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The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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The cell cycle regulation directs how a cell proceeds from one phase to the next and begins mitosis. The cell cycle control system includes intracellular regulatory molecules and external triggers. They provide "stop" or "advance" signals and operate at specific cell cycle stages termed checkpoints to ensure that a particular process is completed before the cell advances to the next phase.
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The cell cycle is an organized set of events that leads the cell to divide into two daughter cells, each containing chromosomes identical to the parent cell. It is the cell cycle that leads to the formation of an entire organism from a single-cell zygote. Besides, cell division also functions in the renewal or repair of tissues in adult multicellular eukaryotes. For example, in the bone marrow, the stem cells divide to form new blood cells. Although essential for several functions, cell...
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Updated: Feb 28, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Cell Cycle Control by PTEN.

Andrew Brandmaier1, Sheng-Qi Hou1, Wen H Shen1

  • 1Department of Radiation Oncology, Weill Cornell Medicine, Cornell University, New York, NY 10065, USA.

Journal of Molecular Biology
|June 13, 2017
PubMed
Summary
This summary is machine-generated.

Phosphatase and tensin homolog (PTEN) is crucial for genomic stability and preventing cancer. PTEN deficiency disrupts cell cycle control, impacting genetic transmission and cell fate.

Keywords:
PTENcell cyclegenetic transmissionquiescencesenescence

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Area of Science:

  • Cell Biology
  • Genetics
  • Oncology

Background:

  • Cell cycle progression requires precise chromosome inheritance for genomic stability and tumor suppression.
  • Disruptions in cell cycle control can lead to malignant transformation and resistance to cancer therapies.
  • Phosphatase and tensin homolog (PTEN) is a key tumor suppressor frequently altered in human cancers.

Purpose of the Study:

  • To review the critical role of PTEN in regulating cell cycle processes.
  • To elucidate how PTEN maintains genomic integrity.
  • To understand the implications of PTEN deficiency in cancer development and cell fate.

Main Methods:

  • Literature review of studies on PTEN function in cell cycle regulation.
  • Analysis of genetic and molecular mechanisms underlying PTEN's role in genomic stability.
  • Synthesis of current knowledge on PTEN's impact on cell cycle progression and cell fate.

Main Results:

  • PTEN deficiency leads to cell cycle deregulation and altered cell fate.
  • Loss of PTEN function impairs fundamental processes of genetic transmission.
  • PTEN acts as a guardian of the genome, essential for maintaining chromosomal integrity.

Conclusions:

  • PTEN plays a vital role in orchestrating cell cycle progression and exit.
  • Maintaining PTEN function is critical for preventing genomic instability and cancer.
  • Understanding PTEN's regulatory functions offers insights into cancer therapy and prevention strategies.