Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.7.49 (reverse transcriptase)
31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have used in situ hybridization and reverse transcriptase polymerase chain reaction (PCR) to study the origins of the extracellular matrix glycoprotein tenascin during the development of the central and peripheral nervous systems. Previous studies have shown that neural crest cells migrate along pathways that are lined with tenascin. In situ hybridization, PCR, and western blotting reveal that these cells themselves are a major source of tenascin both in vitro and in the embryo. Thus, tenascin is probably not acting as a guidance molecule but is more likely to be promoting neural crest cell motility in a more general way. Similarly, subpopulations of proliferating and migrating glia make tenascin in the developing central nervous system, as do the radial glia that are used as a substratum for migrating neuronal cell bodies. In the adult, tenascin continues to be expressed in the cerebellum by Golgi epithelial cells. This expression, as well as the expression of tenascin in connective tissue, indicates that this molecule may also be playing a role in regulating differentiation. Finally, the distribution of tenascin transcripts in the developing brain and spinal cord is similar to the distribution of mRNAs encoding receptors for platelet-derived growth factor-AA and basic fibroblast growth factor. In vitro studies indicate that both of these factors are potential regulators of tenascin expression.
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PMID:Cellular origins of tenascin in the developing nervous system. 753 Jan 47

Two distinct mRNA-splice isoforms of tenascin (TN) are expressed differentially during rat lung development. The unique temporal expression pattern of two TN isoforms suggests the expression of tenascin is strictly developmentally regulated in rat lung tissue. We investigated molecular mechanisms which modulate alternative-splicing expression of TN in lung development. The effect of transforming growth factor-beta 1 (TGF-beta 1) on regulation of expression of TN isoforms was examined by in vitro lung explant culture. Immunoblotting with anti-TN antibody detected two TN polypeptides in rat lung explant culture, the larger [relative molecular weight (M(r)) 230, TN230] polypeptide and the smaller (M(r) 180, TN180). TGF-beta 1 markedly induced the TN180 isoform and caused only a moderate increase of the TN230 isoform. The effects of TGF-beta 1 were shown to be dose dependent over a physiological range of TGF-beta 1 protein concentration. The induction of TN isoform biosynthesis by TGF-beta 1 was detected 12 h after addition of the growth factor, and the effects endured for up to 48 h at a dose of 5 ng/ml. By reverse transcriptase-polymerase chain reaction through amplification of the entire fibronectin type III (FN-III) splicing domain, two distinct TN isoforms were detected in total RNA isolated from gestational day 21 rat lung explant culture treated with TGF-beta 1 and from postnatal day 8 rat lung. The larger isoform contained five FN-III alternative splicing repeats [1,420 base pairs (bp)], but the shorter splicing isoform lacked four FN-III alternative splicing repeats (340 bp).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:TGF-beta regulates expression of tenascin alternative-splicing isoforms in fetal rat lung. 753 67

Tenascin and thrombospondin belong to the growing family of extracellular matrix glycoproteins believed to have an anti-adhesive function during development. Immunohistochemistry has been used to identify these proteins in the developing central nervous system, in the matrix surrounding peripheral neurons, and in connective tissue. The antibodies used in most of these studies, however, could not distinguish between different splice variants (tenascin) nor different genetic forms (thrombospondin). For this reason, we used the reverse transcriptase polymerase chain reaction to generate DNA probes that are specific to the transcripts of high M(r) tenascin and thrombospondin 2. These probes were then used for an in situ hybridization study to determine the cellular origins of specific tenascin and thrombospondin forms throughout the development of the chick. The mRNA encoding high M(r) tenascin was found associated with motile cells and in tissues undergoing dynamic modeling: migrating glia, epithelial glia used as a substratum for migrating neurons, the growing tips of lung buds, and during osteogenesis. In contrast, the mRNAs of low M(r) tenascin were concentrated in areas of cartilage deposition and chondrocyte proliferation. Thrombospondin 2 mRNA was not detected in the developing central nervous system at any time during development by in situ hybridization. In contrast, it was found in embryonic mesenchyme, perichondrium, epimysium, and endothelial cells. Thrombospondin 2 mRNA was detected in poly(A) RNA isolated from embryonic spinal cord and cerebellum by polymerase chain reaction, though it was not detected in poly(A) RNA from the avascular retina. Thus, thrombospondin 2 mRNA may be present in the developing brain at low levels in endothelial cells or blood cells. These data support the notion that tenascin splice variants have distinct roles during development, and that thrombospondin 2 is more likely to be playing a role associated with the morphogenesis of connective tissue than neuronal development.
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PMID:The in situ localization of tenascin splice variants and thrombospondin 2 mRNA in the avian embryo. 769 13

We found that mice transgenic for native bovine growth hormone (bGH) gene had increased body size and rapidly progressive glomerulosclerosis, whereas mice transgenic for a mutated bGH gene (bGH-m11) had near normal body size and slowly progressive glomerulosclerosis. The aim of this study was to determine whether rapidly and slowly progressive glomerulosclerosis had distinct glomerular extracellular matrix (ECM) and growth factor mRNA levels. ECM and growth factors were quantitated by competitive reverse transcriptase-PCR in microdissected glomeruli from bGH, bGH-m11, and nontransgenic littermate control mice. In rapid progressors (bGH mice) at 2 to 3 months, the levels of mRNA-coding for some glomerular ECM and growth factors were increased (alpha 1(IV) collagen, 7.3-fold; laminin B1, 3.9-fold; tenascin, 8-fold; and tumor growth factor (TGF)-beta 1, 3.4-fold). These levels underwent a further 2.3-fold increase at 6 to 9 months. Platelet-derived growth factor (PDGF)-B mRNA was high at 2 to 3 months (7.4-fold) and 6 to 9 months (9.5-fold) and was associated with an increased [3H]-thymidine-labeling index and glomerular cell number. In slow progressors (bGH-m11 mice), the mRNA levels at 2 to 3 months were approximately one half that of rapid progressors (alpha 1(IV) collagen, 3.4-fold; laminin B1 1.9-fold; tenascin, 3-fold; TGF-beta 1, 2.2-fold). PDGF-B levels were normal. At 6 to 9 months, alpha 1(IV) collagen, TGF-beta 1, and PDGF-B mRNA levels doubled, whereas tenascin and laminin B1 levels remained stable. At 12 to 18 months, the alpha 1(IV) collagen, TGF-beta 1, and tenascin levels increased by nearly another 50%. The labeling index and PDGF levels were not increased at any time. The levels of expression of several glomerular ECM mRNA and growth factors of rapid progressors at 2 to 3 months of age was nearly double that of slow progressors, nearly doubling again by 6 to 9 months. In slow progressors, alpha 1(IV) collagen and TGF-beta 1 mRNA levels continued to increase at a slow rate, but tenascin and laminin mRNA levels were only further increased at 12 to 18 months. Thus, the initial levels of these mRNA and their rate of change correlated with the severity of glomerulosclerosis.
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PMID:Differential expression of glomerular extracellular matrix and growth factor mRNA in rapid and slowly progressive glomerulosclerosis: studies in mice transgenic for native or mutated growth hormone. 911 9

The tenascin-R (TN-R) gene encodes a multidomain extracellular matrix protein belonging to the tenascin family, previously detected only in the central nervous system. In this report, we describe the structure of the 5' region of the human TN-R gene and characterize the activity of its promoter. We cloned two previously unreported nontranslated exons (exons 1 and 2, 539 and 101 bp in length, respectively) separated by a large (> or = 40-kb) intron. The intron between exons 2 and 3 (containing the ATG codon) is 122 kb in length. Tenascin-R transcripts in fetal, adult, and neoplastic human brain contain both exons 1 and 2, as demonstrated by S1 nuclease analysis and reverse transcriptase-polymerase chain reaction. The human TN-R promoter displays relatively unusual features in terms of sequence in that it lacks any TATA box, CAAT box, GC-rich regions, or initiator element. The promoter displays its activity only in cultured cells of neural and glial origin, not in transformed epithelial cells and melanoma cells. All the elements required for the full and cell-specific activity of the promoter are contained in the 57-bp sequence closest to the transcription startpoint.
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PMID:Structure of 5' region of human tenascin-R gene and characterization of its promoter. 953 7

We examined the expression of selected growth factors, growth factor receptors, elements of extracellular matrix and cell adhesion molecules in the germinal matrix layer (GML) utilizing immunohistochemistry and reverse transcriptase polymerase chain reaction. At autopsy brain samples from 10 neonatal infants were used. Epidermal growth factor receptor (EGFR) was significantly expressed in the matrix cells. While transforming growth factor alpha and heparin-binding epidermal growth factor-like growth factor were found in the matrix cells or vascular wall as ligands, epidermal growth factor was not expressed. EGFR and its ligands are thought to be important factors for the maintenance of the matrix cells and cell-to-cell interactions. Insulin like growth factor I, its receptor Ibeta and tenascin were found in the stroma of the GML and periventricular region. Vascular endothelial growth factor and receptor Flk-1, laminin A and B2, fibronectin, collagen type IV and integrins such as beta3, alpha5beta1 and alphaVbeta3 were found mainly in or around the vascular wall indicating their important roles for vascularization. Transforming growth factor beta2 and its receptor II were expressed in the matrix cells and/or vascular wall suggesting a role in proliferation and/or regression of the vasculature. CD44 and Thy-1 were also expressed in the matrix cells.
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PMID:Growth factors in infant germinal matrix: relationship to extracellular matrix and cell adhesion molecules. 973 49

Tenascin (TN) is a hexameric extracellular matrix glycoprotein that is temporally and spatially restricted during lung development. This study examines the expression and regulation of TN in early lung organogenesis. Two TN isoforms were detected in total RNA isolated from embryonic day 14 rat lung tissues by reverse transcriptase polymerase chain reaction. The localization of TN in embryonic day 14 rat lung tissues was investigated by using in situ hybridization performed with an antisense RNA probe. TN mRNA was expressed exclusively by the mesenchyme but not by the epithelium of embryonic rat lungs. The intense expression of TN was observed in the mesenchyme that immediately surrounds the growing epithelial cells of the developing bronchi. The effect of the synthetic glucocorticoid hormone dexamethasone on the regulation of TN expression was examined by in vitro lung explant culture. Two TN polypeptides, the larger (M(r) 230 kDa, TN230) polypeptide and the smaller (M(r) 180 kDa, TN180) isoform, were detected in embryonic day 21 rat lungs by immunoblot analysis with anti-TN antibody. Dexamethasone inhibited both TN230 and TN180 biosynthesis. The study demonstrates the expression of TN at the early stage of lung organogenesis and presents evidence of hormonal regulation of TN in lung development, suggesting a potential role of TN in the communication between the epithelial and mesenchymal cells during lung branching morphogenesis.
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PMID:Tenascin is expressed in the mesenchyme of the embryonic lung and down-regulated by dexamethasone in early organogenesis. 1051 24

We studied expressions of various growth factors, their receptors, cell adhesion molecules and extracellular matrix components in Warthin's tumor of the salivary gland with immunohistochemistry and reverse transcriptase-polymerase chain reaction (RT-PCR). Various growth factors and their receptors, such as transforming growth factor-alpha (TGF-alpha), heparin-binding epidermal growth factor-like growth factor (HB-EGF), TGF-beta2, TG-beta3, insulin-like growth factor (IGF)-I and -II, vascular endothelial growth factor (VEGF), EGF receptor (EGFR), erb-B4, TGF-betaRI and II, Flt and Flk-1 and IGF receptor Ibeta, were found in epithelial cells and/or in some lymphoid cells. Fibronectin, laminin, collagen type IV and tenascin were found in stroma of the lymphoid tissue. Integrins such as alpha3beta1 and beta3, Thy-1, CD44 and VCAM-1 were also expressed in epithelial and/or lymphoid cells. These various proteins may interact and regulate the proliferation and cell attachment of both epithelial and lymphoid components in this unique tumor.
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PMID:Growth factors, extracellular matrix components and cell adhesion molecules Warthin's tumor. 1133 65

Tenascin-C is a protein of the extracellular matrix which has been suggested to regulate organogenesis. We have analysed the expression of tenascin-C mRNA during mouse tooth development. We show that it is transiently expressed during epithelial budding in the condensed dental mesenchyme, and that it reappears later in the dental papilla mesenchyme where it persists in the dental pulp but is downregulated in odontoblasts. Probes corresponding to the domains A4, B, and D of the differentially spliced and domain 7 of the constant region of the FNIII-like domain show similar patterns of hybridization. Dental epithelium has been shown to induce tenascin-C in early dental mesenchyme, and we show that growth factors in the transforming growth factor beta (TGFbeta) and fibroblast growth factor (FGF) families can mimic this effect. FGF-4, -8 and TGFbeta-1 proteins were applied locally by beads on dissected dental mesenchyme, and tenascin-C expression was analysed after 24 h culture by reverse transcriptase-polymerase chain reaction (RT-PCR) in situ hybridization, and immunohistochemistry. FGF-4 and TGFbeta-1 stimulated tenascin-C expression in E12 dental mesenchymes. RT-PCR showed induction of several tenascin-C isoforms by both TGFbeta-1 and FGFs. We conclude that several splice forms are expressed during mouse tooth development, and that TGFbeta- and FGF-family growth factors may act as epithelial signals inducing tenascin expression in the dental mesenchyme.
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PMID:Tenascin-C in developing mouse teeth: expression of splice variants and stimulation by TGFbeta and FGF. 1134 55

Acute asthma is characterized by a decrease in the pH of the exhaled breath condensate and bronchoconstriction. These perturbations may injure the epithelium in a chronic, intermittent pattern, leading to subepithelial fibrosis. We used an in vitro three-dimensional model of the bronchial mucosa to elucidate the response to a repeated chemical or physical insult to the epithelium in the postcontraction phase. We used enzyme-linked immunosorbent assay and reverse transcriptase--polymerase chain reaction to assess the production of the following proteins: matrix metalloproteinase (MMP) 3, MMP-9, tissue inhibitor of MMP-1, transforming growth factor beta 1, thrombospondin 1, tenascin, and fibronectin. The presence of the epithelium enhanced the degree of tissue contraction (50.1 +/- 4.4% of original area versus 75.4 +/- 2.3%). In the absence of injury, tenascin, fibronectin, MMP-3, and tissue inhibitor of MMP-1 are actively expressed. However, the chronic chemical wound markedly inhibited the expression of all proteins. We conclude that the epithelium, wound type, and age of the tissue (contracting versus postcontraction) impact the expression of key proteins in an in vitro model of subepithelial fibrosis in asthma.
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PMID:Expression of matrix proteins in an in vitro model of airway remodeling in asthma. 1263 76


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