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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Epigenetic changes alter the physical structure of the DNA without changing the genetic sequence and often regulate whether genes are turned on or off. This regulation ensures that each cell produces only proteins necessary for its function. For example, proteins that promote bone growth are not produced in muscle cells. Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
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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.
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Histone Variants at the Centromere02:30

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Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3...
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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.
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Related Experiment Video

Updated: May 1, 2026

Extraction of Histones from Clinical Specimens for Epigenetic Profiling by Mass Spectrometry
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Extraction of Histones from Clinical Specimens for Epigenetic Profiling by Mass Spectrometry

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Recognizing methylated histone variant H3.3 to prevent tumors.

Swaminathan Venkatesh1, Jerry L Workman1

  • 1Stowers Institute for Medical Research, 1000 E. 50th Street, Kansas City, MO 64110, USA.

Cell Research
|April 16, 2014
PubMed
Summary

Tumor suppressor protein ZMYND11 exclusively reads methylated histone variant H3.3. This finding reveals new insights into how transcription regulation suppresses tumors.

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Cancer Research

Background:

  • Histone modifications store regulatory information.
  • Effector proteins, or 'readers,' interpret these marks.
  • This interpretation dictates the specificity of cellular responses.

Purpose of the Study:

  • To identify novel proteins that read specific histone marks.
  • To elucidate the role of ZMYND11 in tumor suppression.
  • To understand the mechanism of transcription regulation in cancer.

Main Methods:

  • Histone mark identification assays.
  • Protein-histone interaction studies.
  • Tumor suppressor activity assays for ZMYND11.

Main Results:

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  • ZMYND11 identified as an exclusive reader of methylated histone variant H3.3.
  • Demonstrated ZMYND11's critical role in transcription regulation.
  • Established a link between ZMYND11 function and tumor suppression.

Conclusions:

  • ZMYND11's exclusive reading of H3.3 methylation is key to its tumor-suppressive function.
  • Highlights the importance of specific histone mark recognition in gene regulation.
  • Opens new avenues for cancer therapy targeting transcription regulation.