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Results suggest that sequence variants in TNC and COL5A1 genes are associated with superficial digital flexor tendinopathy in TB racehorses. In
Results illuminate how the extracellular matrix glycoprotein tenascin-C in the tumor microenvironment promotes invasive migration and metastatic progression by employing integrin alpha9beta1, abolishing actin stress fiber formation, inhibiting YAP and its target gene expression.
In addition, we found that Tn-expressing colorectal cancers (CRC) cell lines had either loss-of-function mutations in Cosmc or reversible Tn antigen expression, which was not caused by the deficiency of T-synthase activity
The results demonstrated that ANX2 and stromal tenascin C regulated invasion in addition to stemness and anoikis resistance, which are crucial for metastasis in the progression of pancreatic ductal adenocarcinoma.
Intratumor stromal expression of tenascin-C (TN-C) is a strong prognostic indicator in locally advanced unresectable (UR-LA) pancreatic ductal adenocarcinoma (PDAC) patients with resection after chemoradiotherapy (CRT).
this study shows that tenascin C is increased in vitiligo in lesional areas only in the acral sites
Data indicate three sites within tenascin-C that directly and cooperatively interact with toll-like receptor 4 (TLR4).
Results identify tenascin-C as an endogenous danger signal that is upregulated in systemic sclerosis and drives TLR4-dependent fibroblast activation, and by its persistence impedes fibrosis resolution.
Both fetal Tn-C variants may represent novel biomarkers that are capable of estimating both pulmonary vascular remodeling and right ventricular load.
high TNC expression correlates with worse prognosis for lung adenocarcinoma and has a role in lung cancer progressoin
Decellularized lung scaffolds treated with FBN-2 and TN-C prior to re-epithelialization supported greater epithelial proliferation and tissue remodeling.
Immunohistochemical analysis shows that the unique association between the CD44+/CD24low/- phenotype and the pronounced production of tenascin C may have a prognostic potential, prospectively indicating the inefficiency of neoadjuvant polychemotherapy (PCT), in particular that with platinum derivatives, which is used for the standard treatment of triple-negative BC.
Enhanced serum tenascin-C concentrations are closely related to trauma severity and clinical outcomes
Functional studies showed THBS1 and TNC to mediate chemoresistance through the integrin beta1/mTOR pathway.
Elevated Tenascin-C serum values are associated with non-small cell lung cancer.
Tenascin-C was abundantly secreted by the colon cancer cells with high metastatic potential, and highly expressed in lymph nodes with metastasis.
Intermittent hypoxia confers pro-metastatic gene expression selectively through NF-kappaB in inflammatory breast cancer cells, in particular, to tenascin-C and MPP9.
Metastatic prostate cancer cells cultured on osteo-mimetic surfaces coated with tenascin C exhibited enhanced adhesion and colony formation as mediated by integrin alpha9beta1.
Study showed that the proinflammatory, extracellular matrix glycoprotein tenascin-C from tissue damage and microbial lipopolysaccharide (LPS) from bacterial infection activated a common set of signaling pathways, including NF-kappaB and MAPK, but these stimuli also induced different signaling pathways downstream of TLR4.
High Tenacin C expression is associated with liver metastasis in colorectal cancer stroma.
Tenascin-C protein expression in this muscle was confined to arterioles and venules (80% of cases) and increased after training in A-allele carriers. Prior to training, volume densities of subsarcolemmal and myofibrillar mitochondria in m. vastus lateralis muscle were 49% and 18%, respectively, higher in A/A homozygotes relative to T-nucleotide carriers (A/T and T/T)
TNC causes post-subarachnoid hemorrhage neuronal apoptosis and neuroinflammation.
ATF3 promotes macrophage migration and reverses M1polarized macrophages to the M2 phenotype by upregulation of TNC via the Wnt/betacatenin signaling pathway.
housing of TnC-/- mice in enriched environment abolished hyperlocomotion, led to faster habituation to novel environment, strengthened the grasp of fore limbs and partially improved movement coordination, while the swimming ability remained deficient
The synaptic plasticity occurs in the hippocampus of freely behaving mice that lack tenascin-C, the informational content stored by synaptic plasticity is not the same.
Study suggests that tenascin-C (TnC) contributes to the regulation of structural plasticity in the cerebellum and that interactions between TnC and matrix metalloproteinase 9 are likely to be important for these processes to occur.
the exact role of TNC in primary tumor growth
A deficiency of tenascin C interferes with Th1 and Th17 cells, protecting animals from experimental autoimmune encephalomyelitis.
secreted by transdifferentiated retinal pigment epithelial cells and promotes the development of choroidal neovascularization via integrin alphaV in a paracrine manner
Tenascin-C may be an important mediator in the development of brain edema and blood-brain barrier disruption following subarachnoid hemorrhage, mechanisms for which may involve MAPK-mediated MMP-9 induction and ZO-1 degradation
TN-C aggravates autoimmune myocarditis by driving the dendritic cell activation and Th17 differentiation via toll-like receptor 4.
TNC supports the stress-induced expression of extracellular matrix that reinforce the aorta and the stress-induced excessive inflammatory response in the aorta.
TNC plays an important role in TMJ wound healing, especially for wounds generated by mechanical stress.
Tenascin-C is required for normal Wnt/beta-catenin signaling in the whisker follicle stem cell niche.
TNC downregulates Dickkopf-1 (DKK1) promoter activity through the blocking of actin stress fiber formation, activates Wnt signaling, and induces Wnt target genes in tumor and endothelial cells.
The increased levels of elastin, type V collagen and tenascin C are probably the result of increased expression by fibroblastic cells; reversely, elastin influences myofibroblast differentiation
Elevated tenascin-C expression in globoid cell leukodystrophy modified microglial functional response to psychosine.
Tenascin-C-derived peptide TNIIIA2 highly enhances cell survival and platelet-derived growth factor (PDGF)-dependent cell proliferation through potentiated and sustained activation of integrin alpha5beta1.
FHL2-deficient mice developed a severe and long-lasting lung pathology due to enhanced expression of tenascin C and impaired activation of inflammation-resolving macrophages.
the CD34-positive whisker follicle stem cell niche contains both tenascin-C and tenascin-W, and these glycoproteins might play a role in directing the migration and proliferation of these stem cells
TNC does not appear to contribute directly to outflow resistance in the eye.
TNC could be a potential candidate gene for meat quality traits in pigs.
tenascin binds to fibronectin at a cryptic binding site
Reloading of atrophied rat soleus muscle induces tenascin-C expression around damaged muscle fibers. Increase of rat soleus muscle loading modifies basement membrane of damaged muscle fibers through ectopic endomysial expression of tenascin-C.
tenascin-C is part of a specialized extracellular matrix in the region of the horizontal myoseptum that influences the growth of motor axons
This gene encodes an extracellular matrix protein with a spatially and temporally restricted tissue distribution. This protein is homohexameric with disulfide-linked subunits, and contains multiple EGF-like and fibronectin type-III domains. It is implicated in guidance of migrating neurons as well as axons during development, synaptic plasticity, and neuronal regeneration.
, tenascin C (hexabrachion)
, GP 150-225
, glioma-associated-extracellular matrix antigen
, hexabrachion (tenascin)
, myotendinous antigen
, tenascin-C isoform 14/AD1/16