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Related Concept Videos

Regulation of the Unfolded Protein Response01:31

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...
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Canonical Wnt Signaling Pathway

The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which results in tumor...
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Restarting Stalled Replication Forks

DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...
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The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
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Updated: May 15, 2026

A Non-random Mouse Model for Pharmacological Reactivation of Mecp2 on the Inactive X Chromosome
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Published on: May 22, 2019

Wip1 regulation: who controls a reset button?

Raimundo Freire1

  • 1Unidad de Investigación, Hospital Universitario de Canarias, Instituto de Tecnologías Biomédicas, La Laguna, Tenerife, Spain. rfreire@ull.es

Cell Cycle (Georgetown, Tex.)
|January 18, 2013
PubMed
Summary
This summary is machine-generated.

This study comments on cell cycle regulation research. It highlights key findings and implications for understanding cell division and proliferation.

Keywords:
APC/CCdc20Cdk1DNA damage responseDNA repairWip1mitosisp53phosphatase

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Area of Science:

  • Cell Biology
  • Molecular Biology

Background:

  • The cell cycle is a fundamental process in cell division.
  • Dysregulation of the cell cycle is implicated in diseases like cancer.

Purpose of the Study:

  • To provide commentary on the findings presented in Macurek L, et al. Cell Cycle 2013; 12:251-62.
  • To discuss the implications of the original study for the broader field of cell cycle research.

Main Methods:

  • This is a commentary, not an original research study.
  • Analysis and discussion of previously published data and conclusions.

Main Results:

  • The commentary likely elaborates on the significance of the original study's findings.
  • Key aspects of cell cycle regulation identified in the original study are discussed.

Conclusions:

  • The original study offers valuable insights into cell cycle control mechanisms.
  • Further research in this area is crucial for understanding cell proliferation and disease.