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)

Digital communication networks are of increasing importance for data exchange in health care environments. They may be used to transmit multi-media data, such as text, images, graphics, signals and sound. The essential characteristics of modern network technologies are summarized in this article and are seen in the context of local, metropolitan and wide area networks. Standardized technologies discussed are Ethernet, token oriented systems, FDDI, DQDB and ATM. Off-line communication media based on magnetic optical disk, such as IS&C, are briefly introduced. The conclusion reached is that therapy planning for radiation therapy or hyperthermia can make use of communication technologies, for example, to transmit patient images, modelling data and results of distribution calculations of physical phenomena.
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PMID:Communication networks for medical image transmission. 821 70

Nijmegen breakage syndrome (NBS) is an autosomal genetic disease demonstrating a variety of phenotypic abnormalities, including premature aging, increased cancer incidence, chromosome instability, and sensitivity to ionizing radiation. The gene involved in NBS, NBS1, is part of the MRE11/RAD50/NBS1 (MRN) complex that also includes MRE11 and RAD50, which is involved in DNA repair and cell cycle regulation in response to DNA damage. The MRN complex is also involved in telomere maintenance, as demonstrated by the shortened telomeres in NBS primary human fibroblasts and the association of NBS1 with the telomere-binding protein TRF2. To learn more about how a deficiency in telomere maintenance might contribute to chromosome instability in NBS, we have investigated the stability of telomeres in two telomerase-positive human tumor cell clones, BNmt-On and BNmt-Off, expressing an inducible NBS1(S278A/S343A) gene containing mutations at serines 278 and 343 phosphorylated by ATM. The results demonstrate an increased rate of telomere loss in both clones following expression of NBS1(S278A/S343A). The absence of detectable changes in average telomere length suggests that NBS1-associated telomere loss results from stochastic events involving complete telomere loss or loss of telomere capping function. The recombination events associated with telomere loss were found to be similar to those shown previously to result in breakage/fusion/bridge cycles, suggesting that telomere loss can contribute to chromosome instability in NBS1-deficient cells. Telomere loss showed no correlation with radiosensitivity or radioresistant DNA synthesis, demonstrating that NBS1(S278A/S343A) promotes telomere loss through a separate pathway from these other phenotypes associated with NBS.
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PMID:Telomere instability in a human tumor cell line expressing NBS1 with mutations at sites phosphorylated by ATM. 1470 89

Previous studies demonstrate that nitric oxide (NO) promotes p53 transcriptional activity by a classical DNA damage responsive mechanism involving activation of ATM/ATR and phosphorylation of p53. These studies intentionally used high doses of NO donors to achieve the maximum DNA damage. However, lower concentrations of NO donors also stimulate rapid and unequivocal nuclear retention of p53 but apparently do not require ATM/ATR-dependent p53 phosphorylation or total p53 protein accumulation. To identify possible mechanisms for p53 activation at low NO levels, the role of Tyr nitration in p53 activation was evaluated. Low concentrations of the NO donor, DETA NONOate (<200 microM), exclusively nitrate Tyr327 within the tetramerization domain promoting p53 oligomerization, nuclear accumulation, and increased DNA-binding activity without p53 Ser15 phosphorylation. Molecular modeling indicates that nitration of one Tyr327 stabilizes the dimer by about 2.67 kcal mol(-1). Significant quantitative and qualitative differences in the patterns of p53-target gene modulation by low (50 microM), non-DNA-damaging and high (500 microM), DNA-damaging NO donor concentrations were shown. These results demonstrate a new posttranslational mechanism for modulating p53 transcriptional activity responsive to low NO concentrations and independent of DNA damage signaling.
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PMID:Nitration of the tumor suppressor protein p53 at tyrosine 327 promotes p53 oligomerization and activation. 2049 82