Sentences with phrase «marks on their chromatin»

Lausanne, Switzerland About Blog Epigenomics and Epigenetics queries the developmental origins of health and disease by cataloguing the sets of physical markings on chromatin that collaborate to stably alter gene expression.

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Currently, enhancers can be identified through chromatin - based assays, such as ChIP - seq, which predict enhancer elements indirectly based on the enhancer's association with specific epigenomic marks, such as transcription factors or molecular tags on DNA - associated histone proteins.

This mark (H3K4me3) modifies chromatin — the complex of DNA and its protein packaging — by adding three identical molecules known as methyl groups at a specific place on a packaging protein known as histone 3.

We interfere with histone modification marks in vivo, both genome - wide (mutant analysis) and gene - specifically (local disruption of chromatin structure), and analyze the effect on transcription and pluripotency.

The idea is that small chemical tags, such as acetylation, on chromatin marking active or inactive genes would self - propagate independently of the underlying DNA sequence and direct the activity of the genome.

This is in accordance with previous reports that decitabine and 5 - azacytidine produce a marked synergistic effect in combination with suberoylanilide hydroxamic acid and romidepsin in T - lymphoma cell lines by modulating cell cycle arrest and apoptosis.26, 27 As a mechanism of action, KMT2D mutations of B - lymphoma cells promote malignant outgrowth by perturbing methylation of H3K4 that affect the JAK - STAT, Toll - like receptor, or B - cell receptor pathway.28, 29 Here our study indicated that dual treatment with chidamide and decitabine enhanced the interaction of KMT2D with the transcription factor PU.1, thereby inactivating the H3K4me - associated signaling pathway MAPK, which is constitutively activated in T - cell lymphoma.13, 30,31 The transcription factor PU.1 is involved in the development of all hematopoietic lineages32 and regulates lymphoid cell growth and transformation.33 Aberrant PU.1 expression promotes acute myeloid leukemia and is related to the pathogenesis of multiple myeloma via the MAPK pathway.34, 35 On the other hand, PU.1 is also shown to interact with chromatin remodeler and DNA methyltransferease to control hematopoiesis and suppress leukemia.36 Our data thus suggested that the combined action of chidamide and decitabine may interfere with the differentiation and / or viability of PTCL - NOS through a PU.1 - dependent gene expression program.

DOT1L is also unique in that it is the only PKMT to methylate histone H3 on Lysine 79 (H3K79), a chromatin mark associated with active chromatin and transcriptional elongation.