Transcriptional regulation of tenascin genes

نویسندگان

  • Francesca Chiovaro
  • Ruth Chiquet-Ehrismann
  • Matthias Chiquet
چکیده

Extracellular matrix proteins of the tenascin family resemble each other in their domain structure, and also share functions in modulating cell adhesion and cellular responses to growth factors. Despite these common features, the 4 vertebrate tenascins exhibit vastly different expression patterns. Tenascin-R is specific to the central nervous system. Tenascin-C is an "oncofetal" protein controlled by many stimuli (growth factors, cytokines, mechanical stress), but with restricted occurrence in space and time. In contrast, tenascin-X is a constituitive component of connective tissues, and its level is barely affected by external factors. Finally, the expression of tenascin-W is similar to that of tenascin-C but even more limited. In accordance with their highly regulated expression, the promoters of the tenascin-C and -W genes contain TATA boxes, whereas those of the other 2 tenascins do not. This article summarizes what is currently known about the complex transcriptional regulation of the 4 tenascin genes in development and disease.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Transcriptional Response of Structural and Regulatory Genes Involved in Isoprene Biosynthesis and its Relation to Essential Oil Biosynthesis in Response to Salicylic Acid and Abscisic Acid in Mentha piperita L.

Background: In peppermint, precursors for the biosynthesis of monoterpenes are provided by plastidial methyl-erythritol-phosphate (MEP) pathways. Objective: In order to increase our understanding of terpene metabolism in M. piperita, the effect of salicylic acid (SA) and abscisic acid (ABA) in the modulation of expression pattern of genes involved in essential oil biosynthesis and secretion wa...

متن کامل

In Silico Genome-Wide Screening for TnrA-Regulated Genes of Bacillus clausii

Bacillus clausii TnrA transcription factor is required for global nitrogen regulation. In order to obtain anoverview of gene regulation by TnrA in B. clausii KSMK16, the entire genome of B. clausii was screened forthe consensus sequence, 5’-TGTNAN7TNACA-3’ known as the TnrA box, and 13 transcription units werefound containing a putative TnrA box. The TnrA targets identified in...

متن کامل

Transcriptional regulation of the endogenous danger signal tenascin-C: a novel autocrine loop in inflammation.

Inappropriate expression of proinflammatory mediators underpins the pathogenesis of autoimmune disease and tumor metastasis. The extracellular matrix glycoprotein tenascin-C is an endogenous activator of innate immunity that promotes the synthesis of inflammatory cytokines via activation of TLR4. Little tenascin-C is observed in most healthy adult tissues, but expression is specifically upregul...

متن کامل

Microarray-based identification of tenascin C and tenascin XB, genes possibly involved in tumorigenesis associated with neurofibromatosis type 1.

PURPOSE Neurofibromatosis type 1 (NF1) is an autosomal dominant disorder with a complex variety of clinical manifestations. The hallmark of NF1 is the onset of heterogeneous (dermal or plexiform) benign neurofibromas. Plexiform neurofibromas can give rise to malignant peripheral nerve sheath tumors, which are resistant to conventional therapies. EXPERIMENTAL DESIGN To identify new signaling p...

متن کامل

Transcriptional regulation of tenascin‐W by TGF‐beta signaling in the bone metastatic niche of breast cancer cells

Tenascin-W is a matricellular protein with a dynamically changing expression pattern in development and disease. In adults, tenascin-W is mostly restricted to stem cell niches, and is also expressed in the stroma of solid cancers. Here, we analyzed its expression in the bone microenvironment of breast cancer metastasis. Osteoblasts were isolated from tumor-free or tumor-bearing bones of mice in...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:

دوره 9  شماره 

صفحات  -

تاریخ انتشار 2015