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C1QTNF5 encodes a member of the a member of the C1q\\/tumor necrosis factor superfamily. Additionally we are shipping C1q and Tumor Necrosis Factor Related Protein 5 Antibodies (82) and C1q and Tumor Necrosis Factor Related Protein 5 Proteins (8) and many more products for this protein.
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Sequencing of C1QTNF5 revealed 28 unique variants although none showed a statistically significant association with dt-GA when compared with 1000G individuals.
Our results provide the first genetic and physiological evidence for CTRP5 as a negative regulator of glucose metabolism and insulin (show INS ELISA Kits) sensitivity. Inhibition of CTRP5 action may result in the alleviation of insulin (show INS ELISA Kits) resistance associated with obesity and diabetes.
Late-onset retinal degeneration, proven to have the p.Ser163Arg mutation in C1QTNF5, and asked whether retina-wide sub-RPE deposit was detectable and quantifiable.
C1QTNF5 monomers can multimerize into a bouquet-like octadecamer.
CTRP-5 might be a novel adipokine that circulates abundantly in human sera.
C1QTNF5 retinopathy is an autosomal dominant LORD resulting in a complex ocular phenotype involving the RPE and ciliary epithelium. SD-OCT (show Plxna2 ELISA Kits) findings revealed widespread photoreceptor loss and diffuse choroidal thinning.
cloning of the bicistronic transcript and characterization of the upstream ORF, MFRP (show MFRP ELISA Kits)
The crystal structure of the trimeric globular domain of human C1QTNF5 at 1.34A resolution reveals unique features of this novel C1q family member.
pathogenic role of C1qtnf5 Ser163Arg mutation
A physiological function for C1QTNF5 (myonectin) in linking insulin (show INS ELISA Kits) resistance with quantitative changes in mtDNA.
Presence of rd8 (Crb1 (show CRB1 ELISA Kits)) mutation does not alter the ocular phenotype of late-onset retinal degeneration mouse model carrying the Ctrp5 mutation.
CTRP-5 is functionally involved in adipocyte biology.
Ets-2 (show ETS2 ELISA Kits) play a key role in transcriptional regulation of CTRP5 in muscle cells.
L-ORMD is due to insufficient levels of secreted C1QTNF5, compromised RPE cell function resulting from ER retention of the mutant protein or both mechanisms.
CTRP5, a secretory and membrane-associated protein, is localized to the lateral and apical membranes of the RPE and CB. Impaired secretion of the mutant protein may underlie the pathophysiology of long anterior zonules and late-onset retinal degeneration.
This gene encodes a member of the a member of the C1q/tumor necrosis factor superfamily. The encoded protein may be a component of basement membranes and may play a role in cell adhesion. This gene is contained entirely within the 3' UTR of the membrane frizzled-related protein gene on chromosome 11q23 and both genes are expressed from a bicistronic transcript. Mutations in this gene have been associated with late-onset retinal degeneration.
C1q and tumor necrosis factor related protein 5
, complement C1q tumor necrosis factor-related protein 5
, C1q TNF-alpha-related protein 5