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Ruth W. Craig

Researcher at Dartmouth College

Publications -  34
Citations -  3212

Ruth W. Craig is an academic researcher from Dartmouth College. The author has contributed to research in topics: Kinase & Apoptosis. The author has an hindex of 24, co-authored 34 publications receiving 3054 citations. Previous affiliations of Ruth W. Craig include Dartmouth–Hitchcock Medical Center & Icahn School of Medicine at Mount Sinai.

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Mcl-1, a Bcl-2 family member, delays the death of hematopoietic cells under a variety of apoptosis-inducing conditions.

TL;DR: Findings provide further parallels between M cl-1 and Bcl-2, showing that Mcl-1 can interact with Bax in hematopoietic FDC-P1 cells and can prolong cell viability under a variety of cytotoxic conditions.
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MCL1 is phosphorylated in the PEST region and stabilized upon ERK activation in viable cells, and at additional sites with cytotoxic okadaic acid or taxol.

TL;DR: A multiple pathway model is presented, which demonstrates that MCL1 can undergo distinct phosphorylation events – mediated through separate signaling processes and involving different target sites – in cells that remain viable in the presence of TPA versus cells destined to die upon exposure to taxol or okadaic acid.
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Exon skipping in Mcl-1 results in a bcl-2 homology domain 3 only gene product that promotes cell death.

TL;DR: The Mcl-1 gene appears ideally designed for the generation of either a Bcl-2-like viability promoting or, as reported here, a BH3 only death-inducing gene product, which was found to promote cell death.
Journal Article

Fibroblast growth factor-2 inhibits endothelial cell apoptosis by Bcl-2-dependent and independent mechanisms.

TL;DR: It is shown that apoptosis induced by growth factor and serum deprivation of endothelial cells occurs at all phases of the cell cycle and can be blocked by fibroblast growth factor-2 (FGF-2) independently of its mitogenic activity.
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MCL1 transgenic mice exhibit a high incidence of B-cell lymphoma manifested as a spectrum of histologic subtypes.

TL;DR: The findings with the transgene underscore the importance of the normal, highly regulated pattern of MCL1 expression, in addition to providing a model for studying tumorigenesis and its inhibition in the presence of a viability promoting BCL2 family member.