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

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal01:22

Role of Ephrin-Eph Signalling in Intestinal Stem Cell Renewal

2.2K
Erythropoietin-producing hepatocellular carcinoma receptor (Eph) and its ligand, Eph receptor-interacting protein (Ephrin) were first discovered in the human carcinoma cell line, hence the name. Ephrin-Eph interaction guides cells to reach their appropriate location in adult tissues. They also play an essential role in the immune system by helping in immune cell migration, adhesion, and activation. Based on their structure and function, Eph is divided into two classes — EphA and EphB.
2.2K
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
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.8K
The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
3.8K
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
Mismatch Repair01:20

Mismatch Repair

4.9K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
4.9K
The Ras Gene02:38

The Ras Gene

6.3K
The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a...
6.3K

You might also read

Related Articles

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

Sort by
Same author

Interplay Between Periodontal Health and Renal Function in Terms of Severity of Chronic Kidney Disease: A Comprehensive Review.

Cureus·2026
Same author

Den-Site Behavior of Bengal Foxes (<i>Vulpes bengalensis</i>) Reveals Persistent Use, Social Interactions, and Coexistence in Shared Spaces.

Ecology and evolution·2026
Same author

Bovine Tuberculosis in Raw Milk: A Herd-Level Prevalence Study by PCR and ELISA Testing in Sylhet Region of Bangladesh.

Veterinary medicine and science·2026
Same author

An Uncommon Complication of Transoral Incisionless Fundoplication.

Cureus·2026
Same author

The 1-1-1 technique: A modified novel approach to feline ovariohysterectomy with minimal incision, rapid recovery and antibiotic free outcomes.

Veterinary and animal science·2026
Same author

A Challenging Decision: Identifying and Managing Hepatic Hydrothorax in the Setting of a Pancreatic Neuroendocrine Tumor.

Case reports in gastrointestinal medicine·2025

Related Experiment Video

Updated: Jul 20, 2025

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation
15:05

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation

Published on: May 20, 2020

8.7K

Colorectal cancer-associated mutations impair EphB1 kinase function.

Yunyoung Kim1, Sultan Ahmed1, W Todd Miller2

  • 1Department of Physiology and Biophysics, Stony Brook University, Stony Brook, New York, USA.

The Journal of Biological Chemistry
|August 1, 2023
PubMed
Summary

Mutations in EphB1, a receptor tyrosine kinase, reduce its activity and tumor suppressor function in colorectal cancer (CRC). These EphB1 mutations impair cell migration and compartmentalization, suggesting a role in CRC progression.

Keywords:
cell compartmentalizationcell migrationcell signalingcolorectal cancerenzyme kineticsenzyme mutationprotein purificationprotein stabilityreceptor tyrosine kinase

More Related Videos

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

6.1K
Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

12.4K

Related Experiment Videos

Last Updated: Jul 20, 2025

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation
15:05

Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation

Published on: May 20, 2020

8.7K
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

6.1K
Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer
28:15

Deficient Pms2, ERCC1, Ku86, CcOI in Field Defects During Progression to Colon Cancer

Published on: July 28, 2010

12.4K

Area of Science:

  • Molecular Biology
  • Cell Biology
  • Oncology

Background:

  • Erythropoietin-producing hepatoma (Eph) receptor tyrosine kinases are crucial for cell migration and adhesion in development and tissue homeostasis.
  • In the intestinal epithelium, Eph signaling dictates cell positioning along the crypt-villus axis.
  • Eph activity has demonstrated tumor-suppressive potential against colorectal cancer (CRC) progression.

Purpose of the Study:

  • To investigate the functional consequences of cancer-associated EphB1 mutations in colorectal cancer.
  • To elucidate the molecular mechanisms by which EphB1 mutations affect its kinase activity, stability, and signaling pathways.
  • To determine the impact of EphB1 mutations on CRC cell behavior, including migration and compartmentalization.

Main Methods:

  • Purification of wild-type (WT) and five cancer-associated mutant EphB1 kinase domains.
  • Development of biochemical assays to assess EphB1 activity and protein stability.
  • Mammalian cell expression systems to evaluate signaling pathway modulation (STAT3, ERK1/2) and cell migration/compartmentalization assays.

Main Results:

  • CRC-associated EphB1 mutations were found to decrease kinase activity and destabilize the protein's folded structure.
  • Mutant EphB1 receptors inhibited STAT3 and ERK1/2 signaling pathways, unlike WT EphB1.
  • Mutant EphB1 receptors failed to suppress human CRC cell migration and impaired cell compartmentalization.

Conclusions:

  • Somatic mutations in EphB1 reduce its kinase-dependent tumor suppressor function in colorectal cancer.
  • Impaired EphB1 activity due to mutations may contribute to CRC progression by affecting cell migration and organization.
  • Understanding these mutations provides insights into novel therapeutic strategies targeting EphB1 in CRC.