rhC1qTNF5, CF (50 UG)

Background: CTRP5/C1qTNF5

CTRP5, also known as C1qTNF5, belongs to the highly conserved family of Acrp30/Adiponectin paralogs known as C1q and TNF‑related protein family (1). All family members share a modular organization comprising an N‑terminal signal peptide, a short variable region with conserved cysteine residues, a collagenous domain for coiled coil structure, and a C‑terminal globular domain (2, 3). CTRP proteins are predicted to have trimeric structures that can assemble into higher order molecular forms (1). Human and mouse CTRP5 share 94% amino acid sequence identity. CTRP5 is highly expressed in the eye, testis and adipose tissue (4). A mutation (S163R) in C1qTNF5 impairs secretion and is associated with early-onset long anterior zonules (LAZ) and late-onset retinal degeneration (L-ORD) (5). In both mouse and human, the 3' untranslated region of the MFRP transcript contains the complete open reading frame of C1qTNF5, suggesting that these genes are dicistronic. MFRP and C1qTNF5 have been shown to directly interact in the retinal pigment epithelium and are likely functionally related (6). Like other C1qTNF family members, C1qTNF5 shares similarities to adiponectin in structure and function and has been shown to stimulate glucose uptake and increase fatty acid oxidation through activation of AMPK in skeletal muscle (3). Conversely, administration of rhC1qTNF5 was shown to attenuate insulin-induced Akt activation in adipocytes and skeletal muscle (7).