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Related Concept Videos

Master Transcription Regulators02:23

Master Transcription Regulators

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Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...
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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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Proteins that regulate transcription can do so either via direct contact with RNA Polymerase or through indirect interactions facilitated by adaptors, mediators, histone-modifying proteins, and nucleosome remodelers. Direct interactions to activate transcription is seen in bacteria as well as in some eukaryotic genes. In these cases, upstream activation sequences are adjacent to the promoters, and the activator proteins interact directly with the transcriptional machinery. For example, in...
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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
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In eukaryotic cells, nascent mRNA transcripts need to undergo many post-transcriptional modifications to reach the cell cytoplasm and translate into functional proteins. For a long time, transcription and pre-mRNA processing were considered two independent events that occur sequentially in the cell. However, it has now been well established that transcription and pre-mRNA processing are two simultaneous processes that are precisely regulated inside the cell.
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Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells
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PRMT4 blocks myeloid differentiation by assembling a methyl-RUNX1-dependent repressor complex.

Ly P Vu1, Fabiana Perna2, Lan Wang3

  • 1Molecular Pharmacology and Chemistry Program, Sloan-Kettering Institute, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA; Gerstner Sloan-Kettering Graduate School of Biomedical Sciences, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.

Cell Reports
|December 17, 2013
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Summary
This summary is machine-generated.

Protein arginine methyltransferase 4 (PRMT4) overexpression blocks myeloid differentiation in acute myelogenous leukemia. Inhibiting PRMT4 promotes differentiation and reduces leukemia cell proliferation, suggesting it as a potential therapeutic target.

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Area of Science:

  • Hematology
  • Epigenetics
  • Molecular Biology

Background:

  • Epigenetic regulators are crucial in hematopoiesis.
  • Aberrant expression of these genes is linked to hematological malignancies.

Purpose of the Study:

  • Investigate the role of PRMT4 in normal and malignant hematopoiesis.
  • Determine PRMT4's function in acute myelogenous leukemia (AML).

Main Methods:

  • Analyzed PRMT4 expression in AML patient samples.
  • Studied PRMT4's effect on human stem/progenitor cells (HSPCs) differentiation.
  • Investigated the molecular mechanism involving RUNX1 methylation and miR-223.

Main Results:

  • PRMT4 is overexpressed in AML patient samples.
  • PRMT4 overexpression inhibits myeloid differentiation of HSPCs.
  • PRMT4 represses miR-223 via RUNX1 methylation, forming a repressor complex.
  • miR-223 post-transcriptionally represses PRMT4, creating a feedback loop.
  • PRMT4 depletion induces myeloid leukemia cell differentiation and reduces proliferation.

Conclusions:

  • PRMT4 plays a critical role in blocking myeloid differentiation in AML.
  • Targeting PRMT4 presents a potential novel therapeutic strategy for AML.