What's new for 'JKB_daily1' in PubMed

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Sender's message: Sepsis or genomics or altitude: JKB_daily1

Sent on Friday, 2010 Apr 09
Search (sepsis[MeSH Terms] OR septic shock[MeSH Terms] OR altitude[MeSH Terms] OR genomics[MeSH Terms] OR genetics[MeSH Terms] OR retrotransposons[MeSH Terms] OR macrophage[MeSH Terms]) AND ("2009/8/8"[Publication Date] : "3000"[Publication Date]) AND (("Science"[Journal] OR "Nature"[Journal] OR "The New England journal of medicine"[Journal] OR "Lancet"[Journal] OR "Nature genetics"[Journal] OR "Nature medicine"[Journal]) OR (Hume DA[Author] OR Baillie JK[Author] OR Faulkner, Geoffrey J[Author]))
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PubMed Results

Items 1 - 3 of 3

1.	Nature. 2010 Mar 25;464(7288):487; author reply 487. Issues raised by use of ethnic-group names in genome study. Schlebusch C. Comment on: Nature. 2010 Feb 18;463(7283):943-7.
	PMID: 20336115 [PubMed - indexed for MEDLINE]
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	Publication Types: Comment Letter MeSH Terms: Ethnic Groups* Human Genome Project Humans Terminology as Topic*

2.	Nature. 2010 Mar 25;464(7288):487. Questions over the scientific basis of epigenome project. Ptashne M, Hobert O, Davidson E. Comment on: Nature. 2010 Feb 4;463(7281):587.
	PMID: 20336114 [PubMed - indexed for MEDLINE]
	Related articles
	Publication Types: Comment Letter MeSH Terms: Animals Biodiversity Epigenesis, Genetic/genetics* Gene Expression Regulation/genetics Genetic Research/ethics Genome/genetics* Humans

3.	Nature. 2010 Mar 25;464(7288):624-7. Epub 2010 Mar 7. Transcription-independent ARF regulation in oncogenic stress-mediated p53 responses. Chen D, Shan J, Zhu WG, Qin J, Gu W. Institute for Cancer Genetics, and Department of Pathology and Cell Biology College of Physicians & Surgeons, Columbia University, 1130 St Nicholas Avenue, New York, New York 10032, USA. Abstract The tumour suppressor ARF is specifically required for p53 activation under oncogenic stress. Recent studies showed that p53 activation mediated by ARF, but not that induced by DNA damage, acts as a major protection against tumorigenesis in vivo under certain biological settings, suggesting that the ARF-p53 axis has more fundamental functions in tumour suppression than originally thought. Because ARF is a very stable protein in most human cell lines, it has been widely assumed that ARF induction is mediated mainly at the transcriptional level and that activation of the ARF-p53 pathway by oncogenes is a much slower and largely irreversible process by comparison with p53 activation after DNA damage. Here we report that ARF is very unstable in normal human cells but that its degradation is inhibited in cancerous cells. Through biochemical purification, we identified a specific ubiquitin ligase for ARF and named it ULF. ULF interacts with ARF both in vitro and in vivo and promotes the lysine-independent ubiquitylation and degradation of ARF. ULF knockdown stabilizes ARF in normal human cells, triggering ARF-dependent, p53-mediated growth arrest. Moreover, nucleophosmin (NPM) and c-Myc, both of which are commonly overexpressed in cancer cells, are capable of abrogating ULF-mediated ARF ubiquitylation through distinct mechanisms, and thereby promote ARF stabilization in cancer cells. These findings reveal the dynamic feature of the ARF-p53 pathway and suggest that transcription-independent mechanisms are critically involved in ARF regulation during responses to oncogenic stress.
	PMID: 20208519 [PubMed - indexed for MEDLINE]
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	Publication Types: Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't MeSH Terms: ADP-Ribosylation Factors/metabolism* Cell Line Fibroblasts/metabolism Gene Expression Regulation* Humans Molecular Sequence Data Nuclear Proteins/metabolism Proto-Oncogene Proteins c-myc/metabolism Stress, Physiological/physiology* Tumor Suppressor Protein p53/metabolism* U937 Cells Ubiquitin-Protein Ligases/metabolism Ubiquitination Substances: MYC protein, human Nuclear Proteins Proto-Oncogene Proteins c-myc Tumor Suppressor Protein p53 nucleophosmin ADP-Ribosylation Factors Ubiquitin-Protein Ligases Secondary Source ID: GENBANK/EU489742