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

Sent on Tuesday, 2011 Jul 12
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. 2011 Jun 29;474(7353):658-61. doi: 10.1038/nature10195. Vpx relieves inhibition of HIV-1 infection of macrophages mediated by the SAMHD1 protein. Hrecka K, Hao C, Gierszewska M, Swanson SK, Kesik-Brodacka M, Srivastava S, Florens L, Washburn MP, Skowronski J. Source Department of Molecular Biology and Microbiology, Case School of Medicine, Cleveland, Ohio 44106, USA. Comment in Nature. 2011 Jun 30;474(7353):587-8. Abstract Macrophages and dendritic cells have key roles in viral infections, providing virus reservoirs that frequently resist antiviral therapies and linking innate virus detection to antiviral adaptive immune responses. Human immunodeficiency virus 1 (HIV-1) fails to transduce dendritic cells and has a reduced ability to transduce macrophages, due to an as yet uncharacterized mechanism that inhibits infection by interfering with efficient synthesis of viral complementary DNA. In contrast, HIV-2 and related simian immunodeficiency viruses (SIVsm/mac) transduce myeloid cells efficiently owing to their virion-associated Vpx accessory proteins, which counteract the restrictive mechanism. Here we show that the inhibition of HIV-1 infection in macrophages involves the cellular SAM domain HD domain-containing protein 1 (SAMHD1). Vpx relieves the inhibition of lentivirus infection in macrophages by loading SAMHD1 onto the CRL4(DCAF1) E3 ubiquitin ligase, leading to highly efficient proteasome-dependent degradation of the protein. Mutations in SAMHD1 cause Aicardi-Goutières syndrome, a disease that produces a phenotype that mimics the effects of a congenital viral infection. Failure to dispose of endogenous nucleic acid debris in Aicardi-Goutières syndrome results in inappropriate triggering of innate immune responses via cytosolic nucleic acids sensors. Thus, our findings show that macrophages are defended from HIV-1 infection by a mechanism that prevents an unwanted interferon response triggered by self nucleic acids, and uncover an intricate relationship between innate immune mechanisms that control response to self and to retroviral pathogens.
	PMID: 21720370 [PubMed - indexed for MEDLINE]
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2.	Nature. 2011 Jun 29;474(7353):609-15. doi: 10.1038/nature10166. Integrated genomic analyses of ovarian carcinoma. Cancer Genome Atlas Research Network. Collaborators: Bell D, Berchuck A, Birrer M, Chien J, Cramer DW, Dao F, Dhir R, DiSaia P, Gabra H, Glenn P, Godwin AK, Gross J, Hartmann L, Huang M, Huntsman DG, Iacocca M, Imielinski M, Kalloger S, Karlan BY, Levine DA, Mills GB, Morrison C, Mutch D, Olvera N, Orsulic S, Park K, Petrelli N, Rabeno B, Rader JS, Sikic BI, Smith-McCune K, Sood AK, Bowtell D, Penny R, Testa JR, Chang K, Dinh HH, Drummond JA, Fowler G, Gunaratne P, Hawes AC, Kovar CL, Lewis LR, Morgan MB, Newsham IF, Santibanez J, Reid JG, Trevino LR, Wu YQ, Wang M, Muzny DM, Wheeler DA, Gibbs RA, Getz G, Lawrence MS, Cibulskis K, Sivachenko AY, Sougnez C, Voet D, Wilkinson J, Bloom T, Ardlie K, Fennell T, Baldwin J, Gabriel S, Lander ES, Ding LL, Fulton RS, Koboldt DC, McLellan MD, Wylie T, Walker J, O'Laughlin M, Dooling DJ, Fulton L, Abbott R, Dees ND, Zhang Q, Kandoth C, Wendl M, Schierding W, Shen D, Harris CC, Schmidt H, Kalicki J, Delehaunty KD, Fronick CC, Demeter R, Cook L, Wallis JW, Lin L, Magrini VJ, Hodges JS, Eldred JM, Smith SM, Pohl CS, Vandin F, Raphael BJ, Weinstock GM, Mardis ER, Wilson RK, Meyerson M, Winckler W, Getz G, Verhaak RG, Carter SL, Mermel CH, Saksena G, Nguyen H, Onofrio RC, Lawrence MS, Hubbard D, Gupta S, Crenshaw A, Ramos AH, Ardlie K, Chin L, Protopopov A, Zhang J, Kim TM, Perna I, Xiao Y, Zhang H, Ren G, Sathiamoorthy N, Park RW, Lee E, Park PJ, Kucherlapati R, Absher M, Waite L, Sherlock G, Brooks JD, Li JZ, Xu J, Myers RM, Laird W, Cope L, Herman JG, Shen H, Weisenberger DJ, Noushmehr H, Pan F, Triche T Jr, Berman BP, Van Den Berg DJ, Buckley J, Baylin SB, Spellman PT, Purdom E, Neuvial P, Bengtsson H, Jakkula LR, Durinck S, Han J, Dorton S, Marr H, Choi YG, Wang V, Wang NJ, Ngai J, Conboy JG, Parvin B, Feiler HS, Speed TP, Gray JW, Levine A, Socci ND, Liang Y, Taylor BS, Schultz N, Borsu L, Lash AE, Brennan C, Viale A, Sander C, Ladanyi M, Hoadley KA, Meng S, Du Y, Shi Y, Li L, Turman YJ, Zang D, Helms EB, Balu S, Zhou X, Wu J, Topal MD, Hayes DN, Perou CM, Getz G, Voet D, Saksena G, Zhang J, Zhang H, Wu CJ, Shukla S, Cibulskis K, Lawrence MS, Sivachenko A, Jing R, Park RW, Liu Y, Park PJ, Noble M, Chin L, Carter H, Kim D, Karchin R, Spellman PT, Purdom E, Neuvial P, Bengtsson H, Durinck S, Han J, Korkola JE, Heiser LM, Cho RJ, Hu Z, Parvin B, Speed TP, Gray JW, Schultz N, Cerami E, Taylor BS, Olshen A, Reva B, Antipin Y, Shen R, Mankoo P, Sheridan R, Ciriello G, Chang WK, Bernanke JA, Borsu L, Levine DA, Ladanyi M, Sander C, Haussler D, Benz CC, Stuart JM, Benz SC, Sanborn JZ, Vaske CJ, Zhu J, Szeto C, Scott GK, Yau C, Hoadley KA, Du Y, Balu S, Hayes DN, Perou CM, Wilkerson MD, Zhang N, Akbani R, Baggerly KA, Yung WK, Mills GB, Weinstein JN, Penny R, Shelton T, Grimm D, Hatfield M, Morris S, Yena P, Rhodes P, Sherman M, Paulauskis J, Millis S, Kahn A, Greene JM, Sfeir R, Jensen MA, Chen J, Whitmore J, Alonso S, Jordan J, Chu A, Zhang J, Barker A, Compton C, Eley G, Ferguson M, Fielding P, Gerhard DS, Myles R, Schaefer C, Mills Shaw KR, Vaught J, Vockley JB, Good PJ, Guyer MS, Ozenberger B, Peterson J, Thomson E. Abstract A catalogue of molecular aberrations that cause ovarian cancer is critical for developing and deploying therapies that will improve patients' lives. The Cancer Genome Atlas project has analysed messenger RNA expression, microRNA expression, promoter methylation and DNA copy number in 489 high-grade serous ovarian adenocarcinomas and the DNA sequences of exons from coding genes in 316 of these tumours. Here we report that high-grade serous ovarian cancer is characterized by TP53 mutations in almost all tumours (96%); low prevalence but statistically recurrent somatic mutations in nine further genes including NF1, BRCA1, BRCA2, RB1 and CDK12; 113 significant focal DNA copy number aberrations; and promoter methylation events involving 168 genes. Analyses delineated four ovarian cancer transcriptional subtypes, three microRNA subtypes, four promoter methylation subtypes and a transcriptional signature associated with survival duration, and shed new light on the impact that tumours with BRCA1/2 (BRCA1 or BRCA2) and CCNE1 aberrations have on survival. Pathway analyses suggested that homologous recombination is defective in about half of the tumours analysed, and that NOTCH and FOXM1 signalling are involved in serous ovarian cancer pathophysiology.
	PMID: 21720365 [PubMed - indexed for MEDLINE]
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3.	Nature. 2011 May 25;474(7353):654-7. doi: 10.1038/nature10117. SAMHD1 is the dendritic- and myeloid-cell-specific HIV-1 restriction factor counteracted by Vpx. Laguette N, Sobhian B, Casartelli N, Ringeard M, Chable-Bessia C, Ségéral E, Yatim A, Emiliani S, Schwartz O, Benkirane M. Source Institut de Génétique Humaine, Laboratoire de Virologie Moléculaire, CNRS UPR1142, Montpellier 34000, France. nadine.laguette@igh.cnrs.fr Comment in Nature. 2011 Jun 30;474(7353):587-8. Abstract The primate lentivirus auxiliary protein Vpx counteracts an unknown restriction factor that renders human dendritic and myeloid cells largely refractory to HIV-1 infection. Here we identify SAMHD1 as this restriction factor. SAMHD1 is a protein involved in Aicardi-Goutières syndrome, a genetic encephalopathy with symptoms mimicking congenital viral infection, that has been proposed to act as a negative regulator of the interferon response. We show that Vpx induces proteasomal degradation of SAMHD1. Silencing of SAMHD1 in non-permissive cell lines alleviates HIV-1 restriction and is associated with a significant accumulation of viral DNA in infected cells. Concurrently, overexpression of SAMHD1 in sensitive cells inhibits HIV-1 infection. The putative phosphohydrolase activity of SAMHD1 is probably required for HIV-1 restriction. Vpx-mediated relief of restriction is abolished in SAMHD1-negative cells. Finally, silencing of SAMHD1 markedly increases the susceptibility of monocytic-derived dendritic cells to infection. Our results demonstrate that SAMHD1 is an antiretroviral protein expressed in cells of the myeloid lineage that inhibits an early step of the viral life cycle.
	PMID: 21613998 [PubMed - indexed for MEDLINE]
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