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

6.9K
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...
6.9K
Notch Signaling Pathway03:14

Notch Signaling Pathway

6.5K
6.5K
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

2.6K
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...
2.6K
Negative Regulator Molecules01:23

Negative Regulator Molecules

38.9K
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.
38.9K
Abnormal Proliferation02:23

Abnormal Proliferation

5.4K
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...
5.4K
Canonical Wnt Signaling Pathway02:54

Canonical Wnt Signaling Pathway

10.9K
The gene encoding the main signaling molecules of the Wnt signaling pathways (the Wnt proteins) was discovered almost four decades ago by Nüsslein-Volhard and Wieschaus. They identified and originally named the gene "wingless" (wg) after a phenotype discovered during their landmark genetic screen in Drosophila for body pattern defects. At around the same time, another researcher named Harold Varmus found that a murine tumor virus activates the mammalian wg homolog, Int-1, which...
10.9K

You might also read

Related Articles

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

Sort by
Same author

The role of the molecular tumor board: learnings from the ROME trial.

NPJ precision oncology·2026
Same author

KCTD1 is a new modulator of the KCASH family of Hedgehog suppressors.

Neoplasia (New York, N.Y.)·2023
Same author

Correction: Circulating miR‑26b‑5p and miR‑451a as diagnostic biomarkers in medullary thyroid carcinoma patients.

Journal of endocrinological investigation·2023
Same author

Trends in severe outcomes in SARS-CoV-2-positive hospitalized patients with rheumatic diseases: a monocentric observational and case-control study in northern Italy.

Reumatismo·2023
Same author

Matrix Gla Protein drives stemness and tumor initiation in ovarian cancer.

Cell death & disease·2023
Same author

MicroRNA loaded edible nanoparticles: an emerging personalized therapeutic approach for the treatment of obesity and metabolic disorders.

Theranostics·2022

Related Experiment Video

Updated: Mar 25, 2026

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

2.5K

Prolyl-isomerase Pin1 controls Notch3 protein expression and regulates T-ALL progression.

G Franciosa1, G Diluvio1, F Del Gaudio1

  • 1Laboratory of Molecular Pathology, Department of Molecular Medicine, Sapienza University, Rome, Italy.

Oncogene
|February 16, 2016
PubMed
Summary
This summary is machine-generated.

The prolyl-isomerase Pin1 targets Notch3, enhancing its activity and promoting T-cell Acute Lymphoblastic Leukemia (T-ALL) cell invasion. Inhibiting both Pin1 and Notch3 reduces T-ALL cell invasiveness and progression.

More Related Videos

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

8.4K
Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors
08:45

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors

Published on: July 17, 2020

6.7K

Related Experiment Videos

Last Updated: Mar 25, 2026

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

2.5K
Stimulation of Notch Signaling in Mouse Osteoclast Precursors
08:01

Stimulation of Notch Signaling in Mouse Osteoclast Precursors

Published on: February 28, 2017

8.4K
Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors
08:45

Assessing Cellular Target Engagement by SHP2 PTPN11 Phosphatase Inhibitors

Published on: July 17, 2020

6.7K

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Immunology

Background:

  • Deregulated Notch signaling is implicated in T-cell Acute Lymphoblastic Leukemia (T-ALL).
  • The role of Notch pathway in leukemia cell invasion is recognized, but molecular mechanisms are unclear.
  • Pin1 is a prolyl-isomerase involved in regulating protein function.

Purpose of the Study:

  • To investigate the role of Pin1 in Notch3-mediated T-ALL progression.
  • To identify Pin1 as a novel regulator of Notch3.
  • To explore the therapeutic potential of targeting the Notch3-Pin1 axis in T-ALL.

Main Methods:

  • Investigated the interaction between Pin1 and Notch3 in TALL-1 cells.
  • Assessed the effect of combined Notch3 and Pin1 inhibition on cell invasiveness and MMP9 expression.
  • Utilized a mouse model of Notch3-induced T-ALL to evaluate Pin1 depletion effects.
  • Performed in silico gene expression analysis of human T-ALL samples.

Main Results:

  • Pin1 directly targets Notch3, regulating its processing and stabilizing the intracellular domain (N3IC).
  • Combined inhibition of Notch3 and Pin1 reduced invasiveness of TALL-1 cells by decreasing MMP9 expression.
  • Pin1 depletion in a mouse model impaired T-ALL cell expansion and invasiveness.
  • Significant correlation observed between Pin1 and Notch3 expression in human T-ALL samples.

Conclusions:

  • The Notch3-Pin1 axis plays a critical role in T-ALL aggressiveness and progression.
  • Combined suppression of Pin1 and Notch3 represents a potential therapeutic strategy for T-ALL.
  • Targeting this axis may offer a novel approach to treat T-ALL by reducing tumor cell invasion.