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C1QTNF5 encodes a member of the a member of the C1q\\/tumor necrosis factor superfamily. Zusätzlich bieten wir Ihnen C1q and Tumor Necrosis Factor Related Protein 5 Antikörper (89) und C1q and Tumor Necrosis Factor Related Protein 5 Proteine (8) und viele weitere Produktgruppen zu diesem Protein an.
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High myonectin expression is associated with Type 2 Diabetes.
In children adipocyte C1QTNF5 expression is already strongly related to the degree of obesity and is associated with obesity-related AT alterations, systemic CTRP5 serum levels as well as circulating markers of metabolic disease and is positively regulated by TNFalpha (zeige TNF ELISA Kits) in vitro
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 (zeige INS ELISA Kits) sensitivity. Inhibition of CTRP5 action may result in the alleviation of insulin (zeige 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 (zeige RPE ELISA Kits) 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 (zeige RPE ELISA Kits) and ciliary epithelium. SD-OCT (zeige Plxna2 ELISA Kits) findings revealed widespread photoreceptor loss and diffuse choroidal thinning.
cloning of the bicistronic transcript and characterization of the upstream ORF, MFRP (zeige 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.
Presence of rd8 (Crb1) 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 (zeige 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 (zeige RPE ELISA Kits) 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 (zeige RPE ELISA Kits) 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