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TNXB encodes a member of the tenascin family of extracellular matrix glycoproteins.
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Human TNXB ELISA Kit for 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. in Investigative ophthalmology & visual science 2014
Study describes a biallelic TNXB variants in patients with congenital adrenal hyperplasia due to CYP21A2 (show CYP21A2 ELISA Kits) 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 (show FKBPL ELISA Kits) and NOTCH4 (show NOTCH4 ELISA Kits) as candidate susceptibility genes.
Combined analysis of tenascin-C (show TNC ELISA Kits) expression and the nodule size improved the prediction of malignancy in this patient cohort.
rs204887 itself or a nearby variant is unlikely to play a major role in the development of schizophrenia although a cumulative contribution of rare variants in the TNXB gene cannot be ruled out.
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 (show TGFB1 ELISA Kits)(1) and downregulation of PPARgamma (show PPARG ELISA Kits).
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 (show FN1 ELISA Kits) and B16 melanoma cells than do wild-type fibroblasts.
Induction of MMP-2 (show MMP2 ELISA Kits) by Tnx deficiency is mediated through the c-Jun N-terminal kinase and protein tyrosine kinase (show YES1 ELISA Kits) 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.
localizations of Tn-X in the leptomeningeal trabecula (TB) of adult mice and in the connective tissue of the choroid plexus (CP) in the brains of mice
Tenascin-X promotes activation of latent TGF-beta1 (show TGFB1 ELISA Kits) 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 (show FN1 ELISA Kits) 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