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Inhibition of Cdk Activity

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...

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...

Separation of Sister Chromatids

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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.
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Related Experiment Video

Updated: Apr 12, 2026

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

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

An inactive geminin mutant that binds cdt1.

Marissa Suchyta¹, Benoit Miotto², Thomas J McGarry^3,4

¹Department of Medicine, Feinberg Cardiovascular Research Institute, Feinberg School of Medicine, Northwestern University Chicago, IL 60610, USA. msuchyta@gmail.com.

|May 20, 2015

Summary

This summary is machine-generated.

Geminin regulates DNA replication by inhibiting Cdt1. A new Geminin mutant (GemininAWA) shows Geminin does not block MCM loading via steric hindrance, suggesting a non-steric mechanism for replication control.

Keywords:

Cdt1 DNA replication HBO1 geminin pre-replication complex

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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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Published on: December 5, 2017

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CD Spectroscopy to Study DNA-Protein Interactions

CD Spectroscopy to Study DNA-Protein Interactions

Published on: February 10, 2022

Area of Science:

Cell Biology
Molecular Biology
Genetics

Background:

DNA replication initiation is tightly regulated to ensure genome duplication occurs only once per cell cycle.
Geminin protein inhibits the replication factor Cdt1 in vertebrate cells, preventing re-replication.
Cdt1 recruits the mini-chromosome maintenance complex (MCM2-7) to DNA replication origins.

Purpose of the Study:

To investigate the mechanism by which Geminin inhibits Cdt1 and MCM2-7 loading.
To characterize a novel inactive Geminin mutant (GemininAWA) and its effect on DNA replication.

Main Methods:

Creation and characterization of an inactive Geminin mutant (GemininAWA).
Assessing GemininAWA's binding affinity to Cdt1.
In vivo analysis of MCM2-7 loading and DNA replication in the presence of GemininAWA.

Main Results:

GemininAWA binds Cdt1 with normal affinity but fails to inhibit DNA replication.
GemininAWA competes with wild-type Geminin for Cdt1 binding, restoring replication.
GemininAWA does not prevent MCM2-7 loading, leading to massive DNA over-replication in a single S phase.

Conclusions:

Geminin inhibits MCM loading by Cdt1 through a non-steric mechanism, not simple steric hindrance.
The findings suggest Geminin may inhibit DNA replication via interaction with other factors, potentially HBO1.