Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.26.9 (ribonuclease)
 6,589 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment of neuroblastoma cells with dibutyryl-adenosine 3':5'-monophosphate or adenine induced axon formation and a three-fold increase in the polyadenylate, poly(A), content of the polysomal mRNA. The extracted poly(A) contained 90% adenylic acid and showed a mobility of 6--7 S in dodecylsulfate-polyacrylamide gel electrophoresis. Treatment with dibutyryl-adenosine 3':5'-monophosphate or adenine, also induced a 4--6 fold increase in a nuclear enzymic activity that incorporated [3H]ATP to an acid-insoluble polymer in a cell-free system. This polymer, like poly(A) extracted from the polysomal mRNA, was bound at high salt concentration to nitrocellulose filters. [3H]ATP incorporation was Mg2+-dependent, sensitive to ribonuclease and EDTA and resistant to deoxyribonuclease and actinomycin D. There was no incorporation of [3H]UTP or [3H]dTTP and addition of TUP, CTP and GTP did not increase the incorporation of [3H]ATP. 5-Bromodeoxyuridine induced axon formation of neuroblastoma cells and poly(A) polymerase activity, without increasing the poly(A) content in the polysomal mRNA. The results indicate that induction of axon formation of neuroblastoma cells is associated with an increase in the activity of poly(A) polymerase. It is suggested that the induction of this enzyme may be generally involved in cell differentiation.
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PMID:Induction of polyadenylate polymerase and differentiation in neuroblastoma cells. 17 99

Transforming growth factor alpha (TGF-alpha) is expressed in the brain and affects cells by binding to the epidermal growth factor receptor (EGF-R). Using a ribonuclease protection assay, we found that TGF-alpha steady state mRNA levels in the mouse striatum peak during the first week of postnatal life. Temporally this peak correlates with the height of gliogenesis in the subependymal layer (SEL), which lies along the striatal border of the lateral ventricle. In vitro studies demonstrate that TGF-alpha can stimulate the proliferation of astrocytes, so glial fibrillary acidic protein (GFAP) mRNA levels were measured as well and it was observed that the peak of GFAP expression followed that of TGF-alpha by 1 week. Furthermore, in a TGF-alpha deficient mouse, waved-1 (wa-1), a significant reduction of GFAP mRNA levels and immunostaining for GFAP was found in the striatum. Bromodeoxyuridine labeling combined with immunohistochemistry of normal postnatal day 6 brain showed that the proliferating cells in the SEL are EGF-R immunoreactive. In the waved-1 SEL, there were fewer BrdU positive cells and there was a reduced level of [3H]thymidine incorporation. EGF-R immunoreactive cells were found in the SEL of the adult mouse brain. Taken together, our data suggest that the TGF-alpha/EGF-R signaling pathway is involved in postnatal mitogenic events in the brain.
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PMID:Striatal TGF-alpha: postnatal developmental expression and evidence for a role in the proliferation of subependymal cells. 765 13