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- Elsik, Christine G., et al.
(författare)
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The Genome Sequence of Taurine Cattle : A Window to Ruminant Biology and Evolution
- 2009
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Ingår i: Science. - : American Association for the Advancement of Science (AAAS). - 0036-8075 .- 1095-9203. ; 324:5926, s. 522-528
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Tidskriftsartikel (refereegranskat)abstract
- To understand the biology and evolution of ruminants, the cattle genome was sequenced to about sevenfold coverage. The cattle genome contains a minimum of 22,000 genes, with a core set of 14,345 orthologs shared among seven mammalian species of which 1217 are absent or undetected in noneutherian (marsupial or monotreme) genomes. Cattle-specific evolutionary breakpoint regions in chromosomes have a higher density of segmental duplications, enrichment of repetitive elements, and species-specific variations in genes associated with lactation and immune responsiveness. Genes involved in metabolism are generally highly conserved, although five metabolic genes are deleted or extensively diverged from their human orthologs. The cattle genome sequence thus provides a resource for understanding mammalian evolution and accelerating livestock genetic improvement for milk and meat production.
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| 2. |
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| 3. |
- Bensby, Thomas, et al.
(författare)
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OGLE-2009-BLG-076S: THE MOST METAL-POOR DWARF STAR IN THE GALACTIC BULGE
- 2009
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Ingår i: Astrophysical Journal. - 0004-637X. ; 699:2, s. 174-177
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Tidskriftsartikel (refereegranskat)abstract
- Measurements based on a large number of red giant stars suggest a broad metallicity distribution function (MDF) for the Galactic bulge, centered on [Fe/H] approximate to -0.1. However, recently, a new opportunity emerged to utilize temporary flux amplification (by factors of similar to 100 or more) of faint dwarf stars in the Bulge which are gravitationally lensed, making them observable with high-resolution spectrographs during a short observational window. Surprisingly, of the first six stars measured, five have [Fe/H] > +0.30, suggesting a highly skewed MDF, inconsistent with observations of giant stars. Here we present a detailed elemental abundance analysis of OGLE-2009-BLG-076S, based on a high-resolution spectrum obtained with the UVES spectrograph at the ESO Very Large Telescope. Our results indicate it is the most metal-poor dwarf star in the Bulge yet observed, with [Fe/H] = -0.76. Our results argue against a strong selection effect disfavoring metal-poor microlensed stars. It is possible that small number statistics is responsible for the giant/dwarf Bulge MDF discrepancy. Should this discrepancy survive when larger numbers of Bulge dwarf stars (soon to be available) are analyzed, it may require modification of our understanding of either Bulge formation models, or the behavior of metal-rich giant stars.
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| 4. |
- Preston, Roger J. S., et al.
(författare)
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Platelet Factor 4 Impairs the Anticoagulant Activity of Activated Protein C
- 2009
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Ingår i: Journal of Biological Chemistry. - 1083-351X. ; 284:9, s. 5869-5875
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Tidskriftsartikel (refereegranskat)abstract
- Platelet factor 4 (PF4) is an abundant platelet alpha-granule chemokine released following platelet activation. PF4 interacts with thrombomodulin and the gamma-carboxyglutamic acid (Gla) domain of protein C, thereby enhancing activated protein C (APC) generation by the thrombin-thrombomodulin complex. However, the protein C Gla domain not only mediates protein C activation in vivo, but also plays a critical role in modulating the diverse functional properties of APC once generated. In this study we demonstrate that PF4 significantly inhibits APC anticoagulant activity. PF4 inhibited both protein S-dependentAPC anticoagulant function in plasma and protein S-dependent factor Va (FVa) proteolysis 3- to 5-fold, demonstrating that PF4 impairs protein S cofactor enhancement of APC anticoagulant function. Using recombinant factor Va variants FVa-R506Q/R679Q and FVa-R306Q/R679Q, PF4 was shown to impair APC proteolysis of FVa at position Arg306 by 3-fold both in the presence and absence of protein S. These data suggest that PF4 contributes to the poorly understood APC resistance phenotype associated with activated platelets. Finally, despite PF4 binding to the APC Gla domain, we show that APC in the presence of PF4 retains its ability to initiate PAR-1-mediated cytoprotective signaling. In summary, we propose that PF4 acts as a critical regulator of APC generation, but also differentially targets APC toward cytoprotective, rather than anticoagulant function at sites of vascular injury with concurrent platelet activation.
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