Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.48 (transcriptase)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We performed high-sensitivity flow cytometry and Western blotting to study the expression of the low-affinity NGF receptor (p75NGFR) and of the transmembrane tyrosine kinase (Trk) family of high-affinity receptors for the different neurotrophic factors on Epstein-Barr virus (EBV)-transformed human B lymphocytes. Reverse transcriptase (RT) polymerase chain reaction (PCR) with single and multiple sets of primers (multiplex RT-PCR) was used to survey the repertoire of neurotrophin receptor transcripts in this cell line. We demonstrated that transformed B cells express detectable levels of Trk b and its mRNA. Conversely, negative results were obtained for p75NGFR, Trk a, and Trk c. Exposure of EBV-transformed B lymphocytes to brain-derived neurotrophic factor (BDNF) triggered the phosphorylation of Trk b, as demonstrated by Western blots of cell lysates probed with monoclonal antibody against phosphotyrosine.
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PMID:Expression of high- and low-affinity neurotrophin receptors on human transformed B lymphocytes. 863 56

The present work investigated whether neurotrophins could differentially affect in vitro growth and maturation of two related subsets of hypothalamic neurons, hypophysiotropic somatostatin (SRIH) neurons projecting from the periventricular area and arcuate SRIH interneurons. For this purpose, the hypothalamus of 17-day-old rat fetuses was sampled and separated into a ventral and a dorsal fragment containing respectively periventricular and arcuate regions. Each fragment was dissociated and seeded separately in defined medium. Brain-derived neurotrophic factor (BDNF) or neurotrophin-3 (NT-3), two important members of the neurotrophin family involved in neuronal differentiation and plasticity, were added to the cultures at seeding time. After 6 or 11 days in vitro, neurons were labeled with an anti-SRIH antiserum and submitted to morphometric analysis. In parallel, SRIH mRNA was estimated by semiquantitative reverse-transcriptase-polymerase chain reaction, and neuronal SRIH content, basal and depolarisation-stimulated releases measured by radioimmunoassay. The response of control, non-labeled neurons was estimated by neuronal counts and by assaying glutamic acid decarboxylase, a marker of a large majority of hypothalamic neurons. BDNF markedly increased the size and the branching number of SRIH periventricular cell bodies. Expression of SRIH mRNA, as well as SRIH content and release into the culture medium, were also stimulated by the neurotrophin. Non-SRIH neurons were not affected by the treatment. Under the same conditions, arcuate neurons exhibited a weak, mostly transient response to BDNF. NT-3 was ineffective on either neuronal subset. Immunoneutralization of Trk receptors provided further evidence for BDNF effect specificity. The results indicate that BDNF is a selective activator of the differentiation of hypophysiotropic SRIH neurons in the periventricular area of the hypothalamus.
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PMID:Brain-derived neurotrophic factor but not neurotrophin-3 enhances differentiation of somatostatin neurons in hypothalamic cultures. 1102 8

Human infection with Trypanosoma brucei may result in meningo-encephalitis, neuronal demyelination, blood-brain-barrier dysfunction, peri-vascular infiltration, astrocytosis and neuronal apoptosis. Prevention of the short- or long-term, parasite-induced, neuronal assault requires a better understanding of the host's responses to the infection at the molecular level. Northern analysis, cDNA micro-arrays, reverse-transcriptase-PCR (RT-PCR), SDS-PAGE and immunohistology were therefore used to investigate global gene and protein expression in the brains of mice infected with T. brucei. Temporal and spatial expression of neuroleukin (NLK), a predominant neurotrophin which is associated with neuronal protection and regeneration during neuronal assault in the brain, was then assessed. Expression of 20 of the 588 genes investigated (representing pro- and anti-inflammatory immuno-modulators, growth factors, neurotransmitters, and pro- and anti-apoptosis factors) was significantly altered (P < 0.05). TUNEL analysis revealed extensive apoptosis at peak parasitaemia, mainly in the cerebellum. RT-PCR analysis of two regulators of apoptosis, Bcl-x(L) (anti-apoptotic) and Bax (pro-apoptotic), revealed equivalent increases in levels of expression. NLK expression was up-regulated in punctated fashion in brain and was mainly localized to abnormal (stellate) catecholamine neurons (CN) in the locus coeruleus (LC) of infected [and, to a lesser degree, the normal (polygonal) cells of uninfected] brainstem. Expression of NLK receptor (NLK-R) was inversely correlated with that of NLK. At peak parasitaemia, trypanosome infection apparently induces cerebellar apoptosis and a corresponding increase in NLK expression. NLK may be modulating inflammation and is probably involved in protecting CN and the cerebellum against apoptosis.
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PMID:Trypanosoma brucei infection induces apoptosis and up-regulates neuroleukin expression in the cerebellum. 1178 34

Several neurotrophic factors (NTFs) are effective in protecting retinal photoreceptor cells from the damaging effects of constant light and slowing the rate of inherited photoreceptor degenerations. It is currently unclear whether, if continuously available, all NTFs can be protective for many or most retinal degenerations (RDs). We used transgenic mice that continuously overexpress the neurotrophin NT-3 from lens fibers under the control of the alphaA-crystallin promoter to test for neuroprotection in light-damage experiments and in four naturally occurring or transgenically induced RDs in mice. Lens-specific expression of NT-3 mRNA was demonstrated both by in situ hybridization in embryos and by reverse-transcriptase polymerase chain reaction (RT-PCR) in adult mice. Furthermore, NT-3 protein was found in abundance in the lens, ocular fluids, and retina by enzyme-linked immunosorbent assay (ELISA) and immunocytochemistry. Overexpression of NT-3 had no adverse effects on the structure or function of the retina for up to at least 14 months of age. Mice expressing the NT-3 transgene were protected from the damaging effects of constant light to a much greater degree than those receiving bolus injections of NT-3. When the NT-3 transgene was transferred into rd/rd, Rds/+, Q344ter mutant rhodopsin or Mertk knockout mice, overexpression of NT-3 had no protective effect on the RDs in these mice. Thus, specificity of the neuroprotective effect of NT-3 is clearly demonstrated, and different molecular mechanisms are inferred to mediate the protective effect in light-induced and inherited RDs.
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PMID:Sustained delivery of NT-3 from lens fiber cells in transgenic mice reveals specificity of neuroprotection in retinal degenerations. 1892 74