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Related Concept Videos

Regulation of Expression at Multiple Steps01:23

Regulation of Expression at Multiple Steps

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The gene expression in cells is regulated at different stages: (i) transcription, (ii) RNA processing, (iii) RNA localization, and (iv) translation. Transcriptional regulation is mediated by regulatory proteins such as transcription factors, activators, or repressors—these control gene expression by initiating or inhibiting the transcription of genes. Once a precursor or pre-mRNA is produced, it undergoes post-transcriptional modification, including 5' capping, splicing, and the...
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Gene expression in prokaryotes is governed by constitutive and regulated systems, allowing cells to balance the production of essential proteins with adaptive responses to environmental changes.Constitutive Gene ExpressionConstitutive, or housekeeping, genes are continuously expressed as they encode proteins vital for fundamental cellular processes. These include enzymes for glycolysis, ribosomal components for protein synthesis, and proteins involved in DNA replication. Their constant...
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Gene expression can be regulated at almost every step from gene to protein. Transcription is the step that is most commonly regulated. This involves the binding of proteins to short regulatory sequences on the DNA. This association can either promote or inhibit the transcription of a gene associated with the respective sequence.
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The biological clock is involved in many aspects of regulating complex physiology in all animals. It was in 1935 when German zoologists, Hans Kalmus and Erwin Bünning, discovered the existence of circadian rhythm in Drosophila melanogaster. However, the internal molecular mechanisms behind the circadian clock remained a mystery until 1984, when Jeffrey C. Hall, Michael Rosbash, and Michael W. Young discovered the expression of the Per gene oscillating over a 24-hour cycle. In subsequent...
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Gene expression is the process in which DNA directs the synthesis of functional products, that is, proteins. Cells can regulate gene expression at various stages. It allows organisms to generate different cell types and enables cells to adapt to internal and external factors.
Genetic Information Flows from DNA to RNA to Protein
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Related Experiment Video

Updated: Mar 1, 2026

Real-time Analysis of Transcription Factor Binding, Transcription, Translation, and Turnover to Display Global Events During Cellular Activation
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Real-time Analysis of Transcription Factor Binding, Transcription, Translation, and Turnover to Display Global Events During Cellular Activation

Published on: March 7, 2018

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SCYL1 does not regulate REST expression and turnover.

Sebastien Gingras1, Emin Kuliyev2, Stéphane Pelletier2

  • 1Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States of America.

Plos One
|June 2, 2017
PubMed
Summary
This summary is machine-generated.

SCYL1 does not regulate REST turnover in triple-negative breast cancer. This study found no evidence that SCYL1 affects REST protein levels or degradation, contradicting previous research.

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Related Experiment Videos

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Biology

Background:

  • A prior study implicated SCYL1 in the oncogenic STP axis, suggesting it promotes triple-negative breast cancer by degrading the REST tumor suppressor.
  • The proposed mechanism involves SCYL1-mediated regulation of REST turnover, a critical process in tumor suppression.

Purpose of the Study:

  • To investigate the role of SCYL1 in regulating REST turnover.
  • To determine if SCYL1 contributes to the degradation of the REST tumor suppressor in triple-negative breast cancer models.

Main Methods:

  • Utilized three distinct genetic approaches to assess SCYL1's function.
  • Compared REST protein levels and turnover in Scyl1+/+ and Scyl1-/- mouse embryonic fibroblasts.
  • Employed CRISPR-Cas9 technology for targeted SCYL1 inactivation in Hek293T cells.
  • Used RNA interference (RNAi) to deplete SCYL1 in Hek293T and MDA-MB-231 cells.

Main Results:

  • REST protein levels and turnover remained unchanged in Scyl1 knockout mouse embryonic fibroblasts compared to wild-type.
  • Targeted inactivation of SCYL1 using CRISPR-Cas9 did not alter REST steady-state levels or turnover in Hek293T cells.
  • RNAi-mediated depletion of SCYL1 in Hek293T and MDA-MB-231 cells showed no effect on REST steady-state levels or turnover.

Conclusions:

  • SCYL1 does not appear to regulate REST turnover.
  • The findings do not support the hypothesis that SCYL1 mediates REST degradation.
  • This study challenges previous assertions regarding SCYL1's role in the oncogenic STP axis and triple-negative breast cancer progression via REST regulation.