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Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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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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M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

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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...
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Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
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Abnormal Proliferation02:23

Abnormal Proliferation

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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Anaphase Promoting Complex00:50

Anaphase Promoting Complex

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The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
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DNA Damage can Stall the Cell Cycle02:37

DNA Damage can Stall the Cell Cycle

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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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Related Experiment Video

Updated: Jun 29, 2025

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
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Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

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CDK12 Loss Promotes Prostate Cancer Development While Exposing Vulnerabilities to Paralog-Based Synthetic Lethality.

Jean Ching-Yi Tien1,2, Yu Chang1,2,3, Yuping Zhang1,2,3

  • 1Michigan Center for Translational Pathology, University of Michigan, Ann Arbor, MI, USA.

Biorxiv : the Preprint Server for Biology
|April 2, 2024
PubMed
Summary

Loss of cyclin-dependent kinase 12 (CDK12) drives prostate cancer development and suggests new therapeutic strategies. CDK12 inactivation sensitizes tumors to immune checkpoint blockade and CDK13 inhibition.

Keywords:
CDK12CDK13PTENimmunotherapyp53paralog-based synthetic lethalityprostate cancersyngeneic model

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Virus Delivery of CRISPR Guides to the Murine Prostate for Gene Alteration
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Virus Delivery of CRISPR Guides to the Murine Prostate for Gene Alteration

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Virus Delivery of CRISPR Guides to the Murine Prostate for Gene Alteration
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Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence
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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Biallelic loss of cyclin-dependent kinase 12 (CDK12) defines a distinct molecular subtype of metastatic castration-resistant prostate cancer (mCRPC).
  • The precise role of CDK12 loss in prostate cancer initiation and progression, and its implications for treatment, remain incompletely understood.

Conclusions:

  • CDK12 acts as a bona fide tumor suppressor gene in prostate cancer.
  • CDK12 inactivation influences tumor progression and therapeutic sensitivity.
  • Paralog-based synthetic lethality targeting CDK13 is a promising strategy for CDK12-mutant mCRPC.