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Benjamin L. Morris

Researcher at Virginia Commonwealth University

Publications -  5
Citations -  146

Benjamin L. Morris is an academic researcher from Virginia Commonwealth University. The author has contributed to research in topics: Regulation of gene expression & Trisomy. The author has an hindex of 4, co-authored 5 publications receiving 119 citations. Previous affiliations of Benjamin L. Morris include University of Massachusetts Medical School.

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Journal ArticleDOI

CtBP- an emerging oncogene and novel small molecule drug target: Advances in the understanding of its oncogenic action and identification of therapeutic inhibitors.

TL;DR: In light of this evidence, the development of novel inhibitors that mitigate CtBP function may provide clinically actionable therapeutic tools and insight into the future development and use of rational combination therapy that may further augment the efficacy of CtBP inhibitors is provided.
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Dose dependent expression of HDAC4 causes variable expressivity in a novel inherited case of brachydactyly mental retardation syndrome.

TL;DR: Gene expression analyses lending evidence to the hypothesis that HDAC4 modulates severity of this disorder in a dosage‐dependent manner and a parent with mild symptoms of the disorder and a child exhibiting a more severe phenotype.
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Structure-guided design of a high affinity inhibitor to human CtBP.

TL;DR: Crystal structures of phenylpyruvate and 2-hydroxyimino-3-phenylpropanoic acid show binding with favorable ring stacking against the CtBP active site tryptophan and alternate modes of stabilizing the carboxylic acid moiety, and enzymatic assays confirm that HIPP substantially inhibits CtBP catalysis.
Journal ArticleDOI

Design, synthesis, and biological evaluation of substrate-competitive inhibitors of C-terminal Binding Protein (CtBP).

TL;DR: Data suggests that substrate-competitive inhibition of CtBP dehydrogenase activity is a potential mechanism to reactivate tumor-suppressor gene expression as a therapeutic strategy for cancer.
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Active-Site Tryptophan, the Target of Antineoplastic C-Terminal Binding Protein Inhibitors, Mediates Inhibitor Disruption of CtBP Oligomerization and Transcription Coregulatory Activities.

TL;DR: A family of CtBP dehydrogenase inhibitors, based on the parent 2-hydroxyimino-3-phenylpropanoic acid (HIPP), that specifically disrupt cancer cell viability, abrogate CtBP’s transcriptional function, and block polyp formation in a mouse model of intestinal polyposis that depends on CtBP's oncogenic functions are developed.