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Helai P. Mohammad

Researcher at Johns Hopkins University

Publications -  15
Citations -  2125

Helai P. Mohammad is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: DNA methylation & Epigenetics. The author has an hindex of 12, co-authored 14 publications receiving 1974 citations. Previous affiliations of Helai P. Mohammad include GlaxoSmithKline & Johns Hopkins University School of Medicine.

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A stem cell–like chromatin pattern may predispose tumor suppressor genes to DNA hypermethylation and heritable silencing

TL;DR: It is hypothesized that cell chromatin patterns and transient silencing of these important regulatory genes in stem or progenitor cells may leave these genes vulnerable to aberrant DNA hypermethylation and heritable gene silencing during tumor initiation and progression.
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Double strand breaks can initiate gene silencing and SIRT1-dependent onset of DNA methylation in an exogenous promoter CpG island.

TL;DR: The data suggest that normal repair of a DNA break can occasionally cause heritable silencing of a CpG island–containing promoter by recruitment of proteins involved in silencing.
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DNMT1 modulates gene expression without its catalytic activity partially through its interactions with histone-modifying enzymes

TL;DR: The findings show that there are genes for which DNMT1 acts as a transcriptional repressor independent from its methyltransferase function and that this repressive function may invoke a role for a scaffolding function of the protein at target genes.
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The NuRD complex cooperates with DNMTs to maintain silencing of key colorectal tumor suppressor genes.

TL;DR: It is found that depletion of CHD4 is synergistic with DNMT inhibition in reducing the viability of colon cancer cells in correlation with reactivation of TSGs, suggesting that their combined inhibition may be beneficial for the treatment of Colon cancer.
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Polycomb CBX7 Promotes Initiation of Heritable Repression of Genes Frequently Silenced with Cancer-Specific DNA Hypermethylation

TL;DR: A potential mechanism through assembly of novel repressive complexes, by which the polycomb component of PRC1 can promote the initiation of epigenetic changes involving abnormal DNA hypermethylation of genes frequently silenced in adult cancers is proposed.