Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Targeted Cancer Therapies02:57

Targeted Cancer Therapies

7.8K
The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against...
7.8K
Combination Therapies and Personalized Medicine02:50

Combination Therapies and Personalized Medicine

5.1K
Combining two or more treatment methods increases the life span of cancer patients while reducing damage to vital organs or tissue from the overuse of a single treatment. Combination therapy also targets different cancer-inducing pathways, thus reducing the chances of developing resistance to treatment.
The combination of the drug acetazolamide and sulforaphane is a good example of combination therapy to treat cancer. The cells in the interior of a large tumor often die due to the hypoxic and...
5.1K
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

6.6K
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...
6.6K
Structure-Activity Relationships and Drug Design01:28

Structure-Activity Relationships and Drug Design

1.0K
Drug design is a dynamic field that involves discovering and developing new medications based on specific biological targets. This process heavily relies on structure-activity relationships (SAR) and quantitative structure-activity relationships (QSAR) to guide the design and optimization of efficient drugs.
SAR studies the intricate relationship between a drug's chemical structure and biological activity. It focuses on understanding how modifications to a drug's structure can influence...
1.0K
Targets for Drug Action: Overview01:26

Targets for Drug Action: Overview

7.4K
Drugs target macromolecules to modify ongoing cellular processes. Primary drug targets include receptors, ion channels, transporters, and enzymes.
Receptors are either membrane-spanning or intracellular proteins, which upon binding a ligand, get activated and transmit the signal downstream to elicit a response. Drugs bind receptors, either mimicking the action of endogenous ligands or blocking the receptor activity to bring about a modified response. Nearly 35% of approved drugs target the G...
7.4K
Abnormal Proliferation02:23

Abnormal Proliferation

4.6K
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...
4.6K

You might also read

Related Articles

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

Sort by
Same author

Data-balanced transformer for accelerated ionizable lipid nanoparticles screening in mRNA delivery.

Briefings in bioinformatics·2024
Same author

Nitrogen and sulfur cycling and their coupling mechanisms in eutrophic lake sediment microbiomes.

The Science of the total environment·2024
Same author

Histopathology language-image representation learning for fine-grained digital pathology cross-modal retrieval.

Medical image analysis·2024
Same author

MFSynDCP: multi-source feature collaborative interactive learning for drug combination synergy prediction.

BMC bioinformatics·2024
Same author

FOXO3/Rab7-Mediated Lipophagy and Its Role in Zn-Induced Lipid Metabolism in Yellow Catfish (<i>Pelteobagrus fulvidraco</i>).

Genes·2024
Same author

A One-Pot Convenient RPA-CRISPR-Based Assay for <i>Salmonella enterica</i> Serovar Indiana Detection.

Microorganisms·2024

Related Experiment Video

Updated: Sep 8, 2025

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
07:49

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Published on: July 17, 2019

6.2K

Mutation-specific structural changes in BRAF: understanding dimerization and drug binding for targeted therapy.

Minjie Zhao1,2, Rabia Zafar3, Saad Serfraz3

  • 1Department of Hepatobiliary Surgery, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.

Journal of Biomolecular Structure & Dynamics
|August 10, 2025
PubMed
Summary
This summary is machine-generated.

Oncogenic BRAF mutations disrupt cancer signaling by altering protein structure and drug interactions. Understanding these structural changes guides precision oncology therapies for better cancer treatment.

Keywords:
BRAFCRAFV600Edimerizationmutationoncology

More Related Videos

Author Spotlight: Integrating BRET-Based Assays and Rare Mutation Analysis to Decipher RAF Kinase Regulation in Live Cells
06:44

Author Spotlight: Integrating BRET-Based Assays and Rare Mutation Analysis to Decipher RAF Kinase Regulation in Live Cells

Published on: March 1, 2024

1.2K
Employing Digital Droplet PCR to Detect BRAF V600E Mutations in Formalin-fixed Paraffin-embedded Reference Standard Cell Lines
10:16

Employing Digital Droplet PCR to Detect BRAF V600E Mutations in Formalin-fixed Paraffin-embedded Reference Standard Cell Lines

Published on: October 8, 2015

13.3K

Related Experiment Videos

Last Updated: Sep 8, 2025

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods
07:49

Characterize Disease-related Mutants of RAF Family Kinases by Using a Set of Practical and Feasible Methods

Published on: July 17, 2019

6.2K
Author Spotlight: Integrating BRET-Based Assays and Rare Mutation Analysis to Decipher RAF Kinase Regulation in Live Cells
06:44

Author Spotlight: Integrating BRET-Based Assays and Rare Mutation Analysis to Decipher RAF Kinase Regulation in Live Cells

Published on: March 1, 2024

1.2K
Employing Digital Droplet PCR to Detect BRAF V600E Mutations in Formalin-fixed Paraffin-embedded Reference Standard Cell Lines
10:16

Employing Digital Droplet PCR to Detect BRAF V600E Mutations in Formalin-fixed Paraffin-embedded Reference Standard Cell Lines

Published on: October 8, 2015

13.3K

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cancer Research

Background:

  • BRAF mutations are key drivers in various cancers, impacting the MAPK/ERK pathway.
  • Understanding the structural and biophysical effects of BRAF mutations is crucial for targeted therapies.

Purpose of the Study:

  • To investigate the structural and biophysical consequences of five BRAF mutations (V600E, G469E, D594G, N581S, E586K).
  • To analyze the impact of these mutations on dimerization, ATP binding, and drug interactions with Sorafenib and U0126.

Main Methods:

  • Utilized molecular dynamics simulations to analyze protein structural changes.
  • Conducted ATP-binding assessments and drug interaction analyses.
  • Performed free energy and compactness analyses to understand conformational landscapes.

Main Results:

  • The V600E mutation promotes a stable, monomeric active form, conferring Sorafenib resistance.
  • G469E shows intermediate activity and drug responsiveness, retaining dimerization dependence.
  • D594G is kinase-inactive but scaffolds CRAF activation, with limited drug sensitivity.
  • Benign mutations maintain wild-type-like structural and functional properties.

Conclusions:

  • Mutation-specific structural alterations in BRAF influence kinase activity, dimerization, and drug response.
  • These findings provide a mechanistic link between BRAF mutation structure and function.
  • Supports the development of mutation-guided therapeutic strategies in precision oncology.