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TNXB encodes a member of the tenascin family of extracellular matrix glycoproteins. De plus, nous expédions TNXB Anticorps (56) et TNXB Protéines (4) et beaucoup plus de produits pour cette protéine.
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Human TNXB Kit ELISA pour Sandwich ELISA - ABIN415102
Kim, Woo, Suh, Ahn, Park, Hong, Lee, Ahn, Hwang, Kim, Park, Lee: Identification of vinculin as a potential plasma marker for age-related macular degeneration. dans Investigative ophthalmology & visual science 2014
Hypermethylated sites at TNXB are associagted with response to starvation in anorexia nervosa.
Study describes a biallelic TNXB variants in patients with congenital adrenal hyperplasia due to CYP21A2 (Montrer CYP21A2 Kits ELISA) deletions resulting in a classical Ehlers-Danlos syndrome phenotype with skin hyperextensibility, widened atrophic scars and joint hypermobility.
patients with the TNX-deficient type EDS typically have generalized joint hypermobility, skin hyperextensibility and easy bruising. In contrast to the classical type, the inheritance pattern is autosomal recessive and atrophic scarring is absent. Molecular analysis of TNXB in a diagnostic setting is challenging.
the identification of a rare missense variant in TNXB in combination with a positive family history of VUR and joint hypermobility may represent a non-invasive method to diagnose PVUR and warrants further evaluation in other cohorts
We then quantified the tenascin-X level in serum of patients and identified tenascin-X as potent marker for ovarian cancer, showing that secretomic analysis is suitable for the identification of protein biomarkers when combined with protein immunoassay.
these results suggest that mutations in TNXB can cause hereditary primary vesicoureteral reflux .
Noticeable decreased expression of tenascin-X in calcific aortic valves.
Tenascin-X haploinsufficiency was associated with Ehlers-Danlos syndrome in patients with congenital adrenal hyperplasia
Genome-wide association study of age-related macular degeneration identifies TNXB, FKBPL (Montrer FKBPL Kits ELISA) and NOTCH4 (Montrer NOTCH4 Kits ELISA) as candidate susceptibility genes.
Combined analysis of tenascin-C (Montrer TNC Kits ELISA) expression and the nodule size improved the prediction of malignancy in this patient cohort.
these wound healing-related properties are affected in a TNX-deficient extracellular environment
Results suggest that tenascin-X secreted from Schwann cells and/or fibroblasts is involved in blood vessel formation in peripheral nerves.
Tenascin-x is an initiator of myocardial fibrosis and ACM development via upregulation of TGFbeta (Montrer TGFB1 Kits ELISA)(1) and downregulation of PPARgamma (Montrer PPARG Kits ELISA).
Altered properties of the force transmission pathways of muscle due to TNX deficiency directly affect muscle function in TNX KO mice. Such effects are likely to contribute to muscle weakness experienced by patients with Ehlers-Danlos syndrome.
Tenascin-X deficiency mimics Ehlers-Danlos syndrome in mice through alteration of collagen deposition
TNX has either a redundant or a very subtle function in the macromolecular organization in the peripheral nerve
Tnx plays a role in the regulation of cell-cell and cell-matrix interactions: Tnx-null fibroblasts exhibit weaker adhesive properties to fibronectin (Montrer FN1 Kits ELISA) and B16 melanoma cells than do wild-type fibroblasts.
Induction of MMP-2 (Montrer MMP2 Kits ELISA) by Tnx deficiency is mediated through the c-Jun N-terminal kinase and protein tyrosine kinase (Montrer YES1 Kits ELISA) phosphorylation pathway.
TNX is unlikely to be involved in matrix deposition in the early phase of wound healing, but it is required in the later phase when remodeling and maturation of the matrix establishes and improves its biomechanical properties.
TNX knockout mice have mild pregnancy-related abnormalities.
Tenascin-X promotes activation of latent TGF-beta1 (Montrer TGFB1 Kits ELISA) and subsequent epithelial to mesenchymal transition in mammary epithelial cells.
mechanical analysis of collagen gels showed an increased compressive resistance of the gels containing tenascin-X, indicating that this protein might be directly involved in determining the mechanical properties of collagen-rich tissues in vivo.
tenascin-X, via trimerization and multiple interactions with components of collagenous fibrils, plays a crucial role in the organisation of extracellular matrices.
Tenascin-X is an elastic protein and the fibronectin (Montrer FN1 Kits ELISA) type III (FnIII) domains can unfold under a stretching force and refold to regain their mechanical stability upon the removal of the stretching force.
This gene encodes a member of the tenascin family of extracellular matrix glycoproteins. The tenascins have anti-adhesive effects, as opposed to fibronectin which is adhesive. This protein is thought to function in matrix maturation during wound healing, and its deficiency has been associated with the connective tissue disorder Ehlers-Danlos syndrome. This gene localizes to the major histocompatibility complex (MHC) class III region on chromosome 6. It is one of four genes in this cluster which have been duplicated. The duplicated copy of this gene is incomplete and is a pseudogene which is transcribed but does not encode a protein. The structure of this gene is unusual in that it overlaps the CREBL1 and CYP21A2 genes at its 5' and 3' ends, respectively. Multiple transcript variants encoding different isoforms have been found for this gene.
growth-inhibiting protein 45
, hexabrachion-like protein
, tenascin XB1
, tenascin XB2
, tenascin X
, tenascin XB
, tenascin Y
, tenascin X B
, tenascin X pseudogene