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Related Concept Videos

DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

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...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
The Cell Cycle Control System01:28

The Cell Cycle Control System

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.
Cyclins and cyclin-dependent kinases (Cdks) are the primary cell cycle regulators and function at the cell...
The Cell Cycle Control System02:11

The Cell Cycle Control System

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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Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
12:02

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

Published on: June 6, 2017

MIF coordinates the cell cycle with DNA damage checkpoints. Lessons from knockout mouse models.

Günter Fingerle-Rowson1, Oleksi Petrenko

  • 1University Hospital Cologne, Clinic I of Internal Medicine, Dept. of Hematology and Oncology, Cologne, Germany. g.fingerle-rowson@gmx.de

Cell Division
|July 21, 2007
PubMed
Summary
This summary is machine-generated.

Macrophage migration inhibitory factor (MIF) deficiency in mice increases resistance to cancer development. MIF and p53 pathways interact, suggesting MIF’s role in early-stage tumors.

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Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis

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Last Updated: Jul 13, 2026

Studying Cell Cycle-regulated Gene Expression by Two Complementary Cell Synchronization Protocols
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Detection of DNA Double-Stranded Breaks in Mouse Oocytes
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08:33

Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis

Published on: December 5, 2017

Area of Science:

  • Oncology
  • Molecular Biology
  • Immunology

Background:

  • Macrophage migration inhibitory factor (MIF) is a pro-inflammatory mediator implicated in cancer.
  • MIF's role in oncogenic transformation and tumor progression requires further elucidation.

Purpose of the Study:

  • To investigate the consequences of MIF gene deletion on cellular proliferation and transformation.
  • To explore the interplay between MIF, p53, and Rb/E2F pathways in tumorigenesis.

Main Methods:

  • Genetic deletion of the MIF gene in mice.
  • Analysis of cellular transformation properties in MIF-deficient cells.
  • Investigation of functional antagonism between MIF and p53.

Main Results:

  • MIF-deficient cells show increased resistance to oncogenic transformation.
  • Inactivation of p53 and Rb/E2F pathways can overcome MIF deficiency-related transformation defects.
  • MIF and p53 functionally antagonize each other, influencing cell survival and tumorigenesis via overlapping pathways.
  • MIF's impact on p53 function is secondary to p53-independent mechanisms regulating genomic integrity.

Conclusions:

  • MIF plays a significant role in cellular transformation and tumor progression.
  • The MIF-p53 interaction is a critical pathway in cancer development.
  • MIF's involvement in p53-independent mechanisms highlights its broad impact on genomic stability.
  • Targeting MIF may offer a therapeutic strategy for early-stage tumors, particularly those with chronic inflammation.