc or ALK4-Fc (.5-5 μg). An estimated Kd of activin AB to ActRIIA-Fc is 333 pM. The affinity of activin AB for ActRIIA-Fc/ALK7-Fc is greater than that for ActRIIA-Fc and has an estimated Kd of 125 pM. This indicates the enhanced activin AB binding to the activin receptors in the presence of ALK7^[5].

Rhesus Macaque

HEK293

C-hFc

F7GDQ6 (G25-E113)

697826  [NCBI]

Approximately 36.6 kDa

Greater than 95% as determined by reducing SDS-PAGE

<1 EU/μg, determined by LAL method.

• [1]. M Rydén, et al. A novel type I receptor serine-threonine kinase predominantly expressed in the adult central nervous system. J Biol Chem. 1996 Nov 29;271(48):30603-9.  [Content Brief]

  [2]. Byung-Chul Kim, et al. Activin receptor-like kinase-7 induces apoptosis through activation of MAPKs in a Smad3-dependent mechanism in hepatoma cells. J Biol Chem. 2004 Jul 2;279(27):28458-65.  [Content Brief]

  [3]. Wen-bo Li, et al. Silencing of activin receptor-like kinase 7 alleviates aortic stiffness in type 2 diabetic rats. Acta Diabetol. 2015 Aug;52(4):717-26.  [Content Brief]

  [4]. Kunihiro Tsuchida, et al. Activin isoforms signal through type I receptor serine/threonine kinase ALK7. Mol Cell Endocrinol. 2004 May 31;220(1-2):59-65.  [Content Brief]