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C1QTNF5 encodes a member of the a member of the C1q/tumor necrosis factor superfamily.
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Human Polyclonal C1QTNF5 Primary Antibody für WB - ABIN2473125
Laine: Helicobacter pylori and non-ulcer dyspepsia. in Gastroenterology 1992
Show all 2 Pubmed References
Human Polyclonal C1QTNF5 Primary Antibody für CyTOF, FACS - ABIN4899276
Wong, Krawczyk, Kitidis-Mitrokostas, Revett, Gimeno, Lodish et al.: Molecular, biochemical and functional characterizations of C1q/TNF family members: adipose-tissue-selective expression patterns, regulation by PPAR-gamma agonist, cysteine-mediated oligomerizations, ... in The Biochemical journal 2008
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 Antikörper) 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 Antikörper) sensitivity. Inhibition of CTRP5 action may result in the alleviation of insulin (zeige INS Antikörper) 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 Antikörper) 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 Antikörper) and ciliary epithelium. SD-OCT (zeige Plxna2 Antikörper) findings revealed widespread photoreceptor loss and diffuse choroidal thinning.
cloning of the bicistronic transcript and characterization of the upstream ORF, MFRP (zeige MFRP Antikörper)
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 (zeige CRB1 Antikörper)) 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 Antikörper) 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 Antikörper) cell function resulting from ER retention of the mutant protein or both mechanisms.
CTRP5, a secretory and membrane-associated protein (zeige PDZK1IP1 Antikörper), is localized to the lateral and apical membranes of the RPE (zeige RPE Antikörper) 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