Cynomolgus ALK-7 / ALK7 / ACVR1C Protein (Cytokine)

Activin A receptor, type IC Protein Datasheet

ALK-7 / ALK7 / ACVR1C Protein Product Information

• Synonym: ACVR1C
• Protein Construction: A DNA sequence encoding the cynomolgus ACVR1C (F7GDQ6) (Leu44-Glu113) was expressed, fused with the Fc region of human IgG1 at the C-terminus.
• Source: Cynomolgus
• Expression Host: Human Cells

ALK-7 / ALK7 / ACVR1C Protein QC Testing

• Purity: > 95 % as determined by SDS-PAGE
• Endotoxin: < 1.0 EU per μg of the protein as determined by the LAL method
• Stability: Samples are stable for up to twelve months from date of receipt at -70℃
• Predicted N terminal: Gly 25
• Molecular Mass: The recombinant cynomolgus ACVR1C is a disulfide-linked homodimer. The reduced monomer comprises 330 amino acids and has a calculated molecular mass of 36.6 KDa.The apparent molecular mass of cynomolgus CD38 is approximately 42-46 KDa respectively in SDS-PAGE.
• Formulation: Lyophilized from sterile PBS, pH7.4
  1. Normally 5 % - 8 % trehalose and mannitol are added as protectants before lyophilization. Specific concentrations are included in the hardcopy of COA.
  2. Please contact us for any concerns or special requirements.
• SDS-PAGE: ALK-7 / ALK7 / ACVR1C protein

ALK-7 / ALK7 / ACVR1C Protein Usage Guide

• Storage: Store it under sterile conditions at -70℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
• Reconstitution: A hardcopy of COA with reconstitution instruction is sent along with the products. Please refer to it for detailed information.

ALK-7 / ALK7 / ACVR1C Protein Description

ALK-7, also known as ALK7 and ACVR1C, is a member of the ALK family. ALK-7 is a serine-threonine kinase that can cause the activation of one of the SMAD signal transducers, SMAD2. It induces cell death by apoptosis through activation of the traditional TGF-beta pathway components in a process involving activation of SMAD2, SMAD3, caspase-3 and caspase-9. ALK-7 has a ligand known as Nodal. Nodal stimulates the secretion of TIMP-1 and inhibits matrix metalloproteinases MMP-2 and MMP-9 activity. The overexpression of Nodal or constitutively active ALK-7 decreases cell migration and invasion, whereas knock-down of Nodal and ALK-7 has the opposite effects.

References

1. Lin YY. et al., 2012, Nature. 482 (7384): 251-5.
2. He C. et al., 2010, Hum Genet. 128 (5) :515-27.
3. Watanabe R. et al., 2008, Biochem Biophys Res Commun. 377 (3): 867-72.