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

Renewal of Skin Epidermal Stem Cells01:12

Renewal of Skin Epidermal Stem Cells

The skin is divided into epidermis, dermis, and hypodermis, the skin's outermost, middle, and inner layers. The human epidermal layer regularly undergoes renewal, where old, dead cells are replaced by new cells. Epidermal stem cells or EpiSCs divide and differentiate to restore the lost cells. For the renewal process, some EpiSCs continuously self-renew. In contrast, few others differentiate into transit-amplifying cells, which later form prickle or spinous cells, followed by granular cells,...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
Direct cell-to-cell contact is needed for the activation of Notch signaling. The signal is initiated when a notch ligand binds to a receptor on an adjacent cell, also...
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
Notch Signaling Pathway03:14

Notch Signaling Pathway

The Notch signaling pathway is a major intracellular signaling pathway that is highly conserved over a broad spectrum of metazoan species. It stands unique from other intracellular signaling mechanisms in animals because notch protein itself acts as the receptor as well as the primary signaling molecule.
The Notch gene came into the limelight in 1914 after the discovery that its mutation in Drosophila melanogaster leads to a serrated (or "notched") wing margin phenotype. It was not until 1985...
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

The Hedgehog gene (Hh) was first discovered due to its control of the growth of disorganized, hair-like bristles phenotype in Drosophila, much like hedgehog spines. Hh plays a crucial role in the development of organs and the maintenance of homeostasis in both invertebrates and vertebrates. However, while Drosophila has only one Hh protein, mammals have multiple functional Hedgehog proteins - Sonic (Shh), Desert (Dhh), and Indian Hedgehog (Ihh). All of these homologous proteins have adapted to...

You might also read

Related Articles

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

Sort by
Same author

In vivo oncogenic conflict triggered by co-existing KRAS and EGFR activating mutations in lung adenocarcinoma.

Oncogene·2016
Same author

Stromal disrupting effects of nab-paclitaxel in pancreatic cancer.

British journal of cancer·2013
Same author

Upregulation of miR-21 by Ras in vivo and its role in tumor growth.

Oncogene·2010
Same author

K-Ras4B phosphorylation at Ser181 is inhibited by calmodulin and modulates K-Ras activity and function.

Oncogene·2010
Same author

Cell cycle and cancer: genetic analysis of the role of cyclin-dependent kinases.

Cold Spring Harbor symposia on quantitative biology·2006
Same author

Evaluation of potential mechanisms underlying genotype-phenotype correlations in multiple endocrine neoplasia type 2.

Oncogene·2006
Same journal

DNA methylation-mediated silencing of STAT5A drives breast cancer metastasis via dual regulation of EMT and immunosuppressive microenvironment.

Oncogene·2026
Same journal

LncRNA IRENA promotes peripheral T-cell lymphoma progression through scaffolding ARHGEF1 and FMNL1 to modulate RHOA GTPase/MAPK signaling.

Oncogene·2026
Same journal

A novel circSLIT2-encoded SLIT2 isoform suppresses neural invasion in gastric cancer.

Oncogene·2026
Same journal

The miR-302 family suppresses tumor growth in tongue squamous cell carcinoma by directly targeting P65.

Oncogene·2026
Same journal

MOV10 suppresses circRNA biogenesis by disrupting reverse complementary matches structure to drive hepatocarcinogenesis.

Oncogene·2026
Same journal

HSP47 is a potential dual cell target and prognostic factor in pancreatic cancer.

Oncogene·2026
See all related articles

Related Experiment Video

Updated: May 9, 2026

Rapid Genetic Analysis of Epithelial-Mesenchymal Signaling During Hair Regeneration
10:09

Rapid Genetic Analysis of Epithelial-Mesenchymal Signaling During Hair Regeneration

Published on: February 28, 2013

Ras signaling is essential for skin development.

M Drosten1, C G Lechuga1, M Barbacid1

  • 1Molecular Oncology Programme, Centro Nacional de Investigaciones Oncológicas (CNIO), Spanish National Cancer Research Center, Madrid, Spain.

Oncogene
|July 9, 2013
PubMed
Summary
This summary is machine-generated.

Ras proteins are essential for skin development. Eliminating Ras in skin cells stops proliferation and causes developmental defects, highlighting their crucial role in epidermal and hair follicle formation.

More Related Videos

Stimulation of Stem Cell Niches and Tissue Regeneration in Mouse Skin by Switchable Protoporphyrin IX-Dependent Photogeneration of Reactive Oxygen Species In Situ
10:05

Stimulation of Stem Cell Niches and Tissue Regeneration in Mouse Skin by Switchable Protoporphyrin IX-Dependent Photogeneration of Reactive Oxygen Species In Situ

Published on: May 8, 2020

Related Experiment Videos

Last Updated: May 9, 2026

Rapid Genetic Analysis of Epithelial-Mesenchymal Signaling During Hair Regeneration
10:09

Rapid Genetic Analysis of Epithelial-Mesenchymal Signaling During Hair Regeneration

Published on: February 28, 2013

Stimulation of Stem Cell Niches and Tissue Regeneration in Mouse Skin by Switchable Protoporphyrin IX-Dependent Photogeneration of Reactive Oxygen Species In Situ
10:05

Stimulation of Stem Cell Niches and Tissue Regeneration in Mouse Skin by Switchable Protoporphyrin IX-Dependent Photogeneration of Reactive Oxygen Species In Situ

Published on: May 8, 2020

Area of Science:

  • Dermatology
  • Molecular Biology
  • Genetics

Background:

  • Epidermal proliferation and differentiation are tightly regulated processes vital for skin development and hair follicle morphogenesis.
  • Ras proteins (H-Ras, N-Ras, K-Ras) are key regulators in cellular signaling pathways, but their specific role in epidermal development is not fully elucidated.

Purpose of the Study:

  • To investigate the essential role of Ras proteins in keratinocyte proliferation and epidermal development.
  • To determine the consequences of eliminating all three Ras loci in epidermal cells both in vitro and in vivo.

Main Methods:

  • Deletion of all three Ras loci (H-Ras, N-Ras, K-Ras) in keratinocytes in vitro.
  • Generation of a K5Cre mouse model to specifically delete Ras loci from the epidermis in vivo.
  • Analysis of keratinocyte proliferation, differentiation, apoptosis, and senescence.
  • Assessment of epidermal and hair follicle development in mouse embryos lacking Ras proteins in epidermal cells.

Main Results:

  • In vitro, Ras elimination in keratinocytes led to cessation of proliferation and induction of senescence, without apoptosis.
  • Constitutive activation of the mitogen-activated protein kinase pathway partially rescued the proliferative defects.
  • In vivo, deletion of Ras loci in mouse embryos resulted in significantly reduced epidermal proliferation, leading to a thinner epidermis and delayed differentiation marker appearance.
  • No apoptotic or senescent cells were detected in Ras-deficient embryos, indicating severe hypoproliferation as the primary defect.

Conclusions:

  • Ras proteins are genetically essential for controlling keratinocyte and epidermal proliferation.
  • Ras signaling is critical for proper epidermis formation and hair follicle morphogenesis during skin development.
  • Loss of Ras function in the epidermis leads to hypoproliferation and developmental abnormalities, rather than apoptosis or senescence in early development.