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Mark S. Longtine

Researcher at Washington University in St. Louis

Publications -  49
Citations -  12348

Mark S. Longtine is an academic researcher from Washington University in St. Louis. The author has contributed to research in topics: Septin & Septin ring. The author has an hindex of 28, co-authored 45 publications receiving 11569 citations. Previous affiliations of Mark S. Longtine include Oklahoma State University–Stillwater & University of North Carolina at Chapel Hill.

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Role of the yeast Gin4p protein kinase in septin assembly and the relationship between septin assembly and septin function.

TL;DR: The organization of the septins observed in gin4Δ cells and in cells responding to pheromone appears to support some aspects of the model for septin organization suggested previously by Field et al.
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The Morphogenesis Checkpoint in Saccharomyces cerevisiae: Cell Cycle Control of Swe1p Degradation by Hsl1p and Hsl7p

TL;DR: It is suggested that Hsl1p and Hsl7p interact directly with Swe1p to promote its recognition by the ubiquitination complex, leading ultimately to its destruction.
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Role of a Cdc42p Effector Pathway in Recruitment of the Yeast Septins to the Presumptive Bud Site

TL;DR: Two-hybrid, in vitro protein binding, and coimmunoprecipitation data indicate that this role involves a direct interaction of the Gic proteins with the septin Cdc12p, and Mutant phenotypes and suppression data suggest that the Cdc42p effectors Gic1p and Gic2p also function in septin recruitment.
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Review: Oxygen and trophoblast biology – A source of controversy

TL;DR: Two studies are described that show cultured villous trophoblasts undergo apoptosis and autophagy with phenotype-related differences in response to hypoxia, and the hotly debated question of what in vitro oxygen percentage reflects the normal and abnormal oxygen concentrations that occur in vivo.
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Villous trophoblast apoptosis is elevated and restricted to cytotrophoblasts in pregnancies complicated by preeclampsia, IUGR, or preeclampsia with IUGR

TL;DR: It is proposed that repression of apoptosis in the syncytiotrophoblast is important to prevent apoptosis sweeping throughout thesyncytium, which would result in widespread death of this essential interface for maternal-fetal exchange.