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Andrew J. Watson

Researcher at University of Exeter

Publications -  531
Citations -  38911

Andrew J. Watson is an academic researcher from University of Exeter. The author has contributed to research in topics: Blastocyst & Embryonic stem cell. The author has an hindex of 88, co-authored 497 publications receiving 34512 citations. Previous affiliations of Andrew J. Watson include Mansfield University of Pennsylvania & Plymouth Marine Laboratory.

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Book ChapterDOI

The Influence of Biomineralisation on the Composition of Seawater

TL;DR: In this paper, five predominant mineral phases have been identified (calcite, aragonite, celestite, barite and opaline silica), which are progressively dissolved from the settling particulate matter and consequently influence the vertical distribution not only of their major constituent elements (Ca, Ba, Sr, C, Si) but also of a range of trace elements (Ge, Se, Zn, Sc, Cr, Be, Cu, Ni).
Journal ArticleDOI

PP2Cdelta (Ppm1d, WIP1), an endogenous inhibitor of p38 MAPK, is regulated along with Trp53 and Cdkn2a following p38 MAPK inhibition during mouse preimplantation development.

TL;DR: Blockage of p38 MAPK activity is associated with embryo stage specific influences on Trp53, Ppm1d, Cdkn2a, and Mapk14 expression during mouse preimplantation development, and results indicate that the p38MAPK pathway regulates Trp 53, PPM1D, and CdKn2a expression.
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SNAI1 and SNAI2 Are Asymmetrically Expressed at the 2-Cell Stage and Become Segregated to the TE in the Mouse Blastocyst

Christine E. Bell, +1 more
- 31 Dec 2009 - 
TL;DR: This study implicates SNAi1 and SNAI2 in the lineage segregation of the trophectoderm and inner cell mass, and provides new insight into these oncogenes.
Journal ArticleDOI

Structure and inhibition of N-acetylneuraminate lyase from methicillin-resistant Staphylococcus aureus.

TL;DR: The analysis of the crystal structure of ligand‐free and 2R‐sialic acid alditol‐bound MRSA N‐acetylneuraminate lyase suggests that subtle dynamic differences in solution and/or altered binding interactions within the active site may account for species‐specific inhibition.
Journal ArticleDOI

Treatment with AICAR inhibits blastocyst development, trophectoderm differentiation and tight junction formation and function in mice.

TL;DR: The results indicate that early embryonic AMPK levels must be tightly regulated to ensure normal preimplantation development and blastocyst formation to occur and use of metformin should be carefully considered during preIMplantation and early post-embryo transfer phases of fertility treatment cycles.