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Related Concept Videos

Epigenetic Regulation01:37

Epigenetic Regulation

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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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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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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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Common myeloid progenitors (CMPs) are oligopotent cells that can differentiate into granulocytes and macrophages. Granulocytes and macrophages are essential for protecting the body against bacterial, viral, or fungal infections. They migrate from the bone marrow into the circulating blood to reach specific tissue sites where they differentiate and help in immune surveillance. However, they survive only for a few days and must be continuously made available to the organism to maintain a robust...
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Combinatorial gene control is the synergistic action of several transcriptional factors to regulate the expression of a single gene. The absence of one or more of these factors may lead to a significant difference in the level of gene expression or repression.
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Nucleosomes are the basic units of chromatin compaction. Each nucleosome consists of the DNA bound tightly around a histone core, which makes the DNA inaccessible to DNA binding proteins such as DNA polymerase and RNA polymerase. Hence, the fundamental problem is to ensure access to DNA when appropriate, despite the compact and protective chromatin structure.
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Polycomb Alterations in Acute Myeloid Leukaemia: From Structure to Function.

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Genetic alterations in Polycomb Repressive Complex 2 (PRC2) factors are common in acute myeloid leukaemia (AML), impacting histone methyltransferase activity and patient outcomes. This review details PRC2 mutations in AML, their prognostic links, and therapeutic implications.

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Area of Science:

  • Hematology
  • Cancer Biology
  • Epigenetics

Background:

  • Epigenetic dysregulation is a key feature of hematological malignancies, particularly acute myeloid leukaemia (AML).
  • Somatic mutations and deletions in Polycomb Repressive Complex 2 (PRC2) components are frequent in AML, disrupting complex assembly and function.
  • Altered PRC2 activity, often reduced histone methyltransferase activity, is linked to poor prognosis and chemoresistance in AML.

Purpose of the Study:

  • To provide a comprehensive overview of genetic alterations affecting PRC2 components in AML.
  • To examine the structural and functional characteristics of PRC2 factors implicated in AML.
  • To review genetic interactions between PRC2 alterations and other AML-associated mutations.

Main Methods:

  • This study is a review of existing literature.
  • Analysis of genetic alterations in PRC2 core factors.
  • Examination of genetic interactions and prognostic data in adult and paediatric AML.

Main Results:

  • Genetic alterations in PRC2 components are prevalent in AML, affecting complex integrity and function.
  • These alterations are associated with reduced histone methyltransferase activity.
  • PRC2 mutations and deletions show significant links to disease outcomes and therapeutic responses in AML.

Conclusions:

  • PRC2 genetic alterations are critical drivers in AML pathogenesis.
  • Understanding these alterations is crucial for predicting prognosis and developing targeted therapies.
  • Further research into PRC2's role may unveil new therapeutic strategies for AML.