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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
Functional studies showed THBS1 (show THBS1 Proteins) and TNC to mediate chemoresistance through the integrin beta1/mTOR (show FRAP1 Proteins) 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 (show IRF6 Proteins)) from bacterial infection activated a common set of signaling pathways, including NF-kappaB (show NFKB1 Proteins) and MAPK (show MAPK1 Proteins), but these stimuli also induced different signaling pathways downstream of TLR4 (show TLR4 Proteins).
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)
Study that recombinant TNC consisting of the epidermal growth factor (EGF (show EGF Proteins)-like repeats induced cerebral arterial constriction via EGF receptor (show EGFR Proteins) and activation of ERK1/2
Tenascin-C was abundant in cortical white and gray matter in brain tissue from Alzheimer's Disease patients.
Overexpression of TNC, SMA (show SMN1 Proteins), and vimentin (show VIM Proteins) were significantly correlated with the lower overall survival in prostate cancer patients.
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 (show MMP9 Proteins) 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 (show HAND1 Proteins) and Th17 cells, protecting animals from experimental autoimmune encephalomyelitis.
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 (show MAPK1 Proteins)-mediated MMP-9 (show MMP9 Proteins) induction and ZO-1 (show TJP1 Proteins) degradation
TN-C aggravates autoimmune myocarditis by driving the dendritic cell activation and Th17 differentiation via toll-like receptor 4 (show TLR4 Proteins).
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 (show WNT2 Proteins)/beta-catenin (show CTNNB1 Proteins) signaling in the whisker follicle stem cell niche.
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 (show FN1 Proteins) 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