CTRP5, MFRP.
Greater than 85.0% as determined by SDS-PAGE.
C1QTNF5 Human produced in E.Coli is a single, non-glycosylated polypeptide chain containing 253 amino acids (16-243.a.a) and having a molecular mass of 26.4kDa. C1QTNF5 Human is fused to a 25 amino acid His-tag at N-terminus & purified by proprietary chromatographic techniques.
CTRP5, MFRP.
MGSSHHHHHH SSGLVPRGSH MGSHMSPPLD DNKIPSLCPG HPGLPGTPGH HGSQGLPGRD
GRDGRDGAPG APGEKGEGGR PGLPGPRGDP GPRGEAGPAG PTGPAGECSV PPRSAFSAKR
SESRVPPPSD APLPFDRVLV NEQGHYDAVT GKFTCQVPGV YYFAVHATVY RASLQFDLVK
NGESIASFFQ FFGGWPKPAS LSGGAMVRLE PEDQVWVQVG VGDYIGIYAS IKTDSTFSGF LVYSDWHSSP VFA.
Complement C1q Tumor Necrosis Factor-Related Protein 5 (C1QTNF5) is a member of the C1q/TNF-related protein (CTRP) family. This family of proteins is known for its role in various physiological processes, including metabolism, inflammation, and immune response. C1QTNF5, in particular, has garnered attention due to its involvement in metabolic regulation and potential implications in various diseases.
C1QTNF5 is characterized by its unique structure, which includes a short variable domain, a C-terminal C1q globular domain, a collagenous domain, and an N-terminal signal peptide . The C1q domain is homologous to the globular domain of the immune complement C1q, which plays a crucial role in the classical pathway of the complement system . This structural similarity suggests that C1QTNF5 may have similar functional properties, including the ability to interact with various ligands and participate in immune responses.
C1QTNF5, like other CTRPs, is secreted by adipose tissues and plays a significant role in regulating lipid and glucose metabolism . It enhances metabolism through the activation of AMP-activated protein kinase (AMPK) and AKT-dependent pathways, which are crucial for maintaining energy homeostasis and insulin sensitivity . Dysregulation of C1QTNF5 expression has been associated with metabolic disorders such as obesity, type 2 diabetes, and non-alcoholic fatty liver disease (NAFLD) .
Mutations in the C1QTNF5 gene have been linked to late-onset retinal degeneration, a condition characterized by progressive vision loss . Additionally, C1QTNF5 expression has been observed in the tumor microenvironment, where it may promote tumor growth and metastasis . This suggests that C1QTNF5 could be a potential target for therapeutic interventions in cancer treatment.
Recent studies have highlighted the potential of C1QTNF5 as a biomarker for early detection and treatment of metabolic disorders . Pharmacological interventions and lifestyle modifications have been shown to alter the expression of C1QTNF5, indicating its responsiveness to therapeutic strategies . Furthermore, ongoing research aims to explore the broader implications of C1QTNF5 in various physiological and pathological conditions.