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Negative Regulator Molecules

Negative Regulator Molecules

Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.

Molecular Factors Affecting Cell Division

Molecular Factors Affecting Cell Division

Several external and internal factors influence the initiation and inhibition of cell division. For instance, the death of nearby cells or the release of human growth hormone (hGH) promotes cell division. In contrast, lack of hGH or crowding of cells can inhibit cell division.
Several proteins function as internal regulators to ensure each cell cycle stage is completed faithfully before proceeding to the next. Regulator molecules may act directly or influence the activity or production of other...

The Retinoblastoma Gene

The Retinoblastoma Gene

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...

Inhibition of Cdk Activity

Inhibition of Cdk Activity

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Positive Regulator Molecules

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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Related Experiment Video

Updated: Mar 6, 2026

Analysis of Cell Cycle Position in Mammalian Cells

Analysis of Cell Cycle Position in Mammalian Cells

Published on: January 21, 2012

Multiple molecular interactions redundantly contribute to RB-mediated cell cycle control.

Michael J Thwaites^1,2, Matthew J Cecchini^1,2, Srikanth Talluri^1,2

¹London Regional Cancer Program, London, Canada.

|March 16, 2017

Summary

The retinoblastoma tumor suppressor (pRB) uses multiple interaction surfaces to control cell cycle progression. Activating this network is key for preventing uncontrolled cell growth and cancer.

Keywords:

Cell cycle Retinoblastoma Structure–function Systems biology Tumor suppressor

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Last Updated: Mar 6, 2026

Analysis of Cell Cycle Position in Mammalian Cells

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Published on: January 21, 2012

In Vivo Detection and Analysis of Rb Protein SUMOylation in Human Cells

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Published on: November 2, 2017

Studying RNA Interactors of Protein Kinase RNA-Activated during the Mammalian Cell Cycle

Studying RNA Interactors of Protein Kinase RNA-Activated during the Mammalian Cell Cycle

Published on: March 5, 2019

Area of Science:

Cell Biology
Molecular Biology
Cancer Research

Background:

The G1-S phase transition is crucial for cell cycle regulation and cancer prevention.
The retinoblastoma tumor suppressor (pRB) is a key regulator of this transition.

Purpose of the Study:

To investigate the structure-function relationships of pRB's interaction surfaces in cell cycle regulation.
To understand how pRB maintains proliferative control.

Main Methods:

Structure-function analysis of pRB.
SAOS2 cell cycle arrest assays.
Evaluation of pRB interaction mutants in mice.

Main Results:

Disruption of three distinct pRB binding surfaces was required to inhibit cell cycle control.
pRB-E2F and pRB-CDH1 interactions are competitive, indicating interchangeable growth arrest functions.
Genetic disruption of similar mechanisms in mice led to ectopic DNA synthesis in the liver.

Conclusions:

pRB employs a network of mechanisms to prevent cell cycle entry.
These findings have implications for developing CDK4/6 inhibitors to target cancer proliferation.