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Related Concept Videos

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

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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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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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Related Experiment Video

Updated: May 27, 2026

Preparation of Primary Acute Lymphoblastic Leukemia Cells in Different Cell Cycle Phases by Centrifugal Elutriation
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Published on: November 10, 2017

Cell cycle-specific function of Ikaros in human leukemia.

Zhanjun Li1, Chunhua Song, Hongsheng Ouyang

  • 1Pennsylvania State University College of Medicine, Hershey, Pennsylvania, USA.

Pediatric Blood & Cancer
|November 23, 2011
PubMed
Summary

Human Ikaros protein function is cell cycle-specific, regulated by CK2 phosphorylation in acute lymphoblastic leukemia (ALL). This discovery highlights unique human Ikaros functions and identifies the CK2 pathway as a potential therapeutic target for ALL.

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Last Updated: May 27, 2026

Preparation of Primary Acute Lymphoblastic Leukemia Cells in Different Cell Cycle Phases by Centrifugal Elutriation
09:09

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Published on: November 10, 2017

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Published on: May 14, 2016

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Ikaros loss is linked to B and T cell leukemia development.
  • Human Ikaros function and regulation, particularly during the cell cycle, remain poorly understood.
  • Previous research primarily utilized murine models, with limited data on human Ikaros.

Purpose of the Study:

  • To investigate the function and regulation of human Ikaros isoforms during the cell cycle in human acute lymphoblastic leukemia (ALL).
  • To elucidate the mechanisms controlling human Ikaros activity throughout the cell cycle.

Main Methods:

  • Electromobility shift assay (EMSA) to assess DNA-binding activity.
  • Confocal microscopy for subcellular localization studies.
  • Phosphopeptide mapping to identify phosphorylation sites.

Main Results:

  • Human Ikaros DNA-binding activity dynamically changes during the cell cycle.
  • In S phase, Ikaros DNA-binding to target genes decreases while binding to pericentromeric heterochromatin is maintained.
  • CK2 kinase-mediated phosphorylation controls these S phase-specific alterations in Ikaros function.
  • Human Ikaros isoform localization differs from murine models, suggesting unique human functions.

Conclusions:

  • Human Ikaros function is cell cycle-dependent and regulated by CK2 phosphorylation during S phase in T-cell and B-cell ALL.
  • Observed differences between murine and human Ikaros underscore the necessity of human cell studies in ALL research.
  • The CK2 pathway is identified as a promising therapeutic target for ALL treatment.