Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.1.30.1 (S1 nuclease)
 3,660 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Three primary isoforms of the dimeric glycolytic enzyme, triosephosphate isomerase (TPI; EC 5.3.1.1), are detected in proliferating human cells. The electrophoretically separable isoforms result from the three possible combinations of constitutive subunits and subunits expressed only in proliferating cells. Only a single primary isoform is observed in quiescent cells. The two subunits, which differ by covalent modification (s), are product of the single structural locus for this enzyme. Expression of the proliferation specific subunit (TPI-2) is detected within 6-10 hr following mitogen stimulation of quiescent human cells, requires RNA synthesis and is inhibited by agents which inhibit interleukin 2 expression or function. Only the constitutive subunit (TPI-1) is detected in proliferating cells from nonhominoid primate species. A single class of TPI mRNA, which is increased greater than 10 fold following stimulation of quiescent cells, is detected on northern blot analysis and S1 nuclease digestion analysis of RNA from quiescent and proliferating human cells. It is similar in size to the TPI mRNA from proliferating cells of the African green monkey, a primate species not expressing TPI-2. Comparison of the structure of the TPI gene from rhesus monkey (nonexpressing species) to the gene from expressing species does not suggest a mechanism for generating TPI-2. Thus, the regulation of the expression of the hominoid restricted, proliferation specific subunit of TPI has been further defined, although the mechanism for generating TPI-2 remains elusive.
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PMID:Hominoid triosephosphate isomerase: regulation of expression of the proliferation specific isozyme. 255 Jul 87

The adult T cell leukemia (ATL) is a T cell neoplasm etiologically associated with human T lymphotropic virus type I (HTLV-I) infection. ATL cells often abnormally express interleukin 2 (IL-2) receptors, and ATL patients may show clinical evidence of hypercalcemia, osteolytic bone lesions, or increased bone turnover. Whereas interleukin 1 (IL-1) is not generally recognized as a product of T cells, this cytokine is capable of both altering IL-2 receptor expression and activating osteoclasts. Thus, we investigated the possibility that primary ATL leukemic T cells and HTLV-I-infected long-term ATL cell lines produce IL-1. S1 nuclease protection assays demonstrated that primary leukemic ATL cells from five out of six patients, as well as one patient with T4+ chronic lymphocytic leukemia, contained considerable quantities of IL-1 beta messenger RNA (mRNA) and small amounts of IL-1 alpha mRNA. These primary leukemic T cells also released biologically active IL-1 protein as evaluated in the murine thymocyte comitogenesis bioassay. In contrast to primary tumor cells, four out of six long-term ATL cell lines produced variable amounts of IL-1 alpha mRNA in the absence of detectable IL-1 beta mRNA as measured by S1 nuclease protection. These data demonstrate that IL-1 gene (especially IL-1 beta) expression occurs in many primary HTLV-I-infected leukemic T cells raising the possibility that this mediator may play a role in the pathological changes associated with this leukemia. Also, these studies show that the pattern of IL-1 alpha and IL-1 beta gene expression differs between primary ATL tumor cells and long-term cultured ATL cell lines, indicating an interesting biological difference in these two HTLV-I-infected cell populations.
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PMID:Interleukin 1 gene expression in adult T cell leukemia. 288 87

We analyzed the effect of several growth factors and cytokines on the expression of amyloid beta protein precursor (APP) mRNAs in cultured mouse neuronal and glial cells. In neuronal cultures from embryonic day-15 brain. Northern blotting revealed that APP mRNAs increased by 1.3- to 2.6-fold when treated with nerve growth factor, basic fibroblast growth factor, interleukin 1, interleukin 2, interleukin 3, interleukin 6 or granulocyte-macrophage colony-stimulating factor but not with tumor necrosis factor alpha. An S1 nuclease protection assay revealed that the enhanced APP mRNA in neuronal cultures was exclusively APP695 mRNA. On the other hand, astrocyte-enriched cultures prepared from postnatal day-2 brain did not show any significant alteration among these factors. We conclude that certain growth factors and cytokines could enhance APP 695 mRNA expression in neurons in vitro.
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PMID:Effect of growth factors and cytokines on expression of amyloid beta protein precursor mRNAs in cultured neural cells. 847 81