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Martin J Walsh, PhD
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About Me
Language
Position
Research Topics
Apoptosis/Cell Death, Bioinformatics, Cancer, Cell Cycle, Cell Division, Cellular Differentiation, Chromatin, Developmental Biology, Drug Design and Discovery, Epigenetics, Gene Regulation, Human Genetics and Genetic Disorders, Mass Spectrometry, Mitosis, Nucleus, Oncogenes, Protein Structure/Function, Proteomics, RNA, Transcription Factors, Transcriptional Activation and Repression
Multi-Disciplinary Training Areas
Genetics and Genomic Sciences [GGS], Pharmacology and Therapeutics Discovery [PTD]
About Me
Language
Position
Research Topics
Apoptosis/Cell Death, Bioinformatics, Cancer, Cell Cycle, Cell Division, Cellular Differentiation, Chromatin, Developmental Biology, Drug Design and Discovery, Epigenetics, Gene Regulation, Human Genetics and Genetic Disorders, Mass Spectrometry, Mitosis, Nucleus, Oncogenes, Protein Structure/Function, Proteomics, RNA, Transcription Factors, Transcriptional Activation and Repression
Multi-Disciplinary Training Areas
Genetics and Genomic Sciences [GGS], Pharmacology and Therapeutics Discovery [PTD]
About Me
Language
Position
Research Topics
Apoptosis/Cell Death, Bioinformatics, Cancer, Cell Cycle, Cell Division, Cellular Differentiation, Chromatin, Developmental Biology, Drug Design and Discovery, Epigenetics, Gene Regulation, Human Genetics and Genetic Disorders, Mass Spectrometry, Mitosis, Nucleus, Oncogenes, Protein Structure/Function, Proteomics, RNA, Transcription Factors, Transcriptional Activation and Repression
Multi-Disciplinary Training Areas
Genetics and Genomic Sciences [GGS], Pharmacology and Therapeutics Discovery [PTD]
Education
BS, State University of New York at Buffalo
PhD, Columbia University
Awards
2010
Senior Scholar Award in Aging
Ellison Medical Foundation
Research
Regulation of chromatin structure by human CUTL1 transcription factor-
Our focus has been directed on two fundamental transcription factors that play key roles in both oncogenic transformation and during development called the CCAAT displacement protein/cut homologue (CUTL1) and zinc finger protein 217 (ZNF217/zfp217). CUTL1 in man and cux in mouse are essential for development and self -renewal in various tissue compartments in metazoan vertebrates. CUTL1 is also a key determinant in promoting tumor cell migration and metastasis. We have previously shown that CUTL1 can mediate the acetylation and methylation of nucleosomal histones through the differential recruitment and of histone acetyltransferase (HAT), histone deacetylase (HDAC), and histone lysine metyltransferase (HMT) activities. We have also demonstrated that CUTL1 is a substrate of many of these enzymes that determine the function of CUTL1. Although, transcription factors have the ability to bind DNA they typically lack the capacity to navigate chromatin structure necessary to access cognate DNA sequences. Many transcriptional co-regulators provide the function to recognize and bind post-translational -modified nucleosomal histone. When tethered to co-regulators, transcription factors attain the ability to associate with highly ordered chromatin structure and impose their regulatory function. Our ongoing studies are investigating the role novel nuclear co-regulators and their conserved protein domains that can "read" the histone code by binding modified histone residues that mark functional domains within chromatin. Identification and analysis by ChIP-Seq of transcriptional co-regulators for CUTL1 and the histone marks they impose will help us determine the "visual scope" and native context for CUTL1 occupation within the human genome.