Disease relevance of Tnc

• These findings reveal a novel role of TN-C in breast cancer progression [1].
• In contrast, TN-C was more strongly expressed in the intercellular spaces and in tumor vessels in high-grade astrocytomas (anaplastic astrocytomas and glioblastomas) than in low-grade astrocytomas [2].
• Invasion of melanoma in double knockout mice lacking tenascin-X and tenascin-C [3].
• CONCLUSION: Although the distributions of ECM molecules are similar during normal and cleft palatogenesis, differences in TN expression are associated with cleft palate formation [4].
• Overexpression of tenascin-C (TN-C) in breast carcinomas has been associated with a migratory or even invasive tumor cell phenotype [5].

Psychiatry related information on Tnc

• Anxiety was evaluated by the "social interaction test." Ten behavioral categories were recorded: body care, digging, nonsocial exploration, exploration from a distance, social investigation, threat, attack, avoidance/flee, defense/submission and immobility [6].
• RESULTS: Ten days of prior stress exposure did not significantly alter the acquisition of limited-access alcohol drinking [7].

High impact information on Tnc

• Sequences that flanked the transgenic integration site were cloned and mapped to mouse chromosome 4, between the Tsha and Hxb loci [8].
• Tenascin-C, tenascin-R and tenascin-X: a family of talented proteins in search of functions [9].
• In Pax6-deficient mice, cortical radial glia cells were altered in their morphology, number, tenascin-C (TN-C) expression, and cell cycle [10].
• They were never exposed to DES and so have been referred to as "DES-lineage mice." Ten uterine adenocarcinomas and 5 ovarian cystadenocarcinomas were found in 40 DES-lineage mice [11].
• RESULTS: Ten minutes after oral administration, OVA was transported to the proximity of MHC class II antigens within LAMP-1-positive vacuoles and to the basolateral membrane of enterocytes from BALB/c strain mice [12].

Chemical compound and disease context of Tnc

• Tenascin-C (TNC), an extracellular matrix glycoprotein, is upregulated in chronic liver disease [13].
• We have identified four different DNA elements within this promoter and show that they contribute in different ways to TN gene expression in NIH 3T3 fibroblasts, C6 glioma cells, and N2A neuroblastoma cells [14].
• Deficiency of tenascin C attenuates allergen-induced bronchial asthma in the mouse [15].

Biological context of Tnc

• Tenascin-C (TN-C) and matrix metalloproteinases (MMPs) are highly expressed in cancer tissues and probably promote cell migration during cancer progression [1].
• Differential effects of the mutations on whisking were found: recovery of function was worse in TNC-deficient and better in TNR null mice compared with wild-type littermates [16].
• Gene expression profiling of cathepsin D, metallothioneins-1 and -2, osteopontin, and tenascin-C in a mouse spinal cord injury model by cDNA microarray analysis [17].
• One of a family of extracellular matrix proteins, tenascin-C (TNC) is expressed in a spatiotemporally restricted pattern associated with tissue remodeling during embryonic development, wound healing, cancer invasion and tissue regeneration [18].
• To gain insights into the relationship between Wallerian degeneration, lesion induced tenascin-C upregulation and regrowth of axons we have investigated C57BL/Wlds (C57BL/Ola) mice, a mutant in which Wallerian degeneration is considerably delayed [19].

Anatomical context of Tnc

• These findings suggest a functional significance for individual Tnc isoforms in neural stem/progenitor cells [20].
• In skin and tissues of the digestive tract often a reciprocal distribution of TN-X and TN-C was observed [21].
• In addition, the expression of tenascin C, another marker of the mammary mesenchyme, is also dependent on PTHrP [22].
• Organization and reorganization of neuromuscular junctions in mice lacking neural cell adhesion molecule, tenascin-C, or fibroblast growth factor-5 [23].
• In this way, tenascin-C and syndecan-4 work together to control fibroblast morphology and signaling and regulate events such as matrix contraction that are essential for efficient tissue repair [24].

Associations of Tnc with chemical compounds

• Consistently, TN-C was associated with lipid rafts of neonatal mouse brain according to sucrose density gradient centrifugation experiments [25].
• Moreover, cholesterol depletion with methyl-beta-cyclodextrin reduced the punctate surface staining of TN-C [25].
• Schwann cells in the distal stumps of lesioned peripheral nerves strongly express the extracellular matrix glycoprotein tenascin-C [19].
• However, the known ligands for integrin alpha8 beta1-fibronectin, vitronectin, and tenascin-C-are not appropriately localized to mediate all alpha8 beta1 functions in the kidney [26].
• We have recently demonstrated that some tenascin (TN) gene-knockout mice display abnormal behaviors, and that these abnormal behaviors stem from a low level of dopamine transmission in the brain [27].

Physical interactions of Tnc

• The c-Jun-induced transformation process involves complex regulation of tenascin-C expression [28].

Regulatory relationships of Tnc

• Our results provide strong evidence that TNC promotes and TNR impedes recovery after nerve lesion [16].
• There was a striking upregulation of TN-C matrix organization in cell lines expressing beta3 and activated Src when compared to cell lines with neither of these attributes [29].
• FAK induces expression of Prx1 to promote tenascin-C-dependent fibroblast migration [30].
• Transient overexpression of c-Jun induced tenascin-C expression in primary REF and in FR3T3, an established fibroblast cell line [28].
• CONCLUSIONS: In suture wounds, TN appears to enhance the amount of FN expression, and a lack of TN may impair stromal cell migration [31].

Other interactions of Tnc

• Syndecan-4 is also required for tenascin-C action [24].
• In the intraspecific backcross, wi was found to be non-recombinant with Orm1 and D4Mit244, 0.3 cM distal of Mup1, and 0.6 cM proximal of Tnc [32].
• No difference in the expression pattern of TNX were observed in TNC knockout and wild mice [18].
• The TN-C-positive cells aligned in the dentate gyrus exhibited the characteristic morphology of unipolar astrocytes as revealed by double labeling with glial fibrillary acidic protein (GFAP)-immunohistochemistry [33].
• Tenascin-C expression during wallerian degeneration in C57BL/Wlds mice: possible implications for axonal regeneration [19].

Analytical, diagnostic and therapeutic context of Tnc

• The Tnc isoform expression in neural stem/progenitor cells was analyzed by reverse transcriptase-PCR and dot blot Southern hybridization [20].
• Results of endpoint RT-PCR, quantitative real-time RT-PCR and gelatin zymography demonstrated that TN-C, strongly and dose dependently, upregulates MMP-9 expression in murine mammary cancer cells [1].
• The present analysis demonstrated their expression during early heart development, using mouse lines containing the lacZ gene targeted to the TNC locus, by RT-PCR, immunohistochemistry, and in situ hybridization [18].
• This study examined astroglial generation, migration, and differentiation in the developing mouse hippocampus by in situ hybridization histochemistry for TN-C mRNA [33].
• To study TNC isoform variability of wound healing in mice, we induced glomerulonephritis by using Habu snake venom (HSV) and examined alternatively spliced regions by the reverse transcription polymerase chain reaction (RT-PCR) technique [34].

References