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

Negative Regulator Molecules01:23

Negative Regulator Molecules

36.7K
Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
36.7K
Neurogenesis and Regeneration of Nervous Tissue01:15

Neurogenesis and Regeneration of Nervous Tissue

1.2K
In the CNS, neurogenesis, the birth of new neurons from stem cells, is limited to the hippocampus in adults. In other regions of the brain and spinal cord, neurogenesis is almost non-existent due to inhibitory influences from neuroglia, especially oligodendrocytes, and the absence of growth-stimulating cues. The myelin produced by oligodendrocytes in the CNS inhibits neuronal regeneration. Furthermore, astrocytes proliferate rapidly after neuronal damage, forming scar tissue that physically...
1.2K
Replicative Cell Senescence02:15

Replicative Cell Senescence

3.9K
Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
3.9K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

2.2K
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...
2.2K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

5.1K
The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
5.1K
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

4.3K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.3K

You might also read

Related Articles

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

Sort by
Same author

Antibody-drug conjugate-related marker heterogeneity between primary tumors and metastatic lymph nodes in advanced urothelial cancers.

Journal of translational internal medicine·2026
Same author

Focused acoustic vortex-mediated targeted aggregation of engineered bacteria for in situ antibody production to enhance immunotherapy.

Acta biomaterialia·2026
Same author

Machine learning prediction of PICC-associated thrombotic complications in critically ill patients.

BMC medical informatics and decision making·2026
Same author

Ultrasonic pre-treatment followed by glycation modifies chickpea protein isolate: structural transformation, pickering emulsion stability and gel properties.

Food research international (Ottawa, Ont.)·2026
Same author

Gelation properties and swallowing characteristics of Chinese shrimp Fenneropenaeus chinensis powders/konjac glucomannan composite gels as dysphagia food.

Food research international (Ottawa, Ont.)·2026
Same author

Synergistic Microstructural Engineering of LiNi<sub>0.8</sub>Co<sub>0.1</sub>Mn<sub>0.1</sub>O<sub>2</sub> Cathodes via pH-Controlled Crystallographic Orientation of Ni<sub>0.8</sub>Co<sub>0.1</sub>Mn<sub>0.1</sub>(OH)<sub>2</sub> Precursors.

Langmuir : the ACS journal of surfaces and colloids·2026

Related Experiment Video

Updated: Oct 21, 2025

Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress
09:51

Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress

Published on: May 7, 2014

15.5K

Rack1 is essential for corticogenesis by preventing p21-dependent senescence in neural stem cells.

Qian Zhu1, Liping Chen1, Ying Li1

  • 1Department of Neurobiology, Beijing Institute of Basic Medical Sciences, 100850 Beijing, China.

Cell Reports
|September 1, 2021
PubMed
Summary

Receptor for activated C kinase (Rack1) prevents neural stem cell senescence, crucial for normal brain development. Its absence causes microcephaly by promoting senescence and reducing neurogenesis.

Keywords:
Rack1TGF-β/Smadcellular senescencemicrocephalyneural stem cellsp21

More Related Videos

Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells NPCs
10:47

Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells NPCs

Published on: March 2, 2018

10.2K
Induction of Protein Deletion Through In Utero Electroporation to Define Deficits in Neuronal Migration in Transgenic Models
12:01

Induction of Protein Deletion Through In Utero Electroporation to Define Deficits in Neuronal Migration in Transgenic Models

Published on: January 12, 2015

10.4K

Related Experiment Videos

Last Updated: Oct 21, 2025

Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress
09:51

Assessing Cell Cycle Progression of Neural Stem and Progenitor Cells in the Mouse Developing Brain after Genotoxic Stress

Published on: May 7, 2014

15.5K
Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells NPCs
10:47

Rapid Detection of Neurodevelopmental Phenotypes in Human Neural Precursor Cells NPCs

Published on: March 2, 2018

10.2K
Induction of Protein Deletion Through In Utero Electroporation to Define Deficits in Neuronal Migration in Transgenic Models
12:01

Induction of Protein Deletion Through In Utero Electroporation to Define Deficits in Neuronal Migration in Transgenic Models

Published on: January 12, 2015

10.4K

Area of Science:

  • Neuroscience
  • Developmental Biology
  • Cell Biology

Background:

  • Normal neurodevelopment depends on balanced neural stem cell (NSC) functions.
  • Disruptions in NSC regulation can lead to neurodevelopmental disorders like microcephaly.
  • Cellular senescence is implicated in impaired neurogenesis and corticogenesis.

Purpose of the Study:

  • To investigate the role of Receptor for Activated C Kinase 1 (Rack1) in neurodevelopment.
  • To elucidate the mechanism by which Rack1 influences neural stem cell fate and proliferation.
  • To understand Rack1's role in preventing microcephaly.

Main Methods:

  • Generated Rack1 knockout mouse models.
  • Analyzed neurogenesis and corticogenesis in developing cortical progenitors.
  • Investigated the involvement of p21 and TGF-β/Smad signaling pathways.
  • Performed in vivo rescue experiments by removing p21.

Main Results:

  • Rack1 deletion in cortical progenitors resulted in a microcephaly phenotype.
  • Absence of Rack1 led to decreased neurogenesis and increased NSC senescence.
  • Rack1 null NSCs showed dramatically activated p21 signaling.
  • Rack1 directly interacts with Smad3 to suppress TGF-β/Smad signaling, inhibiting p21-mediated senescence.
  • Removal of p21 significantly rescued the Rack1-knockout phenotype in vivo.

Conclusions:

  • Rack1 is essential for normal cortical development by inhibiting NSC senescence.
  • Rack1's interaction with Smad3 suppresses the TGF-β/Smad pathway, preventing p21-induced senescence.
  • Inhibition of p21-induced NSC senescence by Rack1 is a critical mechanism for neurogenesis and corticogenesis.