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

TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

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 are of three kinds RI, RII, and RIII. The RI...
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Assembly of Signaling Complexes01:30

Assembly of Signaling Complexes

Multiprotein signaling complexes are formed in a dynamic process involving protein-protein interactions at the cytoplasmic domain of transmembrane receptors or enzymatic and non-enzymatic proteins associated with the receptor. These complexes ensure the activation and propagation of intracellular signals that regulate cell functions.
Interaction domains in cell signaling
Interaction domains recognize exposed features of their binding partners containing post-translationally modified sequences,...
Coat Assembly and GTPases01:33

Coat Assembly and GTPases

Vesicles incorporate different coat protein subunits in different cell locations, which changes the properties of the coat, such as the shape and geometry of the transport vesicles. Thus, vesicle coat proteins also play a significant role in cargo selection.
Coat assembly depends on the local availability of phosphatidylinositol phosphates or PIPs and GTP-binding proteins. Adaptor proteins, which link the coat proteins to the membrane, bind to these PIPs and play a crucial role in controlling...
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

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 activation may...
Pinching-off of Coated Vesicles01:32

Pinching-off of Coated Vesicles

Vesicle budding is orchestrated by distinct cytosolic proteins such as adaptor proteins, coat proteins, and GTPases. To initiate vesicle budding, membrane-bending proteins containing crescent-shaped BAR domains bind to the lipid heads in the bilayer and distort the membrane to form a protein-coated vesicle bud. Adaptors proteins such as AP2 for clathrin-coated vesicles can nucleate on the deformed membrane. Finally, coat proteins such as clathrin or COPI and COPII assemble into a coat forming...

You might also read

Related Articles

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

Sort by
Same author

TGF-β1 and TGF-β2 family members differentially modulate tumor initiation and invasiveness of primary liver cancer in a MMP14-dependent manner.

Carcinogenesis·2026
Same author

Phosphatidylserine-Dependent Clearance of Damaged Red Blood Cells by Liver Sinusoidal Endothelial Cells in Alcohol-Related Liver Disease.

Biology·2026
Same author

Long-term Dynamic Virological Response Patterns and Clinical Outcomes in Hepatitis B Virus-related Cirrhosis: A Real-world 10-year Cohort Study.

Journal of clinical and translational hepatology·2026
Same author

Semi-automated isolation of parenchymal and non-parenchymal liver cells from mice and humans with enhanced stellate cell fraction.

Cell & bioscience·2026
Same author

Erratum: Follistatin-controlled activin-HNF4α-coagulation factor axis in liver progenitor cells determines outcome of acute liver failure.

Hepatology (Baltimore, Md.)·2025
Same author

Transforming Growth Factor-β Signaling in Alcohol-Associated Liver Disease: A Multicellular Perspective.

The American journal of pathology·2025
Same journal

Mt1-Ca<sup>2+</sup>-Mitochondrial Metabolic Axis Maintains Temporomandibular Joint Condylar Cartilage Homeostasis Under Low Oxygen and Hypoxic Condition.

Journal of cellular physiology·2026
Same journal

Correction to "IRE1α/NOX4 Signaling Pathway Mediates Ros-Dependent Activation of Hepatic Stellate Cells in NaAsO<sub>2</sub>-Induced Liver Fibrosis".

Journal of cellular physiology·2026
Same journal

Lipocalin-2 Restores Mitochondrial and Antioxidant Adaptation in a Strain-Specific Manner During LPS Induced Sepsis.

Journal of cellular physiology·2026
Same journal

Dysregulation of Non-Muscle Myosin IIA Assembly and Phosphorylation in S100A4 Null Mouse Lens.

Journal of cellular physiology·2026
Same journal

Corrigendum to "A Probiotic Combination of Limosilactobacillus reuteri and Clostridium butyricum Ameliorates 5-Fluorouracil-Induced Intestinal Mucositis in Rats by Strengthening Barrier Integrity and Modulating Immuno-Microbial Homeostasis".

Journal of cellular physiology·2026
Same journal

Sexually Dimorphic Regulation of MiR-29a/c-3p in Human Endothelial Cells: Cell Functions and Transcriptome.

Journal of cellular physiology·2026
See all related articles

Related Experiment Video

Updated: May 12, 2026

Studying TGF-&#946; Signaling and TGF-&#946;-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

Caveolin and TGF-β entanglements.

Christoph Meyer1, Yan Liu, Steven Dooley

  • 1Medical Faculty Mannheim, Section Molecular Hepatology, Department of Medicine II, Heidelberg University, Mannheim, Germany. christoph.meyer@medma.uni-heidelberg.de

Journal of Cellular Physiology
|April 6, 2013
PubMed
Summary
This summary is machine-generated.

Caveolin proteins and transforming growth factor-beta (TGF-β) signaling pathways are intricately linked, influencing cell behavior and disease progression. Their reciprocal regulation impacts cellular responses to TGF-β, affecting development and disorders like cancer.

More Related Videos

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication
09:52

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication

Published on: September 20, 2016

Visualization and Quantification of TGF&#946;/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay
11:38

Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay

Published on: September 14, 2021

Related Experiment Videos

Last Updated: May 12, 2026

Studying TGF-&#946; Signaling and TGF-&#946;-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells
06:54

Studying TGF-β Signaling and TGF-β-induced Epithelial-to-mesenchymal Transition in Breast Cancer and Normal Cells

Published on: October 27, 2020

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication
09:52

A Mimic of the Tumor Microenvironment: A Simple Method for Generating Enriched Cell Populations and Investigating Intercellular Communication

Published on: September 20, 2016

Visualization and Quantification of TGF&#946;/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay
11:38

Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay

Published on: September 14, 2021

Area of Science:

  • Cellular Biology
  • Molecular Signaling
  • Biochemistry

Background:

  • Transforming growth factor-beta (TGF-β) is a crucial cytokine regulating development, tissue homeostasis, and disease.
  • Caveolin proteins are involved in endocytosis and modulate various signaling pathways, including those implicated in cancer and fibrosis.
  • Dysregulation of TGF-β signaling is associated with numerous pathological conditions.

Purpose of the Study:

  • To provide a comprehensive overview of the complex relationship between caveolin proteins and TGF-β signaling.
  • To elucidate how caveolin modulates TGF-β-induced cellular responses.
  • To highlight the reciprocal regulation and in vivo implications of this crosstalk in disease.

Main Methods:

  • Literature review of studies investigating caveolin and TGF-β interactions.
  • Analysis of molecular mechanisms underlying caveolin's influence on TGF-β/Smad and non-Smad pathways.
  • Examination of gene expression and miRNA regulation in the context of caveolin-TGF-β crosstalk.

Main Results:

  • Caveolin proteins significantly impact TGF-β signaling pathways, affecting cellular outcomes.
  • Reciprocal regulation exists between caveolin and TGF-β at the levels of gene expression and miRNA.
  • In vivo evidence demonstrates the role of this crosstalk in disease development and progression.

Conclusions:

  • The interplay between caveolin and TGF-β is multifaceted and critical for cellular signaling.
  • Understanding this relationship is essential for deciphering disease mechanisms and developing therapeutic strategies.
  • Further research into this crosstalk may reveal novel insights into cancer and fibrosis.