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

---

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

A distinct subset of patients with peripheral T-cell lymphoma (PTCL) is described which reacts with Leu-19 (CD56), an antibody that has been shown to identify the neural cell adhesion molecule (NCAM). These NCAM-positive PTCL patients (11 of a series of 46 PTCL; 24%) exhibited a striking predilection for unusual anatomic sites of involvement: central nervous system (36%), muscle (18%), gastrointestinal tract, and nasopharynx (27% each). Additional extranodal sites of involvement included the pituitary, thyroid, parathyroids, adrenals, and pancreas. The NCAM-positive subset also exhibited a characteristic phenotypic profile, with significantly lower expression of CD3 and CD5 compared with the NCAM-negative group. RNA transcripts consistent with the NCAM gene were detected in tissue samples from five Leu-19-positive cases using a reverse transcriptase-polymerase chain reaction assay, supporting the idea that Leu-19 recognizes NCAM in these patient samples. This suggests that the expression of the NCAM plays a role in the behavior and localization of lymphomas. Because of the unique clinical and phenotypic characteristics of this group it may be designated as "NCAM-positive peripheral T-cell lymphoma."
...
PMID:Neural cell adhesion molecule-positive peripheral T-cell lymphoma: a rare variant with a propensity for unusual sites of involvement. 138 3

The development of the CNS is associated with an increasing use of the 30-bp variable alternative, spliced exon (VASE) in neural cell adhesion molecule (NCAM). We have assessed the relative usage of VASE by reverse transcriptase-linked polymerase chain reaction in the developing cerebellum and hippocampus at times when neurons isolated from these tissues can respond to substrate-associated NCAM by increased axonal growth and also at later developmental stages, when they are no longer responsive to substrate-associated NCAM. Neurons isolated from the developing cerebellum at postnatal day 6 respond to NCAM with increased neurite growth. NCAM transcripts from these cells were found to have negligible levels of VASE usage. In contrast, neurons that are isolated at later stages of development (postnatal days 8, 10, and 11) and do not respond to NCAM were found to synthesise a much higher proportion of NCAM transcripts containing VASE. In the hippocampus, embryonic day 18 neurons, which are responsive to NCAM, express low levels of VASE, whereas postnatal days 4 and 5 neurons, which are not responsive to NCAM, have a greater proportion of transcripts containing VASE. Thus, the level of NCAM VASE exon usage by neurons appears to be a good indicator of the ability of these cells to respond to non-VASE-containing NCAM (expressed in a cellular substratum) by increased neurite outgrowth.
...
PMID:Use of the neural cell adhesion molecule VASE exon by neurons is associated with a specific down-regulation of neural cell adhesion molecule-dependent neurite outgrowth in the developing cerebellum and hippocampus. 140 33

Perlecan is a modular heparan sulfate proteoglycan that harbors five domains with homology to the low density lipoprotein receptor, epidermal growth factor, laminin and neural cell adhesion molecule. Using a monoclonal antibody directed against the laminin-like domain of perlecan, we have recently shown that perlecan is widely expressed in all lymphoreticular systems. To investigate further this observation we have studied the expression of perlecan in two human leukemic cell lines. Using reverse transcriptase-PCR, ribonuclease protection assay, and metabolic labeling we detected significant perlecan expression in the multipotential cell line K562, originally derived from a patient with chronic myelogenous leukemia. In contrast, the promyelocytic cell line HL-60 expressed perlecan at barely detectable levels. These results were intriguing because the K562 cells do not assemble or produce a classical basement membrane. Following induction with either sodium butyrate or the phorbol diester 12-0-tetradecanoylphorbol-13-acetate (TPA), K562 and HL-60 differentiate into early progenitor cells with erythroid or megakaryocytic properties, respectively. Following treatment of K562 and HL-60 cells with either of these agents, perlecan expression was markedly increased in K562 cells. In contrast, we could detect perlecan protein synthesis in HL-60 cells only at very low levels, even after induction with TPA or sodium butyrate. Collectively, these results indicate that perlecan is actively synthesized by bone marrow derived cells and suggest that this proteoglycan may play a role in hematopoietic cell differentiation.
...
PMID:The proteoglycan perlecan is expressed in the erythroleukemia cell line K562 and is upregulated by sodium butyrate and phorbol ester. 754 67

Ito cells (lipocytes, stellate cells) are regarded as the principle matrix-producing cell of the liver and have been shown recently to express glial fibrillary acidic protein, an intermediate filament typically found in glia cells of the nervous system. The present study examines 1) whether Ito cells of rat liver express central nervous system typical adhesion molecules, namely, neural cell adhesion molecule (N-CAM), in a cell-type-specific manner and 2) whether N-CAM expression is affected by activation of Ito cells in vitro and during rat liver injury in vivo. As assessed by reverse transcriptase polymerase chain reaction, Northern blotting, Western blotting, and immunocytochemistry of freshly isolated and cultivated hepatic cells, N-CAM expression was restricted to Ito cells and was absent in hepatocytes, Kupffer cells, and sinusoidal endothelial cells. Ito cells expressed predominantly N-CAM-coding transcripts of 6.1 and 4.8 kb in size and 140-kd isoforms of the N-CAM protein, which was localized on the cell surface membrane of Ito cells. In parallel to glial fibrillary acidic protein down-regulation and smooth muscle alpha-actin up-regulation, N-CAM expression was increased during in vitro transformation of Ito cells from resting to activated (myofibroblast-like) cells and by the fibrogenic mediator transforming growth factor-beta 1. By immunohistochemistry, N-CAM was detected in normal rat liver in the portal field as densely packed material and in a spot as well as fiber-like pattern probably representing nerve structures. However, after liver injury, N-CAM expression became detectable in mesenchymal cells within and around the necrotic area and within fibrotic septae. In serially cut tissue sections, N-CAM-positive cells were predominantly co-distributed with smooth muscle alpha-actin-positive cells rather than glial fibrillary acidic protein-positive cells, especially in fibrotic livers. The experimental results illustrate that N-CAM positivity in the liver cannot be solely ascribed to nerve endings as, among the different types of resident liver cells, Ito cells specifically express N-CAM in vitro and presumably in vivo. In addition to its role as potential cell-type-specific marker protein for activated Ito cells, the induction of N-CAM expression might illustrate a mechanism by which mesenchymal cell proliferation might be inhibited when tissue repair is concluded.
...
PMID:Cell-type-specific expression of neural cell adhesion molecule (N-CAM) in Ito cells of rat liver. Up-regulation during in vitro activation and in hepatic tissue repair. 870 84

Tissue and stage-specific pre-mRNA splicing events are important for posttranscriptional gene control, yet the diversity of such regulatory pathways has been largely unexplored at the single-cell level. Here we use a less conventional approach, which combines the whole-cell patch clamp method and the reverse transcriptase-polymerase chain reaction, to examine five neuron-specific splicing events in individual Purkinje neurons during postnatal development in live slices of rat cerebellum. Within the dimensions of the slice, the neurons sampled in this manner remain connected in their natural circuits and express multiple neuron-specific mRNAs, unlike established cell lines. In contrast to invariant splicing of control mRNAs, significant changes in splicing regulation during development are displayed by regulated exons of the GABA(A) receptor gamma2 subunit, clathrin light chain B, neural cell adhesion molecule, and N-methyl-D-aspartate receptor R1 mRNAs. Whereas two of the neuron-specific exons are regulated in parallel in Purkinje neurons, these same substrates are regulated differentially in cerebellar Granule neurons during the same course of development. These results illustrate how two types of specialized neurons contribute to splicing regulation in the natural environment of the complex tissue. In addition, these results provide a larger view of splicing regulation, favoring models in which cell-specific machineries operate in a more selective, rather than widespread manner, in these neuronal cell types.
...
PMID:Cell- and stage-specific splicing events resolved in specialized neurons of the rat cerebellum. 897 73

Type 1B astrocytes of the human optic nerve head (ONH) constitutively express neural cell adhesion molecule (NCAM) in vivo and in vitro. Increased synthesis of NCAM has been detected in reactive astrocytes in the glaucomatous ONH of human donor eyes. Several NCAM isoforms are generated through alternate RNA splicing in tissue- and disease-specific patterns. In this study, we analyzed expression of NCAM isoforms in ONH of normal donors at different ages and in glaucoma. Total RNA was extracted from ONH of fetal, normal adult and glaucomatous eyes, and cultured human ONH astrocytes, fetal brain astrocytes and an astrocytoma cell line, for reverse transcriptase-polymerase chain reaction (RT-PCR) analysis. To distinguish between NCAM 180 and 140 isoforms, exon-specific primer sets covering exons 13-19 were used. Isoform-specific riboprobes were used for in situ hybridization (ISH) in glaucomatous and in age-matched ONH. By RT-PCR, NCAM 140 was the predominant isoform in adult ONH as well as in all cultured cells. NCAM 180 mRNA was strongly expressed in glaucoma, whereas in normal adult tissues it was not detectable. ISH confirmed expression of NCAM in normal adult ONH and localized NCAM 140 mRNA to astrocytes. ISH demonstrated expression of NCAM 180 mRNA in reactive astrocytes in glaucomatous ONH. Our results demonstrate that the NCAM 180 isoform is induced in glaucoma. NCAM 180 may play a role in astrocyte interaction with extracellular matrix (ECM), vessels, axons and other astrocytes and, through its expanded cytoplasmic domain, serve as a signaling molecule for reactive astrocytes during remodeling of the ONH in glaucoma.
...
PMID:Differential expression of neural cell adhesion molecule isoforms in normal and glaucomatous human optic nerve heads. 1064 Jun 77

The aim of this work was to study which genes upregulated by the IFN-gamma/STAT1 system in human muscle might be involved in the process of muscle fiber atrophy in dermatomyositis (DM). These proteins included proteases (cathepsins B and L, calpain), proteins implicated in apoptosis and cell cycle (Bcl-x(l), Fas, p21), structural proteins (beta-actin, utrophin, desmin), and other proteins whose expression is known to be modified by IFN-gamma (neural cell adhesion molecule (N-CAM), major histocompatibility complex-I (MHC-I)). We performed immunocytochemistry, Western blot, and semiquantitative reverse transcriptase-polymerase chain reaction using human muscle cultures. We found upregulation of cathepsins B and L, bcl-x(l) and p21 while N-CAM, calpain, utrophin, desmin, beta-actin and Fas remained at basal levels. Immunohistochemistry on frozen sections from biopsies of patients with different muscle diseases showed upregulation of cathepsin L and calpain in perifascicular muscle fibers in DM. In view of these results, the increased expression of cathepsins L and B after IFN-gamma stimulation in muscle cultures and its inhibition using fludarabine, a STAT1 blocker, further support our previous studies and suggest that the increased expression of cathepsins detected in perifascicular muscle fibers in DM is mediated by IFN-gamma/STAT1 and contributes to their atrophy.
...
PMID:Cathepsins are upregulated by IFN-gamma/STAT1 in human muscle culture: a possible active factor in dermatomyositis. 1155 41

Transforming growth factor (TGF) beta1 and ethanol retard the migration of young, post-mitotic neurons to the developing cerebral cortex. The coordination of this migration depends upon cell adhesion proteins (CAPs). We examined the effects of TGFbeta1 and ethanol on genes related to both TGF and CAPs. Rat B104 neuroblastoma cells were treated with TGFbeta1 (0 or 10 ng/mL) and ethanol (0 or 400 mg/dL) for 6-48 h. Total RNA was purified from each sample and analyzed using the Rat U34A GeneChip (Affymetrix). Candidate genes were those up- or down-regulated by either TGFbeta1 or ethanol. Twenty transcripts of CAPs were identified as being expressed by B104 cells and as being affected by treatment with TGFbeta1 or ethanol. The expression was verified for five representative genes (neural cell adhesion molecule, L1, and integrins alpha1, alpha7, and beta1) using assays with real-time reverse transcriptase-polymerase chain reactions. Each of these genes showed time-dependent changes. The changes were reflected in increases in protein expression that appeared within 24 or 48 h. Thus, the effects of TGFbeta1 and ethanol on CAPs parallel changes described in vivo and likely underlie changes associated with ethanol-induced alterations in neuronal migration.
...
PMID:Transforming growth factor beta1 and ethanol affect transcription and translation of genes and proteins for cell adhesion molecules in B104 neuroblastoma cells. 1668 95

We investigated the toxic effects of carbendazim and n-butyl isocyanate (BIC), metabolites of the fungicide benomyl, on development in the African clawed frog, Xenopus laevis. To test the toxic effects, frog embryo teratogenesis assays using Xenopus were performed. Embryos were exposed to various concentrations of carbendazim (0-7 microM) and BIC (0-0.2 microM). LC(100) for carbendazim and BIC were 7 and 0.2 microM, respectively, and the corresponding LC(50), determined by probit analysis, were 5.606 and 0.135 microM. Exposure to carbendazim concentrations > or = 3 microM and BIC concentrations > or = 0.1 microM resulted in 10 different types of severe external malformation. Histological examinations revealed dysplasia of the brain, eyes, intestine, and somatic muscle, and swelling of the pronephric ducts. These phenomena were common in both test groups. The tissue-specific toxic effects were investigated with an animal cap assay. Neural tissues are normally induced at a high frequency by activin A, however, the induction of neural tissues was strongly inhibited by the addition of carbendazim. Conversely, the addition of BIC resulted in weak inhibition of neural tissues. Electron micrographs of animal cap explants revealed degeneration of cell junctions in the carbendazim-treated group, but not in the BIC-treated group. Numerous residual yolk platelets and mitochondrial degeneration were commonly observed in both test groups. The gene expression of cultivated animal cap explants was investigated by reverse transcriptase-polymerase chain reaction and revealed that expression of the neural-specific marker neural cell adhesion molecule was more strongly inhibited in the carbendazim-treated group than in the BIC-treated group.
...
PMID:Toxic effects of carbendazim and n-butyl isocyanate, metabolites of the fungicide benomyl, on early development in the African clawed frog, Xenopus laevis. 1821 21

Suppressor of cytokine signaling-2 (SOCS-2) has recently been identified as an important regulator involved in neuronal differentiation and maturation. However, the role of SOCS-2 in ischemia-induced hippocampal neurogenesis remains to be clarified. Here we investigated the spatiotemporal expression of SOCS-2 in the rat hippocampus following transient forebrain ischemia, and particular attention was paid to changes in the dentate gyrus. SOCS-2 mRNA was constitutively expressed in hippocampal neurons and astrocytes in control animals. However, its upregulation occurred specifically in reactive astrocytes in the hippocampus proper, in particular the CA1 and dentate hilar regions, at day 3 after reperfusion, and was sustained for more than 2 weeks. In addition to the CA1 and hilar regions, SOCS-2 was transiently increased in the subgranular zone (SGZ) of the dentate gyrus on days 3-7 after reperfusion. This correlated with the post-ischemic upregulation of SOCS-2 in the CA1 or dentate gyrus subfield, including the SGZ detected by semiquantitative reverse transcriptase-polymerase chain reaction analysis. The majority of the SOCS-2-expressing cells in the SGZ were co-labeled with glial fibrillary acidic protein (GFAP), and a subpopulation of GFAP/SOCS-2 double-labeled cells in the SGZ co-expressed the neural progenitor marker nestin, or the proliferation marker proliferating cellular nuclear antigen. In addition, a subset of SOCS-2-labeled cells in the SGZ expressed the immature neuronal marker polysialic acid-neural cell adhesion molecule. These data suggest that SOCS-2 may be involved in glial reactions, and possibly adult hippocampal neurogenesis during ischemic insults.
...
PMID:Enhanced expression of SOCS-2 in the rat hippocampus after transient forebrain ischemia. 1946 88


1

---