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

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
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

Juvenile Myelomonocytic Leukemia Presenting with Unusual Immunonologic Manifestations: Report of a Case with Multiple Somatic Genetic Aberrations Including <i>KRAS</i> and Novel <i>ETV6</i> Mutations.

Pediatric and developmental pathology : the official journal of the Society for Pediatric Pathology and the Paediatric Pathology Society·2026
Same author

Early α-synuclein-mediated mitochondrial dysfunction in a human cell model of Parkinson's disease dementia.

Communications biology·2026
Same author

An Interpretable 3D Bag-Of-Visual-Words Pipeline for Volumetric Microscopy Classification.

bioRxiv : the preprint server for biology·2026
Same author

Dominant clones leverage developmental epigenomic states to drive ependymoma.

Nature·2026
Same author

ZFTA-RELA ependymomas make itaconate to epigenetically drive fusion expression.

Nature·2026
Same author

Childhood brain tumors instruct cranial hematopoiesis and immunotolerance.

Nature genetics·2026

Related Experiment Video

Updated: May 19, 2026

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

Pten deletion causes mTorc1-dependent ectopic neuroblast differentiation without causing uniform migration defects.

Guo Zhu1, Lionel M L Chow, Ildar T Bayazitov

  • 1Department of Developmental Neurobiology, St Jude Children's Research Hospital, Memphis, TN 38105, USA.

Development (Cambridge, England)
|August 10, 2012
PubMed
Summary

The PI3K-Akt-mTorc1 pathway regulates neuroblast migration and differentiation. Pten deletion causes pathway activation, leading to premature differentiation and enlarged brain regions, but migration itself is not uniformly impaired.

More Related Videos

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

Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development
09:32

Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development

Published on: June 15, 2017

Related Experiment Videos

Last Updated: May 19, 2026

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells
09:37

Defining Gene Functions in Tumorigenesis by Ex vivo Ablation of Floxed Alleles in Malignant Peripheral Nerve Sheath Tumor Cells

Published on: August 25, 2021

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

Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development
09:32

Light-mediated Reversible Modulation of the Mitogen-activated Protein Kinase Pathway during Cell Differentiation and Xenopus Embryonic Development

Published on: June 15, 2017

Area of Science:

  • Neuroscience
  • Cell Biology
  • Developmental Biology

Background:

  • Adult neurogenesis occurs in the subventricular zone (SVZ), with precursors migrating to the olfactory bulb (OB) via the rostral migratory stream (RMS).
  • The PI3K-Akt-mTorc1 signaling pathway plays crucial roles in cell growth, proliferation, and survival.
  • Pten (Phosphatase and tensin homolog) is a tumor suppressor that negatively regulates the PI3K-Akt-mTorc1 pathway.

Purpose of the Study:

  • To investigate the role of the PI3K-Akt-mTorc1 pathway in the migration and differentiation of neuroblasts.
  • To determine the effect of Pten deletion on neuroblast migration and the PI3K-Akt-mTorc1 pathway.
  • To elucidate the mechanisms underlying migration defects observed in Pten-deficient neuroblasts.

Main Methods:

  • Analysis of PI3K-Akt-mTorc1 pathway activity in migrating neuroblasts.
  • Generation of a mouse model with postnatal deletion of Pten in neuroblasts.
  • Live imaging of neuroblast migration in acute brain slices.
  • Pharmacological inhibition of mTorc1.

Main Results:

  • The PI3K-Akt-mTorc1 pathway is inactivated in migrating neuroblasts in the SVZ and RMS, and activated upon reaching the OB.
  • Postnatal Pten deletion leads to aberrant PI3K-Akt-mTorc1 activation, resulting in enlarged SVZ and RMS.
  • Pten deletion causes premature termination of migration and differentiation of neuroblasts, which is rescued by mTorc1 inhibition.
  • Live imaging reveals that Pten-null neuroblasts do not exhibit uniform migration defects; instead, a subpopulation shows altered morphology and reduced movement, suggesting premature differentiation.

Conclusions:

  • The PI3K-Akt-mTorc1 pathway is dynamically regulated during neuroblast migration and differentiation.
  • Pten deletion disrupts this regulation, leading to ectopic differentiation and secondary migration defects.
  • These findings suggest that impaired migration in Pten-null neurons may be a consequence of premature differentiation rather than a primary defect in migratory mechanics.