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Related Concept Videos

Anaphase Promoting Complex00:50

Anaphase Promoting Complex

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...
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

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...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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...
Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.

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Identification of Cyclin-dependent Kinase 1 Specific Phosphorylation Sites by an In Vitro Kinase Assay
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The c-MYC-AP4-p21 cascade.

Peter Jung1, Heiko Hermeking

  • 1Experimental and Molecular Pathology, Institute of Pathology, Ludwig-Maximilians-University Munich, Munich, Germany.

Cell Cycle (Georgetown, Tex.)
|March 10, 2009
PubMed
Summary

The c-MYC protein represses the p21 gene by inducing the AP4 transcription factor. AP4 then binds near the p21 promoter, inhibiting its expression and promoting cell cycle progression, particularly in colorectal cancer.

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Gene Regulation

Background:

  • The p21 gene encodes a cyclin-dependent kinase (CDK) inhibitor, crucial for anti-proliferative responses.
  • c-MYC is known to promote cell cycle progression, but its mechanism for repressing p21 has been under investigation.

Purpose of the Study:

  • To elucidate the novel mechanism by which c-MYC represses p21 transcription.
  • To explore the role of the transcription factor AP4 (TFAP4) in this process.
  • To discuss the implications of the c-MYC-AP4-p21 axis in colorectal cancer.

Main Methods:

  • Investigated the transcriptional cascade initiated by c-MYC.
  • Identified AP4 (TFAP4) as a direct target gene of c-MYC.
  • Analyzed the binding of AP4 to the p21 promoter region.

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  • Examined the functional consequences of AP4-mediated p21 repression.

    • Main Results:

    • c-MYC directly induces the expression of the AP4 transcription factor.
    • AP4 binds to motifs near the p21 promoter, mediating transcriptional repression.
    • AP4 interferes with p21 induction via DNA damage/p53 and TGFbeta/Smad pathways, and during differentiation.
    • Expression patterns of c-MYC and AP4 overlap in colonic epithelium and colorectal cancer.

    Conclusions:

    • A novel mechanism reveals c-MYC represses p21 via AP4 induction, facilitating cell cycle progression.
    • AP4 plays a key role in c-MYC's function and is implicated in colorectal cancer.
    • The c-MYC-AP4 pathway presents potential targets for cancer diagnosis and therapy.