What's new for 'JKB_daily1' in PubMed

This message contains My NCBI what's new results from the National Center for Biotechnology Information (NCBI) at the U.S. National Library of Medicine (NLM).
Do not reply directly to this message.

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

Sent on Thursday, 2011 Feb 10
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]))
Click here to view complete results in PubMed. (Results may change over time.)
To unsubscribe from these e-mail updates click here.

PubMed Results

Items 1 - 3 of 3

1.	Nature. 2011 Jan 6;469(7328):23-5. What lies ahead. [No authors listed]
	PMID: 21209640 [PubMed - indexed for MEDLINE]
	Related citations

2.	Nature. 2011 Jan 6;469(7328):12. New year, new science. Van Noorden R, Ledford H, Mann A.
	PMID: 21209635 [PubMed - indexed for MEDLINE]
	Related citations

3.	Nature. 2011 Jan 6;469(7328):112-5. Epub 2010 Dec 12. CENP-B preserves genome integrity at replication forks paused by retrotransposon LTR. Zaratiegui M, Vaughn MW, Irvine DV, Goto D, Watt S, Bähler J, Arcangioli B, Martienssen RA. Cold Spring Harbor Laboratory, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA. Abstract Centromere-binding protein B (CENP-B) is a widely conserved DNA binding factor associated with heterochromatin and centromeric satellite repeats. In fission yeast, CENP-B homologues have been shown to silence long terminal repeat (LTR) retrotransposons by recruiting histone deacetylases. However, CENP-B factors also have unexplained roles in DNA replication. Here we show that a molecular function of CENP-B is to promote replication-fork progression through the LTR. Mutants have increased genomic instability caused by replication-fork blockage that depends on the DNA binding factor switch-activating protein 1 (Sap1), which is directly recruited by the LTR. The loss of Sap1-dependent barrier activity allows the unhindered progression of the replication fork, but results in rearrangements deleterious to the retrotransposon. We conclude that retrotransposons influence replication polarity through recruitment of Sap1 and transposition near replication-fork blocks, whereas CENP-B counteracts this activity and promotes fork stability. Our results may account for the role of LTR in fragile sites, and for the association of CENP-B with pericentromeric heterochromatin and tandem satellite repeats.
	PMID: 21151105 [PubMed - indexed for MEDLINE]
	Related citations