Recombinant Human C1qTNF9 stimulates CXCL10 secretion by RAW 264.7 mouse monocyte/macrophage cells. The ED50 for this effect is typically 1.5-7.5 μg/mL.
C1qTNF9, also known as CTRP9, is an approximately 40 kDa member of the C1q and TNF-related protein family (1). Like all members of this protein family, C1qTNF9 consists of a short variable region, a collagenous domain that can be hydroxylated, and a C1q-like globular domain (1). Human C1qTNF9 shares 85% amino acid sequence identity with the mouse and rat orthologs. Both the mouse and human C1qTNF9 proteins are expressed in adipose tissue, but the mouse protein has also been detected in the heart, lung, muscle, kidney, testis, lymph node, smooth muscle, prostate, thymus, and uterus (1, 2). They have both also been shown to be secreted as trimers and higher order multimers and also to form hetero-oligomers with Adiponectin (1, 2). Mouse C1qTNF9 can stimulate the phosphorylation of AMPK, Akt, and eNOS (1, 3, 4). Also in mice, C1qTNF9 may have an important role in cardiac and metabolic health. Its expression has a cardioprotective effect following acute myocardial infarction that may be dependent on AMPK activation (4-6). Additionally, transgenic mice overexpressing C1qTNF9 are resistant to high fat diet‑induced obesity (7). This metabolic role may be conserved, since C1qTNF9 serum levels have been shown to inversely correlate with metabolic syndrome in humans (8).
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C1q and Tumor Necrosis Factor Related Protein 9
Entrez Gene IDs:
AQL1; C1q and tumor necrosis factor related protein 9; C1QTNF9AComplement C1q tumor necrosis factor-related protein 9; complement C1q tumor necrosis factor-related protein 9A; CTRP9; MGC48915
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