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 Experiment Videos

The c-Cbl oncoprotein

M L Lupher1, C E Andoniou, D Bonita

  • 1Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

The International Journal of Biochemistry & Cell Biology
|July 24, 1998
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

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

Sort by
Same author

The ten-year experience of firework injuries treated at a uk regional burns & plastic surgery unit.

Annals of burns and fire disasters·2018
Same author

Recombinant human serum amyloid P in healthy volunteers and patients with pulmonary fibrosis.

Pulmonary pharmacology & therapeutics·2013
Same author

Suicide watch: how cytomegalovirus interferes with the cell-death pathways of infected cells.

Tissue antigens·2010
Same author

The role of cooperativity with Src in oncogenic transformation mediated by non-small cell lung cancer-associated EGF receptor mutants.

Oncogene·2009
Same author

Virally mediated inhibition of Bax in leukocytes promotes dissemination of murine cytomegalovirus.

Cell death and differentiation·2008
Same author

Progesterone induces apoptosis in malignant mesothelioma cells.

Anticancer research·2002
Same journal

Corrigendum to "Sodium butyrate down-regulation of indoleamine 2, 3-dioxygenase at the transcriptional and post-transcriptional levels" [Int. J. Biochem. Cell Biol. 42 (2010) 1840-1846].

The international journal of biochemistry & cell biology·2026
Same journal

Whole-brain spatial metabolomics reveals metabolic gradient shifts in a murine glioma model following boron neutron capture therapy (130 characters).

The international journal of biochemistry & cell biology·2026
Same journal

LCN2 modulates Th17/Treg balance in vitro and is associated with an adaptive response to intestinal ischemia-reperfusion injury under Hmox1-deficient conditions.

The international journal of biochemistry & cell biology·2026
Same journal

Chloroquine modulates the redox-sensitive signalling via inhibiting the AMPK-ULK1 under LPS induced state in murine splenic macrophages.

The international journal of biochemistry & cell biology·2026
Same journal

The vicious cycle of hyperglycemia and oxidative stress: Novel mechanistic insights into a pathogenic alliance.

The international journal of biochemistry & cell biology·2026
Same journal

Fibroblast growth factors (FGF) in the pathogenesis and treatment of inflammatory bowel diseases (IBD): An overview.

The international journal of biochemistry & cell biology·2026
See all related articles

Cbl protein regulates tyrosine kinase signaling pathways. Oncogenic Cbl mutants activate signaling, suggesting therapeutic potential for controlling tyrosine kinases.

Area of Science:

  • Molecular Biology
  • Cell Signaling
  • Oncogenesis

Background:

  • Cbl is a signal transducing protein downstream of tyrosine kinase receptors.
  • It is the product of the c-cbl proto-oncogene and has distinct functional domains (Cbl-N and Cbl-C).
  • Wild-type Cbl is non-transforming, while certain deletions render it oncogenic.

Purpose of the Study:

  • To elucidate the role of Cbl in tyrosine kinase signaling pathways.
  • To investigate the function of Cbl domains and its interaction with other signaling molecules.
  • To explore the therapeutic potential of targeting Cbl in cancer.

Main Methods:

  • Analysis of Cbl protein structure and function, including domain deletions.
  • Investigating Cbl's interaction with tyrosine kinases and adaptor proteins (Grb2, Crk, PI-3-kinase).

Related Experiment Videos

  • Studying Cbl homologs in model organisms (C. elegans, Drosophila) and oncogenic Cbl mutant effects in fibroblasts.

    • Main Results:

    • Cbl acts as a substrate for tyrosine kinases and binds to key signaling adaptors.
    • Oncogenic Cbl mutants, particularly those with deletions, activate signaling cascades.
    • Cbl homologs function as negative regulators of receptor tyrosine kinases in model organisms.

    Conclusions:

    • Cbl is a central regulator of tyrosine kinase signaling.
    • Understanding Cbl's regulatory mechanisms and binding motifs offers therapeutic avenues.
    • Targeting Cbl may provide novel strategies for controlling aberrant tyrosine kinase activity in diseases like cancer.