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

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...
Pleiotropy01:33

Pleiotropy

Pleiotropy is the phenomenon in which a single gene impacts multiple, seemingly unrelated phenotypic traits. For example, defects in the SOX10 gene cause Waardenburg Syndrome Type 4, or WS4, which can cause defects in pigmentation, hearing impairments, and an absence of intestinal contractions necessary for elimination. This diversity of phenotypes results from the expression pattern of SOX10 in early embryonic and fetal development. SOX10 is found in neural crest cells that form melanocytes,...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

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.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Non-LTR Retrotransposons03:18

Non-LTR Retrotransposons

As the name suggests, non-LTR retrotransposons lack the long terminal repeats characteristic of the LTR retrotransposons. Additionally, both LTR and non-LTR retrotransposons use distinct mechanisms of mobilization. Non-LTR retrotransposons are further divided into two classes - Long interspersed nuclear elements (LINEs) and short interspersed nuclear elements (SINEs), both of which occur abundantly in most mammals, including humans. Some of the active non-LTR retrotransposons in humans are L1...
Abnormal Proliferation02:23

Abnormal Proliferation

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 daughter...

You might also read

Related Articles

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

Sort by
Same author

MICU2 controls mitochondrial calcium signaling and migration in neurons during development.

Cell reports·2025
Same author

Feasibility of a Smart Label-Enabled Remote Therapeutic Monitoring Intervention to Support Cyclin-Dependent Kinase 4/6 Inhibitor Adherence in Breast Cancer Care.

JCO clinical cancer informatics·2025
Same author

Neural Progenitors as a Novel Pathogenic Mechanism in Microcephaly.

bioRxiv : the preprint server for biology·2025
Same author

Altered extracellular matrix structure and elevated stiffness in a brain organoid model for disease.

Nature communications·2025
Same author

Examining the NEUROG2 lineage and associated gene expression in human cortical organoids.

Development (Cambridge, England)·2024
Same author

A framework for neural organoids, assembloids and transplantation studies.

Nature·2024
Same journal

Population codes for context-dependent decision-making.

Current opinion in neurobiology·2026
Same journal

Cichlid fish as a model for understanding social dysfunction.

Current opinion in neurobiology·2026
Same journal

On aims and methods in field neuroethology: Investigating neural mechanisms of behavior in semi-natural and natural contexts.

Current opinion in neurobiology·2026
Same journal

Neurobiological interfaces connecting environmental change to monarch butterfly migration.

Current opinion in neurobiology·2026
Same journal

Learning how to experience the world: From circuits to cell types to genes.

Current opinion in neurobiology·2026
Same journal

Editorial overview for neurobiology of disease 2026.

Current opinion in neurobiology·2026
See all related articles

Related Experiment Video

Updated: May 8, 2026

Validation of a Mouse Model to Disrupt LINC Complexes in a Cell-specific Manner
09:02

Validation of a Mouse Model to Disrupt LINC Complexes in a Cell-specific Manner

Published on: December 10, 2015

LIS1 functions in normal development and disease.

Orly Reiner1, Tamar Sapir

  • 1Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel.

Current Opinion in Neurobiology
|August 27, 2013
PubMed
Summary
This summary is machine-generated.

LIS1 gene mutations cause brain malformations like lissencephaly or developmental delays. Its interaction with cytoplasmic dynein is crucial for neuronal migration and cortical development.

More Related Videos

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry
10:16

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry

Published on: January 6, 2017

ALS - Motor Neuron Disease: Mechanism and Development of New Therapies
15:48

ALS - Motor Neuron Disease: Mechanism and Development of New Therapies

Published on: July 29, 2007

Related Experiment Videos

Last Updated: May 8, 2026

Validation of a Mouse Model to Disrupt LINC Complexes in a Cell-specific Manner
09:02

Validation of a Mouse Model to Disrupt LINC Complexes in a Cell-specific Manner

Published on: December 10, 2015

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry
10:16

SorLA and CLC:CLF-1-dependent Downregulation of CNTFRα as Demonstrated by Western Blotting, Inhibition of Lysosomal Enzymes, and Immunocytochemistry

Published on: January 6, 2017

ALS - Motor Neuron Disease: Mechanism and Development of New Therapies
15:48

ALS - Motor Neuron Disease: Mechanism and Development of New Therapies

Published on: July 29, 2007

Area of Science:

  • Neuroscience
  • Genetics
  • Developmental Biology

Background:

  • LIS1 is the first identified gene linked to neuronal migration disorders.
  • It's a dosage-sensitive gene critical for cortical development.
  • LIS1 dysfunction leads to lissencephaly (deletions) or developmental delays (duplications).

Purpose of the Study:

  • To elucidate the cellular functions of LIS1 in cortical development.
  • To understand the regulatory interaction between LIS1 and cytoplasmic dynein.
  • To investigate the role of LIS1-dynein interaction in neuronal migration and transport.

Main Methods:

  • Analysis of LIS1 gene deletions and duplications.
  • Investigating LIS1's effects on progenitor proliferation and cell division.
  • Studying LIS1's role in nuclear positioning and neuronal migration.
  • Examining the in vitro and in vivo interaction of LIS1 with cytoplasmic dynein.

Main Results:

  • LIS1 regulates progenitor proliferation, spindle orientation, and nuclear movements.
  • LIS1 impacts neuronal nucleokinesis and migration.
  • LIS1 binding to cytoplasmic dynein affects motor velocity in vitro and in vivo.
  • This interaction is potentially vital for high-load transport in neurons.

Conclusions:

  • LIS1 plays a multifaceted role in cortical development by influencing cell proliferation and neuronal migration.
  • The interaction between LIS1 and cytoplasmic dynein is central to its cellular functions.
  • Understanding LIS1-dynein dynamics offers insights into neuronal transport and developmental disorders.