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Shiv I. S. Grewal

Researcher at National Institutes of Health

Publications -  99
Citations -  20281

Shiv I. S. Grewal is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Heterochromatin & Heterochromatin assembly. The author has an hindex of 61, co-authored 95 publications receiving 19125 citations. Previous affiliations of Shiv I. S. Grewal include Cold Spring Harbor Laboratory & Laboratory of Molecular Biology.

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Regulation of heterochromatic silencing and histone H3 lysine-9 methylation by RNAi.

TL;DR: It is proposed that double-stranded RNA arising from centromeric repeats targets formation and maintenance of heterochromatin through RNAi.
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Role of Histone H3 Lysine 9 Methylation in Epigenetic Control of Heterochromatin Assembly

TL;DR: In vivo evidence is provided that lysine 9 of histone H3 (H3 Lys9) is preferentially methylated by the Clr4 protein at heterochromatin-associated regions in fission yeast, defining a conserved pathway wherein sequential histone modifications establish a “histone code” essential for the epigenetic inheritance of heterochROMatin assembly.
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RNAi-Mediated Targeting of Heterochromatin by the RITS Complex

TL;DR: The purification of an RNAi effector complex termed RITS (RNA-induced initiation of transcriptional gene silencing) that is required for heterochromatin assembly in fission yeast is described and a mechanism for the role of the RNAi machinery and small RNAs in targeting of heterochROMatin complexes and epigenetic genesilencing at specific chromosomal loci is suggested.
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Heterochromatin and Epigenetic Control of Gene Expression

TL;DR: An unexpected role for noncoding RNAs and RNA interference in the formation of epigenetic chromatin domains has been uncovered.
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Establishment and Maintenance of a Heterochromatin Domain

TL;DR: It is demonstrated that a centromere-homologous repeat present at the silent mating-type region is sufficient for heterochromatin formation at an ectopic site, and that its repressive capacity is mediated by components of the RNA interference (RNAi) machinery.