Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004135 (ATM)
13,001 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have used a multi-parameter flow-cytometric technique to analyse changes in cell-cycle phase distribution (early and late G1, S and G2+M phases) for normal and X-ray-sensitive (ataxia-telangiectasia, A-T) lymphoblastoid cells exposed to X-irradiation and sodium butyrate (either alone or in combination). Sodium butyrate, an inhibitor of histone deacetylase, is a useful pharmacological tool for determining the proposed role of a histone acetylation-based chromatin surveillance system in controlling cell-cycle responses to DNA damage. We report that X-irradiated A-T cells (acute doses up to 1.5 Gy) demonstrate deficiencies in the capacity to traverse G1 and G2+M phases, although we can find no evidence of the specific involvement of a sodium butyrate-sensitive process in normal cells or abnormalities in the responses of A-T cells to the drug. We conclude that abnormal cellular control of G1 transition in A-T may be the basis of disturbed cellular differentiation in vivo, particularly in non-proliferating tissues under conditions of accumulated environmental or spontaneous DNA damage.
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PMID:Effects of X-irradiation and sodium butyrate on cell-cycle traverse on normal and radiosensitive lymphoblastoid cells. 241 68

The induction of partial maturation in an in vitro derived Abelson virus-transformed murine lymphoid cell subline (ABC-1/AT1) is described. Pre-B (cytoplasmic, mu chain-positive) lymphocytes were induced from presumptive B cell precursors by prostaglandin E1, butyric acid, lipopolysaccharide and interferon. Maturation was independent of alterations in cellular growth rate and could be achieved in the absence of cell division. The AT1 subline was found to be restricted to the expression of a single light chain type (lambda) indicating a possible B cell lineage-committed precursor as the target for viral transformation.
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PMID:Partial maturation and light chain restriction of Abelson virus-transformed B cell precursors. 678 33

Brain angiotensin II (Ang II) induces tonic sympathoexcitatory effects through AT1 receptor stimulation of glutamatergic neurons and sympathoinhibitory effects via GABAergic neurons in the rostral ventrolateral medulla, the brainstem 'pressor area'. NADPH-derived superoxide production and reactive oxygen species signalling is critical in these actions, and AT2 receptors in the rostral ventrolateral medulla appear to mediate opposing effects on sympathetic outflow. In the hypothalamic paraventricular nucleus, Ang II has AT1 receptor-mediated sympathoexcitatory effects and enhances nitric oxide formation, which in turn inhibits the Ang II effects through a GABAergic mechanism. Ang II also decreases the tonic sympathoinhibitory effect of gamma amino butyric acid within the paraventricular nucleus. Angiotensin III and Angiotensin IV increase blood pressure via brain AT1 receptor stimulation. Angiotensin (1-7) influences cardiovascular function through a specific Mas-receptor. This review examines the evidence that brain angiotensin peptides, glutamate, gamma amino butyric acid and nitric oxide interact within the rostral ventrolateral medulla and paraventricular nucleus to control sympathetic tone and blood pressure.
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PMID:Brain angiotensin peptides regulate sympathetic tone and blood pressure. 2050 52