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

Anaphase Promoting Complex00:50

Anaphase Promoting Complex

3.3K
The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
3.3K
Determination01:51

Determination

20.7K
During embryogenesis, cells become progressively committed to different fates through a two-step process: specification followed by determination. Specification is demonstrated by removing a segment of an early embryo, “neutrally” culturing the tissue in vitro—for example, in a petri dish with simple medium—and then observing the derivatives. If the cultured region gives rise to cell types that it would normally generate in the embryo, this means that it is specified. In...
20.7K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

2.4K
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...
2.4K
Hedgehog Signaling Pathway02:33

Hedgehog Signaling Pathway

9.8K
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...
9.8K
Cadherins in Tissue Organization01:19

Cadherins in Tissue Organization

3.9K
The cadherins are a superfamily of cell adhesion molecules comprising over 180 variants, with specific tissues expressing a particular combination of cadherin types. Cadherins generally exhibit homophilic binding; i.e., cadherins on one cell bind to cadherins of the same or closely related type on another cell. Thus, cells of the same type have a specific affinity to bind to each other and sort themselves into clusters to form tissues.
Cell Sorting During Development
Cell sorting plays an...
3.9K
Mechanism of Filopodia Formation01:39

Mechanism of Filopodia Formation

3.0K
Filopodia are thin, actin-rich cellular protrusions that play an important role in many fundamental cellular functions. They vary in their occurrence, length, and positioning in different cell types, suggesting their diverse roles.
Their main function is to guide migrating cells during normal tissue morphogenesis or cancer metastasis by recognizing and making initial contacts with the extracellular matrix. However, they can also act as stationary cell anchors or help to establish communication...
3.0K

You might also read

Related Articles

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

Sort by
Same author

Effectiveness of beetroot juice on aerobic and anaerobic exercise performance: systematic review and meta-analysis.

Frontiers in nutrition·2026
Same author

A Synergistic C<sub>2+</sub> Alcohols/Olefins-Intermediated Pathway Boosts CO<sub>2</sub> Hydrogenation to Aromatics.

Angewandte Chemie (International ed. in English)·2026
Same author

FGF18 mediates fibroblast-leukemia crosstalk to promote acute myeloid leukemia progression.

Blood·2026
Same author

Inhibiting METTL3 synergizes with Notch blockade to treat ESCC by targeting cancer stemness via m6A-JAG2.

Journal of gastroenterology·2026
Same author

A Comprehensive Review of Biomimicry in Food: Biomimetic Foods, Food Processing, Food Packaging, Food Freezing, and Food Quality Inspection.

Comprehensive reviews in food science and food safety·2026
Same author

Author Correction: Gut microbiota-modulated glutamic acid rejuvenates the quality of oocytes deteriorated by advanced reproductive age.

EMBO molecular medicine·2026

Related Experiment Video

Updated: Jan 13, 2026

Assessing Signaling Properties of Ectodermal Epithelia During Craniofacial Development
09:25

Assessing Signaling Properties of Ectodermal Epithelia During Craniofacial Development

Published on: March 24, 2011

9.9K

The E3 Ubiquitin Ligase DCAF13 Is Essential for Craniofacial Development.

Li Liu1, Xiaoming Xu1, Peijun Huang2

  • 1Institute of Life Sciences, College of Life and Environmental Science, Wenzhou University, Wenzhou, China.

Genesis (New York, N.Y. : 2000)
|January 6, 2026
PubMed
Summary

DDB1- and CUL4-associated factor 13 (DCAF13) is essential for craniofacial development. Its deficiency impairs neural crest cell proliferation and differentiation by affecting PTEN-PI3K/AKT signaling, leading to malformations.

Keywords:
DCAF13PI3K/AKT signaling pathwaycraniofacial developmentneural crest cells

More Related Videos

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
07:26

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis

Published on: April 1, 2022

2.4K
Analyzing Craniofacial Morphogenesis in Zebrafish Using 4D Confocal Microscopy
09:16

Analyzing Craniofacial Morphogenesis in Zebrafish Using 4D Confocal Microscopy

Published on: January 30, 2014

11.5K

Related Experiment Videos

Last Updated: Jan 13, 2026

Assessing Signaling Properties of Ectodermal Epithelia During Craniofacial Development
09:25

Assessing Signaling Properties of Ectodermal Epithelia During Craniofacial Development

Published on: March 24, 2011

9.9K
Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis
07:26

Isolation of Whole Cell Protein Lysates from Mouse Facial Processes and Cultured Palatal Mesenchyme Cells for Phosphoprotein Analysis

Published on: April 1, 2022

2.4K
Analyzing Craniofacial Morphogenesis in Zebrafish Using 4D Confocal Microscopy
09:16

Analyzing Craniofacial Morphogenesis in Zebrafish Using 4D Confocal Microscopy

Published on: January 30, 2014

11.5K

Area of Science:

  • Developmental Biology
  • Cell Biology
  • Genetics

Background:

  • Craniofacial morphogenesis depends on neural crest cell development.
  • DDB1- and CUL4-associated factor 13 (DCAF13) has known roles in embryogenesis and cancer.
  • The function of DCAF13 in neural crest development is unexplored.

Purpose of the Study:

  • To investigate the role of DCAF13 in craniofacial development.
  • To elucidate the molecular mechanisms by which DCAF13 regulates neural crest cell functions.

Main Methods:

  • Conditional knockout of Dcaf13 in neural crest lineages.
  • Analysis of craniofacial phenotypes.
  • Investigation of signaling pathways, including PTEN-PI3K/AKT.

Main Results:

  • Conditional Dcaf13 knockout caused severe craniofacial malformations.
  • Impaired skeletal growth and differentiation in affected embryos.
  • DCAF13 deficiency led to PTEN accumulation, inhibiting PI3K/AKT signaling.
  • Suppressed proliferation and differentiation of cranial neural crest (CNC)-derived cells.

Conclusions:

  • DCAF13 is a critical regulator of craniofacial morphogenesis.
  • DCAF13 controls CNC cell proliferation and differentiation via the PTEN-PI3K/AKT pathway.
  • This study reveals a novel function of DCAF13 in embryonic development.