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Tenascin C

Tenascin, tenascin-C, TnC
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. [provided by RefSeq, Jul 2011] (from NCBI)
Top mentioned proteins: CAN, fibronectin, HAD, V1a, CD45
Papers on Tenascin
Local trauma in human patellar tendon leads to widespread changes in the tendon gene expression.
Kjaer et al., Nottingham, United Kingdom. In J Appl Physiol, Feb 2016
Results for DNA content were inconclusive, and no changes were detected in expression of Insulin-like growth factor-I, connective tissue growth factor, scleraxis, decorin, fibromodulin, tenascin-C, tenomodulin, VEGFa, CD68, IL-6, MMP12 and MMP13.
Tenogenic induction of equine mesenchymal stem cells by means of growth factors and low-level laser technology.
Spaas et al., Padova, Italy. In Vet Res Commun, Feb 2016
PB-MSCs were used to study the effects of the addition of some growth factors (GFs) as TGFβ3 (transforming growth factor), EGF2 (Epidermal growth factor), bFGF2 (Fibroblast growth factor) and IGF-1 (insulin-like growth factor) in presence or without Low Level Laser Technology (LLLT) on the mRNA expression levels of genes important in the tenogenic induction as Early Growth Response Protein-1 (EGR1), Tenascin (TNC) and Decorin (DCN).
Significance of myocardial tenascin-C expression in left ventricular remodelling and long-term outcome in patients with dilated cardiomyopathy.
Anzai et al., Suita, Japan. In Eur J Heart Fail, Feb 2016
Myocardial tenascin-C (TNC) is known to appear under pathological conditions, possibly to regulate cardiac remodelling.
Tuning microenvironment modulus and biochemical composition promotes human mesenchymal stem cell tenogenic differentiation.
Kloxin et al., Newark, United States. In J Biomed Mater Res A, Feb 2016
Increasing modulus and collagen mimetic peptide content increased relevant gene expression and protein production or retention (scleraxis, collagen I, tenascin-C).
The role of extracellular matrix in spinal cord development.
Faissner et al., Bochum, Germany. In Exp Neurol, Dec 2015
Recent research has also provided strong evidence that depletion of single matrix molecules like Tenascin C (TnC) can lead to developmental changes within the progenitor pools.
Inflammatory and Fibrotic Responses of Cardiac Fibroblasts to Myocardial Damage Associated Molecular Patterns (DAMPs).
Turner, Leeds, United Kingdom. In J Mol Cell Cardiol, Dec 2015
These include intracellular molecules released by necrotic cells (heat shock proteins, high mobility group box 1 protein, S100 proteins), proinflammatory cytokines (interleukin-1α), specific ECM molecules up-regulated in response to tissue injury (fibronectin-EDA, tenascin-C) or molecules modified by a pathological environment (advanced glycation end product-modified proteins observed with diabetes).
Molecular identity of human outer radial glia during cortical development.
Kriegstein et al., San Francisco, United States. In Cell, Oct 2015
By analyzing gene expression across single cells, we find that outer radial glia preferentially express genes related to extracellular matrix formation, migration, and stemness, including TNC, PTPRZ1, FAM107A, HOPX, and LIFR.
The Function of Matricellular Proteins in the Lamina Cribrosa and Trabecular Meshwork in Glaucoma.
O'Brien et al., Dublin, Ireland. In J Ocul Pharmacol Ther, Sep 2015
Matricellular proteins are a family of nonstructural secreted glycoproteins, which enable cells to communicate with their surrounding ECM, including CTGF, also known as CCN2, TSPs, SPARC, periostin, osteonectin, and tenascin-C and -X, and other ECM proteins.
Tenascin-C: Its functions as an integrin ligand.
Chiquet-Ehrismann et al., Davis, United States. In Int J Biochem Cell Biol, Aug 2015
This review summarizes the experimental evidence of tenascin-C/integrin interactions, emphasizing the identification of integrin binding sites and the effects of specific interactions on cell behavior.
Tenascin-X: beyond the architectural function.
Bartholin et al., Lyon, France. In Cell Adh Migr, 2014
Tenascin-X is the largest member of the tenascin (TN) family of evolutionary conserved extracellular matrix glycoproteins, which also comprises TN-C, TN-R and TN-W.
Effluent Tenascin-C Levels Reflect Peritoneal Deterioration in Peritoneal Dialysis: MAJOR IN PD Study.
Nagata et al., Tochigi, Japan. In Biomed Res Int, 2014
In the MGO-treated rats, tenascin-C (TN-C) levels in the peritoneal effluents were remarkably high and a cluster of TN-C-positive mesothelial cells with epithelial-to-mesenchymal transition- (EMT-) like change excessively proliferated at the peritoneal surface, but not in the FA-treated rats.
Tenascin C regulates proliferation and differentiation processes during embryonic retinogenesis and modulates the de-differentiation capacity of Müller glia by influencing growth factor responsiveness and the extracellular matrix compartment.
Faissner et al., Bochum, Germany. In Dev Biol, 2012
Both cycling G2-phase cells and early post-mitotic neurons were significantly increased in the retina due to Tnc-deficiency. Further investigations suggested that Tnc regulates these processes via the Wnt-signaling cascade.
Engineered troponin C constructs correct disease-related cardiac myofilament calcium sensitivity.
Davis et al., Columbus, United States. In J Biol Chem, 2012
Rationally engineered TnC constructs corrected the abnormal Ca(2+) sensitivities of the thin filament, reconstituted actomyosin ATPase activity
Extracellular matrix protein tenascin-C is required in the bone marrow microenvironment primed for hematopoietic regeneration.
Kubota et al., Tokyo, Japan. In Blood, 2012
Mice lacking TN-C (TN-C(-/-)) mice showed normal steady-state hematopoiesis; however, they failed to reconstitute hematopoiesis after bone marrow ablation and showed high lethality.
Effect of hypertrophic cardiomyopathy-linked troponin C mutations on the response of reconstituted thin filaments to calcium upon troponin I phosphorylation.
Tikunova et al., United States. In Biochemistry, 2012
Cardiomyopathy-linked TnC mutations affect the response of reconstituted thin filaments to calcium upon cardiac troponin (Tn)I phosphorylation.
Matricellular proteins in cardiac adaptation and disease.
Frangogiannis, United States. In Physiol Rev, 2012
Thrombospondin (TSP)-1, -2, and -4 as well as tenascin-C and -X secreted protein acidic and rich in cysteine (SPARC), osteopontin, periostin, and members of the CCN family (including CCN1 and CCN2/connective tissue growth factor) are involved in a variety of cardiac pathophysiological conditions, including myocardial infarction, cardiac hypertrophy and fibrosis, aging-associated myocardial remodeling, myocarditis, diabetic cardiomyopathy, and valvular disease.
Disease-related cardiac troponins alter thin filament Ca2+ association and dissociation rates.
Davis et al., Columbus, United States. In Plos One, 2011
The disease-related protein modifications alter Ca(2+) binding by influencing both the association and dissociation rates of thin filament Ca(2+) exchange.
Breast cancer cells produce tenascin C as a metastatic niche component to colonize the lungs.
Massagué et al., New York City, United States. In Nat Med, 2011
We report that breast cancer cells that infiltrate the lungs support their own metastasis-initiating ability by expressing tenascin C (TNC).
Tenascin-C is an endogenous activator of Toll-like receptor 4 that is essential for maintaining inflammation in arthritic joint disease.
Foxwell et al., London, United Kingdom. In Nat Med, 2009
tenascin-C as a novel endogenous activator of TLR4-mediated immunity that mediates persistent synovial inflammation and tissue destruction in arthritic joint disease.
Candidate genes on chromosome 9q33-34 involved in the progression of childhood ependymomas.
Vassal et al., Paris, France. In J Clin Oncol, 2009
Using a candidate-gene strategy, we found an overexpression of two potential oncogenes at the locus 9qter: Tenascin-C and Notch1.
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