Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Abnormal Proliferation

Abnormal Proliferation

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...

DNA Damage can Stall the Cell Cycle

DNA Damage can Stall the Cell Cycle

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...

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.

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...

Interactions Between Signaling Pathways

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Structure-Guided Design of Peptide Inhibitors Targeting Class I Viral Fusion Proteins.

Pathogens (Basel, Switzerland)·2026

Same author

Conformational trajectory of the HIV-1 fusion peptide during CD4-induced envelope opening.

Nature communications·2025

Same author

Inter-protomer opening cooperativity of envelope trimers positively correlates with HIV-1 entry stoichiometry.

mBio·2025

Same author

Differentiating Cell Entry Potentials of SARS-CoV-2 Omicron Subvariants on Human Lung Epithelium Cells.

Viruses·2024

Same author

Understanding ADC variation by fat content effect using a dual-function MRI phantom.

European radiology experimental·2024

Same author

Administration of Bevacizumab and the Risk of Chronic Kidney Disease Development in Taiwan Residents: A Population-Based Retrospective Cohort Study.

International journal of molecular sciences·2024

Search research articles

Related Experiment Video

Updated: Nov 7, 2025

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

S100P Interacts with p53 while Pentamidine Inhibits This Interaction.

Revansiddha H Katte¹, Deepu Dowarha¹, Ruey-Hwang Chou^2,3

¹Department of Chemistry, National Tsing Hua University, Hsinchu 30013, Taiwan.

|April 30, 2021

Summary

Pentamidine disrupts the S100P-p53 interaction, inhibiting cancer cell growth. This drug reactivates the p53-21 pathway, offering a new therapeutic strategy against cancer progression.

Keywords:

1H-5N HSQC spectrum HADDOCK program S100P biomolecular docking p53-TAD (73 amino acids)protein-protein interactions

More Related Videos

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors

Published on: July 17, 2020

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method

Published on: September 10, 2017

Related Experiment Videos

Last Updated: Nov 7, 2025

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors

Published on: July 17, 2020

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method

Procedure and Key Optimization Strategies for an Automated Capillary Electrophoretic-based Immunoassay Method

Published on: September 10, 2017

Area of Science:

Biochemistry
Molecular Biology
Cancer Research

Background:

S100P protein binds to p53, potentially inactivating its tumor-suppressive functions.
The interaction between S100P and p53 is a potential target for cancer therapy.

Purpose of the Study:

To investigate the molecular interaction between S100P and p53.
To evaluate pentamidine as an antagonist of the S100P-p53 complex.
To assess the therapeutic potential of targeting this interaction.

Main Methods:

¹H-¹⁵N HSQC experiments to study protein interactions.
Molecular modeling to visualize binding sites.
Cell proliferation assays on breast cancer cells (ZR-75-1).

Main Results:

Pentamidine disrupts the S100P-p53 complex by competing for the same binding site.
Pentamidine treatment reduces breast cancer cell proliferation.
Pentamidine increases levels of p53 and p21 proteins, indicating pathway re-activation.

Conclusions:

Pentamidine effectively antagonizes the S100P-p53 interaction.
Targeting the S100P-p53 association with pentamidine shows promise for cancer therapy.
This approach offers a novel strategy to inhibit cancer progression by re-activating the p53-21 pathway.