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:3.1.27.1 (RNase)
16,360 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The DNA fraction from a line of bovine embryonic kidney cells originally exposed as primary cultures several months earlier to a temperature-sensitive (ts) mutant of respiratory syncytial (RS) virus could be used to transfect human HEp-2 cells with the production of infectious RS virus. The DNA donor cells, designated BEK/RS ts, retained their healthy fibroblastic appearance during continuous cultivation at a temperature (39 degrees) restrictive for growth of the original infecting mutant and showed no evidence for RS virus replication or viral antigen synthesis when directly examined for these activities by conventional methods. The infectious property of the DNA from BEK/RS ts cells was abolished by exposure of the nucleic acid preparation to DNase (but not RNase) or by pretreatment of recipient HEp-2 cells with actinomycin D or mitomycin C. The latter drug treatments substantially enhanced the replication of infecting wild-type RS virus in HEp-2 cells. Viral isolates derived from the progeny of a DNA transfection included clones possessing several genetic markers of the RS ts mutant originally used to infect BEK/RS ts cells and other virus clones that appeared to be either hybrid or wild-type for phenotypic properties such as their temperature sensitivity. An infectious proviral DNA was also detected in a line of virogenic HEp-2 cells (HEp-2/RS) persistently infected with respiratory syncytial virus after exposure to the wild-type strain 2 years earlier.
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PMID:Recovery of infectious proviral DNA from mammalian cells infected with respiratory syncytial virus. 110 42

We have developed a functional screen in yeast to identify ligands for receptor tyrosine kinases. Using this method, we cloned two Xenopus genes that activate the fibroblast growth factor (FGF) receptor. These encode novel secreted proteins, designated FRL1 and FRL2, distantly related to the epidermal growth factor and angiogenin/ribonuclease families, respectively. Both genes activate the FGF receptor in Xenopus oocytes as well as in yeast. Overexpression induces mesoderm and neural-specific genes in Xenopus explants; induction is blocked by a dominant negative inhibitor of the FGF receptor. FRL1 is broadly expressed during gastrulation and neurulation, while FRL2 is expressed principally in the axial mesoderm and brain at later stages. Our results indicate that despite their lack of similarity with FGF, FRL1 and FRL2 are ligands for the FGF receptor that play distinct roles in development.
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PMID:The identification of two novel ligands of the FGF receptor by a yeast screening method and their activity in Xenopus development. 758 65

Goitre was induced in adult rats by acute (1 or 2 weeks) or chronic (4 or 10 weeks) administration of methimazole together with a low iodine diet. Involution of thyroid growth was then observed at 16 weeks, 4 weeks after withdrawal of goitrogens and reversion to a normal diet. Experimental animals quickly became hypothyroid compared with controls and exhibited thyroid hyperplasia (control (n = 10): total serum thyroxine (T4) 66 +/- 4 nmol/l, thyroid weight 5 +/- 1 mg/100 g body weight, means +/- S.D.; experimental (n = 10): T4 undetectable, thyroid weight 27 +/- 4 mg/100 g body weight after 2 weeks of treatment). Thyroid growth rate subsequently slowed between 2 and 10 weeks. Messenger RNA for basic fibroblast growth factor (basic FGF) and for the high-affinity FGF receptor, was compared in the thyroids and livers of control and goitrous rats by ribonuclease protection assay. Low levels of mRNA for basic FGF and its receptor were detectable in thyroids from control rats at all times, while none was detected in the livers from any animal. Basic FGF and receptor mRNAs increased, and were detected at greatest abundance in hyperplastic thyroids at 1 and 2 weeks respectively, during goitre formation, but subsequently declined in parallel with thyroid growth rate at 4 and 10 weeks. When quantified by radioimmunoassay, basic FGF extracted from thyroids was fivefold greater than in controls after 1 week of goitrogen treatment (control (n = 4): 24 +/- 9 pmol/micrograms DNA; goitre (n = 4): 100 +/- 16 pmol/micrograms DNA; P < 0.05). Basic FGF and FGF receptor mRNAs localized by in situ hybridization predominantly to the epithelial cell population within follicles. Localization by immunohistochemistry demonstrated that basic FGF was present in the thyroids of control rats, and was largely associated with the basement membrane of follicles. During thyroid hyperplasia, increased basic FGF immunoreactivity appeared over the cytoplasm of follicular epithelial cells and was lost from the extracellular matrix. Thyroid involution following removal of goitrogen/low iodine treatment was associated with a decrease in mRNA for basic FGF or its receptor, and a loss of immunoreactive basic FGF from the cytoplasm of follicular cells. These results suggest that autocrine expression of basic FGF and FGF receptor could contribute to thyroid hyperplasia in rats.
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PMID:Increase of basic fibroblast growth factor (FGF) and FGF receptor messenger RNA during rat thyroid hyperplasia: temporal changes and cellular distribution. 793 Oct 5

Recent observations suggest that fibroblast growth factors (FGFs) and their receptors are involved in the control of embryogenesis. Several FGF receptor genes have been identified so far and their expression is differentially regulated. As part of a continuing effort to analyse the differential expression of FGF receptors and their potential role during amphibian development, we have isolated a Pleurodeles homolog of FGF receptor 3 (FGFR-3), which we designated PFR-3 because of its highest homology to human FGFR-3 (75% overall identity). PFR-3 is a maternally derived mRNA. While a low level of expression persists during the cleavage and gastrula stages, a significant increase in the mRNA was observed at the end of the gastrula stage. RNase protection analysis on dissected tissues showed that PFR-3 mRNA was mainly localized to the ectoderm at the early gastrula stage and then shifted to the embryonic neural tissues, whereas adult brain had decreased levels of PFR-3 mRNA expression. Consistent with the loss of FGF receptors during skeletal muscle terminal differentiation, PFR-3 as well as other FGF receptor mRNAs were undetectable in the adult skeletal muscle. However, highest levels of PFR-3 mRNA expression were found in the testis. In situ hybridization revealed strong expression in the germinal epithelium of the embryonic brain (especially the diencephalon and rhombencephalon) and neural tube, in the lens and the cranial ganglia. The epithelium of the developing gut, like the pharynx and esophagus, also prominently expressed PFR-3 mRNA. Other sites of expression were found in the liver and in the mesenchymal condensation sites of branchial arches.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Isolation and developmental expression of the amphibian homolog of the fibroblast growth factor receptor 3. 800 62

In the present study, we attempted to clarify the controversial question whether basic fibroblast growth factor (bFGF, FGF-2) mRNA is present or absent in the embryonic central nervous system (CNS). For this purpose we analyzed the expression of the FGF-2 mRNA in the embryonic and adult forebrain, brainstem, and spinal cord using the highly specific ribonuclease protection assay. Using this method we were able to detect FGF-2 mRNA in the rat CNS of embryonic day (E) 16 and 17, however, at lower levels compared to adult FGF-2 mRNA levels. In addition, we show that a FGF-2 antisense transcript is expressed in embryonic CNS tissue. Furthermore, using this method, we demonstrate FGF receptor 1 mRNA in the rat embryonic and adult CNS. The presence of FGF-2 and FGF receptor 1 suggests a physiological role for this growth factor during the development of the embryonic CNS.
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PMID:Fibroblast growth factor (FGF)-2 sense and antisense mRNA and FGF receptor type 1 mRNA are present in the embryonic and adult rat nervous system: specific detection by nuclease protection assay. 855 92

In order to clarify the physiological function of fibroblast growth factor (FGF-2) in the adrenal medulla the regulation of FGF-2 and FGF receptor 1 (FGFR1) was studied in vitro and in vivo in response to glucocorticoids. To assess the effects of glucocorticoids, in vivo extracts of adrenal medulla and adrenal cortex were analyzed by RNase protection assay and Western blot analysis. PC12 cells were chosen as a model system to study the effects of glucocorticoids in vitro. In PC12 cells, dexamethasone (DEX) was found to stimulate dramatically the expression of both FGF-2 mRNA and protein. Western blot analysis revealed that exclusively the 21-kDa FGF-2 isoform was enhanced. In contrast to the FGF-2 mRNA level FGFR1 was not affected by treatment with glucocorticoids. In vivo FGF-2 mRNA level and 21-kDa FGF-2 isoform level are significantly enhanced in the adrenal medulla 24 h after DEX injection. In vivo application of DEX leads to an increase of the medullary and cortical FGFR1 transcript levels. Glucocorticoid effects on FGF-2 expression were not found in adrenal cortex, heart, skeletal muscle, and kidney, respectively, in vivo and in L6 rat myoblasts in vitro. In addition to adrenal medullary cells glucocorticoids elevated the FGF-2 mRNA and protein level also in vivo in the brain and in vitro in immortalized Schwann cells. The present results suggest that the 21-kDa FGF-2 isoform mediates a physiological function specific for neuronal tissue which is modulated by glucocorticoids.
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PMID:In vivo and in vitro effect of glucocorticoids on fibroblast growth factor (FGF)-2 and FGF receptor 1 expression. 866 54

Fibroblast growth factor-2 (FGF-2) has marked pharmacological neurotrophic effects on lesioned spinal autonomic neurons following target removal of the adrenal medulla, yet expression and axonal transport in autonomic neurons remain to be shown. We show here FGF-2 and FGF receptor type 1 (FGFR1) protein and mRNA expression in preganglionic intermediolateral neurons of the rat thoracic spinal cord. While immunoreactivity of both FGF-2 and FGFR1 co-localize to intermediolateral neurons, mRNA transcripts of FGFR1, but not of FGF-2, are detectable in intermediolateral preparations by RNase protection analysis, suggesting protein translocation in vivo. Unilateral microinjection of 125iodinated FGF-2 into the adrenal medulla (a major target of intermediolateral neurons) results in significant accumulation of specific radioactivity in thoracic spinal cord tissue, including the intermediolateral neurons, and the ipsilateral splanchnic nerve. Emulsion autoradiography demonstrated labelling over ipsilateral intermediolateral neurons only. Neuronal co-localization of FGF-2/FGFR1 protein, differential mRNA expression, specific retrograde axonal transport and the known neurotrophic actions in vivo, strongly suggest unique physiological roles of FGF-2 in the autonomic nervous system.
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PMID:Localization, differential expression and retrograde axonal transport suggest physiological role of FGF-2 in spinal autonomic neurons of the rat. 905 56

The heparin-binding acidic and basic fibroblast growth factors (aFGF, bFGF) and their receptors in the bovine oviduct are described. By means of western blot analysis one 18 kDa aFGF and two bFGF proteins (16 and 18 kDa, respectively) were detected in oviductal flushings. Different concentrations of these two growth factors could be measured in oviductal flushings during the oestrous cycle: concentrations of aFGF protein were significantly higher at ovulation (mean +/- SEM; 5.3 +/- 0.5 ng ml-1) than during the luteal phase (3.0 +/- 0.3 ng ml-1); concentrations of bFGF were higher at the preovulatory stage (3.5 +/- 0.7 ng ml-1) than at the post-ovulatory stage (1.3 +/- 0.15 ng ml-1). Immunohistochemical studies using a/bFGF-specific antibodies indicated that these growth factors were localized mainly in oviduct epithelial cells. The sequence of the bovine FGF receptor (FGFR) was partly determined. Quantification of mRNAs by an RNase-protection assay (RPA) showed that expression of aFGF and bFGF was different during the oestrous cycle, indicating that the regulation of aFGF is separate from that of bFGF. Only mRNA encoding bFGF and FGFR could be detected in cumulus-oocyte complexes by reverse transcription PCR. In summary, the components of the FGF system were found in the bovine oviduct suggesting an autocrine or paracrine regulation involving oviduct cells and cumulus-oocyte complexes.
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PMID:Detection of mRNA and immunoreactive proteins for acidic and basic fibroblast growth factor and expression of the fibroblast growth factor receptors in the bovine oviduct. 915 30

We have studied the expression of basic fibroblast growth factor 2 (FGF-2) and FGF receptor 1 (FGFR1) in the hypoglossal motor system during degeneration and regeneration by using an RNase protection assay, in situ hybridization, and Western blot analysis. The FGF-2 transcript was found to be weakly expressed in the hypoglossal motoneurons of the adult rat. Both peripheral transection and crush injury of the hypoglossal nerve resulted in a marked up-regulation of the FGF-2 mRNA in motoneurons of the hypoglossal nucleus (with a peak at 10 and 11 days postlesion) as well as in the proximal and distal nerve stumps. The FGFR1 transcript was strongly expressed by hypoglossal motoneurons of unlesioned rats. Neither axotomy nor crush lesion of the hypoglossal nerve revealed any alteration of the expression level and cellular localization in the hypoglossal nucleus, but they did result in a significant increase of the FGFR1 mRNA level in the proximal and distal nerve stump. Western blot analysis of the hypoglossal nucleus revealed the presence of the 21 kD and 23 kD isoforms and of a weak expression of the 18 kD isoform. Hypoglossal nerve transection resulted in a complete down-regulation of the FGF-2 protein 3 days after lesion. After 14 days, however, the level of the three isoforms was increased above the control level. The regulation of FGF-2 in hypoglossal motoneurons after experimental nerve injury is in agreement with the idea of a lesion-related function of FGF-2. Together with previously reported neurotrophic effects, these results suggest that FGF-2 provides trophic support for lesioned motoneurons. At the injury site, FGF-2 could be involved in the regulation of the myelination.
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PMID:Expression of fibroblast growth factor-2 in hypoglossal motoneurons is stimulated by peripheral nerve injury. 918 88

Keratinocyte growth factor (KGF) belongs to the fibroblast growth factor (FGF) family, and its activity seems to be restricted to epithelial cells. It elicits its biological effects through binding to the KGF receptor (KGFR), a splicing transcript variant of FGF receptor 2 (FGFR2). The presence of multiple isoforms of FGFR2 and the overlapping specificities of the FGFs with respect to their receptors do not allow the use of anti-FGFR antibodies as specific immunocytochemical tools. Here we used a chimeric protein recently obtained by the fusion of KGF to the HFc portion of immunoglobulin G (La Rochelle et al., J. Cell Biol., 129: 357-366, 1995) to analyze the expression and distribution of KGFRs in human keratinocytes cultured in chemically defined medium and incubated with different Ca2+ concentrations to modulate their differentiation. We observed at both immunofluorescence and electron microscopic levels and by Western blot analysis of proliferation (K6) or differentiation (K1) markers that KGFR expression is up-modulated during keratinocyte differentiation. Cytofluorimetric and Western blot analysis revealed that exposure to the high Ca2+ differentiation signal resulted in a significant increase in KGFRs. RNase protection assay using a KGFR-specific cDNA probe demonstrated that this effect was correlated with a > 4-fold increase in KGFR transcript level. Our results suggest that the expression of KGFR, unlike that of the epidermal growth factor receptor, may control the proliferative-differentiative program from basal to suprabasal cells in human skin.
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PMID:Modulation of keratinocyte growth factor receptor expression in human cultured keratinocytes. 930 Jan 81


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