ACVR2B Protein, Mouse (HEK293, His-hFc)

Activin receptor type-2B (ACVR2B), also known as ActR-IIB and MGC116908, is an activin type II receptor. Type I receptors are essential for signaling; and type II receptors are required for binding ligands and for expression of type I receptors^[1].
The sequence of amino acids in ACVR2B proteins from different species is very stable, which leads to the conclusion that in the process of evolution, ACVR2B has been only slightly altered, and that both in humans and in animals, its function is similar.
Activins and growth differentiation factors (GDF) bind to ACVR2B, which in turn activate type I receptors such as activin receptor-like kinases (ALK) ALK4 and ALK5, activating downstream molecule SMAD2/3. SMADSs regulate a number of myogenic genes, such as myoD, myogenin, and Myf5, that are involved in cellular hypertrophy, proliferation, or differentiation. Noncanonical ACVR2B pathways have also been shown to regulate MAP kinases. ACVR2B blocks signaling of myostatin, its close homolog GDF11, as well as activin A, activin B, and BMP10^[1]. Activin A primarily binds to the type 1 receptors ALK4 or ALK7 in complex with ACVR2A or ACVR2B, causing activation of SMAD2 or SMAD3^[2].
In myeloma cells, BMP-6- and BMP-9-induced activation of SMAD1/5/8 through ACVR2A/ACVR2B/ALK2 is inhibited by activin A treatment^[2]. ACVR2B has been shown to preserve muscle mass and prolong survival in tumor hosts, and to increase bone mass in models of osteogenesis imperfecta and muscular dystrophy^[3].

Recombinant mouse ACVR2B (2 ng/mL; added 3 min before hypoxia) antagonizes SMAD2 signaling and cell death in cardiomyocytes that are subjected to hypoxic stress^[1].

Recombinant mouse ACVR2B (1 mg/kg; s.c.; once) shows cardioprotection activity in ischemia-reperfusion (IR) injury mouse. ACVR2B= modifies cardiac metabolism, left ventricular mitochondrial respiration, as well as cardiac phenotype toward physiological hypertrophy. By blocking myostatin, ACVR2B potentially reduces cardiomyocyte death and modifies cardiomyocyte metabolism for hypoxic conditions to protect the heart from IR injury^[1].