Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

The Spindle Assembly Checkpoint02:19

The Spindle Assembly Checkpoint

The spindle assembly checkpoint is a molecular surveillance mechanism ensuring the fidelity of chromosome segregation during anaphase. The checkpoint monitors the completion of all the prerequisite steps before chromosome segregation to determine whether the segregation process should proceed or be delayed.
Many proteins function together to control the spindle assembly checkpoint. Mutations affecting these proteins may allow cells to proceed into anaphase prematurely, resulting in the...
The Spindle Assembly Checkpoint02:19

The Spindle Assembly Checkpoint

The spindle assembly checkpoint is a molecular surveillance mechanism ensuring the fidelity of chromosome segregation during anaphase. The checkpoint monitors the completion of all the prerequisite steps before chromosome segregation to determine whether the segregation process should proceed or be delayed.
Many proteins function together to control the spindle assembly checkpoint. Mutations affecting these proteins may allow cells to proceed into anaphase prematurely, resulting in the...
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...
Separation of Sister Chromatids02:17

Separation of Sister Chromatids

At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

The contribution of apical stimulation to Mandarin speech perception in users of the MED-EL COMBI 40+ cochlear implant.

Acta oto-laryngologica·2010
Same author

[Scapular belt for the treatment of comminuted fractures of scapula].

Zhongguo gu shang = China journal of orthopaedics and traumatology·2010
Same author

Manipulation of ordered nanostructures of protonated polyoxometalate through covalently bonded modification.

Chemistry (Weinheim an der Bergstrasse, Germany)·2010
Same author

Developments in nonsteroidal antiandrogens targeting the androgen receptor.

ChemMedChem·2010
Same author

Dynamic presentation of immobilized ligands regulated through biomolecular recognition.

Journal of the American Chemical Society·2010
Same author

[Research on crop-weed discrimination using a field imaging spectrometer].

Guang pu xue yu guang pu fen xi = Guang pu·2010

Related Experiment Video

Updated: Jun 24, 2026

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

CDK5RAP2 is required for spindle checkpoint function.

Xiaoying Zhang1, Dongyun Liu, Shuang Lv

  • 1Laboratory of Cancer Biology, Capital Normal University College of Life Science, Beijing, China.

Cell Cycle (Georgetown, Tex.)
|March 14, 2009
PubMed
Summary
This summary is machine-generated.

CDK5RAP2 is crucial for spindle checkpoint function. Its inhibition leads to resistance against paclitaxel and doxorubicin chemotherapy, suggesting CDK5RAP2 as a potential therapeutic target in cancer treatment.

More Related Videos

Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes
10:09

Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes

Published on: September 13, 2022

Studying Mitotic Checkpoint by Illustrating Dynamic Kinetochore Protein Behavior and Chromosome Motion in Living Drosophila Syncytial Embryos
13:59

Studying Mitotic Checkpoint by Illustrating Dynamic Kinetochore Protein Behavior and Chromosome Motion in Living Drosophila Syncytial Embryos

Published on: June 14, 2012

Related Experiment Videos

Last Updated: Jun 24, 2026

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

Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes
10:09

Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes

Published on: September 13, 2022

Studying Mitotic Checkpoint by Illustrating Dynamic Kinetochore Protein Behavior and Chromosome Motion in Living Drosophila Syncytial Embryos
13:59

Studying Mitotic Checkpoint by Illustrating Dynamic Kinetochore Protein Behavior and Chromosome Motion in Living Drosophila Syncytial Embryos

Published on: June 14, 2012

Area of Science:

  • Cell Biology
  • Molecular Oncology
  • Genetics

Background:

  • Paclitaxel and doxorubicin are cornerstone chemotherapies.
  • CDK5RAP2 mutations are linked to primary microcephaly.
  • The role of CDK5RAP2 in cancer chemotherapy resistance is unknown.

Purpose of the Study:

  • To investigate the role of CDK5RAP2 in chemotherapy resistance.
  • To elucidate the mechanism by which CDK5RAP2 affects spindle checkpoint function.

Main Methods:

  • CDK5RAP2 knockdown in cancer cells.
  • Analysis of chromosome segregation and spindle checkpoint proteins (BUBR1, MAD2, CDC20).
  • Assessment of cellular response to paclitaxel and doxorubicin.

Main Results:

  • CDK5RAP2 inhibition causes chromosome mis-segregation and spindle checkpoint failure.
  • CDK5RAP2 regulates BUBR1 and MAD2 transcription.
  • CDK5RAP2 knockdown confers resistance to paclitaxel and doxorubicin, which is reversed by restoring CDK5RAP2.
  • Paclitaxel and doxorubicin treatment decrease CDK5RAP2 levels in cancer cells.

Conclusions:

  • CDK5RAP2 is essential for maintaining spindle checkpoint integrity.
  • Reduced CDK5RAP2 expression is a mechanism of resistance to paclitaxel and doxorubicin.
  • Targeting CDK5RAP2 may overcome chemotherapy resistance in cancer.