scispace - formally typeset
Journal ArticleDOI

Transcriptional regulation by Polycomb group proteins.

TLDR
The current knowledge of the PRC complexes is discussed, how they are targeted to chromatin and how the high diversity of the PcG proteins allows these complexes to influence cell identity.
Abstract
Polycomb group (PcG) proteins function within Polycomb repressive complexes (PRCs), which modify histones and other proteins and silence target genes. This Review highlights new insights into the role of PcG proteins in gene regulation, specifically in controlling self-renewal and differentiation of embryonic stem cells, and into how PRCs are targeted to chromatin.

read more

Citations
More filters
Journal ArticleDOI

Unique features of long non-coding RNA biogenesis and function

TL;DR: This Review describes special events in the lifetimes of lncRNAs — before, during and after transcription — and discusses how these events ultimately shape the unique characteristics and functional roles of lNCRNAs.
Journal ArticleDOI

Targeting EZH2 in cancer

TL;DR: A unifying perspective is synthesized that the promotion of cancer arises from disruption of the role of EZH2 as a master regulator of transcription.
Journal ArticleDOI

Cancer Epigenetics: Tumor Heterogeneity, Plasticity of Stem-like States, and Drug Resistance

TL;DR: The possible role of epigenetic abnormalities as well as genetic alterations in such dynamics and in the creation of cellular heterogeneity in cancers of all types are discussed.
Journal ArticleDOI

Interpreting the language of histone and DNA modifications

TL;DR: Key recent advances in the understanding of the epigenetic language encompassing histone and DNA modifications are highlighted and foreshadow challenges that lie ahead as the authors continue the quest to decipher the fundamental mechanisms of chromatin regulation.
Journal ArticleDOI

Transcriptional plasticity promotes primary and acquired resistance to BET inhibition

TL;DR: The results identify and validate WNT signalling as a driver and candidate biomarker of primary and acquired BET resistance in leukaemia, and implicate the rewiring of transcriptional programs as an important mechanism promoting resistance to BET inhibitors and, potentially, other chromatin-targeted therapies.
References
More filters
Journal ArticleDOI

NuRD-mediated deacetylation of H3K27 facilitates recruitment of Polycomb Repressive Complex 2 to direct gene repression

TL;DR: It is shown that histone deacetylation by NuRD specifies recruitment for Polycomb Repressive Complex 2 (PRC2) in embryonic stem (ES) cells and proposes a gene‐specific mechanism for modulating expression of transcriptionally poised genes whereby NuRD controls the balance between acetylation and methylation of histones, thereby precisely directing the expression of genes critical for embryonic development.
Journal ArticleDOI

TrxG and PcG Proteins but Not Methylated Histones Remain Associated with DNA through Replication

TL;DR: It is suggested that histone modification enzymes may re-establish the histone code on newly assembled unmethylated histones and thus may act as epigenetic marks.
Journal ArticleDOI

Roles of the Polycomb group proteins in stem cells and cancer

TL;DR: The roles of Polycomb proteins in stem cell biology, and the impact their misregulation can have on cancer are recapitulate.
Journal ArticleDOI

Role of the Polycomb Repressive Complex 2 in Acute Promyelocytic Leukemia

TL;DR: It is shown that in leukemic cells knockdown of SUZ12, a key component of Polycomb repressive complex 2 (PRC2), reverts not only histone modification but also induces DNA demethylation of PML-RARalpha target genes.
Journal ArticleDOI

General transcription factors bind promoters repressed by Polycomb group proteins.

TL;DR: It is shown that binding of PcG proteins to repressed promoters does not exclude general transcription factors (GTFs) and that depletion of P cG proteins by double-stranded RNA interference leads to de-repression of developmentally regulated genes, and it is suggested that Pcg complexes maintain silencing by inhibiting GTF-mediated activation of transcription.
Related Papers (5)