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Related Concept Videos

Histone Modification02:32

Histone Modification

The histone proteins have a flexible N-terminal tail extending out from the nucleosome. These histone tails are often subjected to post-translational modifications such as acetylation, methylation, phosphorylation, and ubiquitination. Particular combinations of these modifications form “histone codes” that influence the chromatin folding and tissue-specific gene expression.
Acetylation
The enzyme histone acetyltransferase adds acetyl group to the histones. Another enzyme, histone deacetylase,...
Spreading of Chromatin Modifications02:25

Spreading of Chromatin Modifications

The histone proteins in the nucleosomes are post-translationally modified (PTM) to increase or decrease access to DNA. The commonly observed PTMs are methylation, acetylation, phosphorylation, and ubiquitination of lysine amino acids in the histone H3 tail region. These histone modifications have specific meaning for the cell. Hence, they are called "histone code". The protein complex involved in histone modification is termed as "reader-writer" complex.
Writers
The writer is an enzyme that can...
Genomic Imprinting and Inheritance02:30

Genomic Imprinting and Inheritance

Diploid organisms inherit genetic material through chromosomes from both parents. Copies of the same gene are known as alleles. In most cases, both alleles are simultaneously expressed and allow various cellular processes to function optimally. If one of the alleles is missing or mutated, the expression of the other allele can compensate; however, this is not true for all genes.
The expression of some genes depends on which parent passed the gene to the offspring, through a phenomenon known as...

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Related Experiment Video

Updated: May 27, 2026

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells
10:26

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells

Published on: January 20, 2019

Epigenetics in Waldenström's macroglobulinemia.

Antonio Sacco1, Irene M Ghobrial, Aldo M Roccaro

  • 1Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA, USA.

Epigenomics
|November 30, 2011
PubMed
Summary

Waldenström's macroglobulinemia (WM) patients exhibit a distinct microRNA (miRNA) signature. Specific deregulated miRNAs, including miR-155 and miR-9*, are key to the pathogenesis of this B-cell lymphoma.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Waldenström's macroglobulinemia (WM) is an incurable low-grade B-cell lymphoma.
  • Disease progression is the primary cause of mortality in WM patients.
  • Limited genetic and epigenetic data exist for WM, hindering understanding of its pathogenesis.

Purpose of the Study:

  • To investigate the molecular underpinnings of WM.
  • To identify specific microRNA (miRNA) signatures associated with WM.
  • To elucidate the role of deregulated miRNAs in WM pathogenesis.

Main Methods:

  • Analysis of miRNA expression profiles in WM patients.
  • Identification of differentially expressed miRNAs.
  • Investigation of the functional roles of key miRNAs in disease pathogenesis.

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Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients
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Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation
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Genome-wide Analysis of HDAC Inhibitor-mediated Modulation of microRNAs and mRNAs in B Cells Induced to Undergo Class-switch DNA Recombination and Plasma Cell Differentiation

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Comprehensive DNA Methylation Analysis Using a Methyl-CpG-binding Domain Capture-based Method in Chronic Lymphocytic Leukemia Patients
13:21

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Published on: June 16, 2017

Main Results:

  • WM patients display a unique miRNA signature.
  • miR-155 and miR-9* were identified as significantly deregulated in WM.
  • These miRNAs play a crucial role in the development and progression of Waldenström's macroglobulinemia.

Conclusions:

  • MicroRNA dysregulation is implicated in WM pathogenesis.
  • miR-155 and miR-9* represent potential therapeutic targets for WM.
  • Further research into miRNA signatures may improve WM diagnosis and treatment.