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

Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

3.0K
Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
3.0K
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

14.0K
Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
14.0K
Abnormal Proliferation02:23

Abnormal Proliferation

5.4K
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...
5.4K
Regulated Protein Degradation02:58

Regulated Protein Degradation

9.3K
It is vital to regulate the activity of enzymatic as well as non-enzymatic proteins inside the cell. This can be achieved either through creating a balance between their rate of synthesis and degradation or regulating the intrinsic activity of the protein. Both these regulation mechanisms play an essential role in the normal functioning of cells.
Protein degradation plays two important roles in the cells. It helps to protect cells from misfolded or damaged proteins before they lead to a...
9.3K
Covalently Linked Protein Regulators02:04

Covalently Linked Protein Regulators

9.9K
Proteins can undergo many types of post-translational modifications, often in response to changes in their environment. These modifications play an important role in the function and stability of these proteins. Covalently linked molecules include functional groups, such as methyl, acetyl, and phosphate groups, and also small proteins, such as ubiquitin. There are around 200 different types of covalent regulators that have been identified.
These groups modify specific amino acids in a protein....
9.9K
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

11.0K
The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
11.0K

You might also read

Related Articles

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

Sort by
Same author

Critical behavior of the order parameter at the nonequilibrium phase transition of the Ising model.

Journal of physics. Condensed matter : an Institute of Physics journal·2018
Same author

MicroRNA-18a promotes hepatocellular carcinoma proliferation, migration, and invasion by targeting Bcl2L10.

OncoTargets and therapy·2018
Same author

Anatomical variation of infra-pyloric artery origination: A prospective multicenter observational study (IPA-Origin).

Chinese journal of cancer research = Chung-kuo yen cheng yen chiu·2018
Same author

Progression in Vascular Cognitive Impairment: Pathogenesis, Neuroimaging Evaluation, and Treatment.

Cell transplantation·2018
Same author

Risk factors analysis for hyperuricemic nephropathy among CKD stages 3-4 patients: an epidemiological study of hyperuricemia in CKD stages 3-4 patients in Ningbo, China.

Renal failure·2018
Same author

Asymptotic analysis of V-BLAST MIMO for coherent optical wireless communications in Gamma-Gamma turbulence.

Optics express·2018

Related Experiment Video

Updated: Apr 8, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

14.0K

E3 ubiquitin ligase Cbl-b suppresses human ORMDL3 expression through STAT6 mediation.

Wei-Xia Yang1, Rui Jin1, Chun-Ming Jiang2

  • 1Department of Pediatrics, The First Affiliated Hospital, Nanjing Medical University, Nanjing, Jiangsu Province 210029, China.

FEBS Letters
|June 27, 2015
PubMed
Summary

Casitas B lineage lymphoma b (Cbl-b) suppresses Orosomucoid 1-Like Protein 3 (ORMDL3) expression in asthma. This mechanism involves Cbl-b reducing signal transducer and activator of transcription 6 (STAT6) phosphorylation, impacting airway immune tolerance.

Keywords:
Casitas B lineage lymphoma bOrosomucoid 1-Like Protein 3Signal transducer and activator of transcription 6Transcriptional regulationWheeze

More Related Videos

Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates
09:47

Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates

Published on: May 10, 2022

3.3K
Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
07:23

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome

Published on: June 15, 2016

9.0K

Related Experiment Videos

Last Updated: Apr 8, 2026

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs
10:44

Chemical Inactivation of the E3 Ubiquitin Ligase Cereblon by Pomalidomide-based Homo-PROTACs

Published on: May 15, 2019

14.0K
Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates
09:47

Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates

Published on: May 10, 2022

3.3K
Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome
07:23

Describing a Transcription Factor Dependent Regulation of the MicroRNA Transcriptome

Published on: June 15, 2016

9.0K

Area of Science:

  • Immunology
  • Genetics

Background:

  • Orosomucoid 1-Like Protein 3 (ORMDL3) is implicated as an asthma candidate gene.
  • Casitas B lineage lymphoma b (Cbl-b), an E3 ubiquitin ligase, is crucial for airway immune tolerance.

Purpose of the Study:

  • To investigate the association between Cbl-b and ORMDL3 in asthma.
  • To elucidate the molecular mechanisms linking Cbl-b and ORMDL3 expression.

Main Methods:

  • Analysis of ORMDL3 expression and Cbl-b levels in peripheral blood of recurrent wheeze patients.
  • In vivo studies to determine Cbl-b's effect on ORMDL3 transcription.
  • Investigation of signal transducer and activator of transcription 6 (STAT6) phosphorylation in relation to interleukin 4 and Cbl-b.

Main Results:

  • ORMDL3 expression significantly increases with decreased Cbl-b in recurrent wheeze patients.
  • Cbl-b was found to suppress ORMDL3 transcriptional activity and mRNA expression.
  • Cbl-b reduced STAT6 phosphorylation, which is induced by interleukin 4 binding to the ORMDL3 promoter.

Conclusions:

  • Cbl-b suppresses human ORMDL3 expression via the STAT6 signaling pathway.
  • This finding provides a molecular link between Cbl-b and ORMDL3 in the context of asthma pathogenesis.