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

Lineage Commitment01:21

Lineage Commitment

Commitment is the  process whereby stem cells:
Forced Transdifferentiation01:28

Forced Transdifferentiation

Transdifferentiation, also known as lineage reprogramming, was first discovered by Selman and Kafatos in 1974 in silkmoths. They observed that the moths’ cuticle-producing cells transformed into salt-producing cells. Many such cases of natural transdifferentiation occur in organisms. In humans, pancreatic alpha cells can become beta cells. In newts, the loss of the eye’s lens causes the pigmented epithelial cells to transdifferentiate into the lens cells.
Artificial transdifferentiation occurs...
Role Of Notch Signalling In Intestinal Stem Cell Renewal01:12

Role Of Notch Signalling In Intestinal Stem Cell Renewal

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...
Determination01:51

Determination

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 contrast, determination...
Cis-regulatory Sequences02:02

Cis-regulatory Sequences

Cis-regulatory sequences are short fragments of non-coding DNA that are present on the same chromosomes as the genes that they regulate. These fragments serve as binding sites for transcriptional regulators, proteins that are responsible for controlling gene transcription and differential gene expression across cell types in eukaryotes. Cis-regulatory sequences can be close to the gene of interest or thousands of bases away in the DNA sequence; however, those sequences that are further away are...
Plasticity00:58

Plasticity

Plasticity is the property where an object loses its elasticity and undergoes irreversible deformation, even after the deformation forces are eliminated. If a material deforms irreversibly without increasing stress or load, then this is called ideal plasticity. For example, when a force is applied to an aluminum rod, it changes its shape, but it does not return to its original shape once the force is removed. Plastic deformation or ductility is thus a permanent deformation or change in the...

You might also read

Related Articles

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

Sort by
Same author

Sphingosine-1-phosphate receptor modulators resensitize FLT3-ITD acute myeloid leukemia cells with NRAS mutations to FLT3 inhibitors.

Leukemia·2026
Same author

Sphingosine-1-phosphate receptor modulators resensitize FLT3-ITD acute myeloid leukemia cells with <i>NRAS</i> mutations to FLT3 inhibitors.

bioRxiv : the preprint server for biology·2025
Same author

SIRT5 inhibition impairs mitochondrial metabolism and enhances venetoclax-induced elimination of acute myeloid leukemia cells.

Leukemia·2025
Same author

Targeting rapid TKI-induced AXL upregulation overcomes adaptive ERK reactivation and exerts antileukemic effects in FLT3/ITD acute myeloid leukemia.

Molecular oncology·2024
Same author

Inhibition of NOTCH4 sensitizes FLT3/ITD acute myeloid leukemia cells to FLT3 tyrosine kinase inhibition.

Leukemia·2024
Same author

NUP98::Nsd1 and FLT3-ITD collaborate to generate acute myeloid leukemia.

Leukemia·2023

Related Experiment Video

Updated: May 21, 2026

Direct Lineage Reprogramming of Adult Mouse Fibroblast to Erythroid Progenitors
11:46

Direct Lineage Reprogramming of Adult Mouse Fibroblast to Erythroid Progenitors

Published on: December 14, 2018

FLT3 in lineage specification and plasticity.

Sarah Greenblatt1, Donald Small

  • 1Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.

Oncotarget
|May 31, 2012
PubMed
Summary

Activating mutations in FMS-like tyrosine kinase 3 (FLT3) can collaborate with other mutations to cause acute leukemia. This study reveals that leukemic cells showing lymphoid and myeloid traits are restricted to myeloid differentiation, offering insights into FLT3

More Related Videos

Lineage Tracing of Inducible Fluorescently-Labeled Stem Cells in the Adult Mouse Brain
09:44

Lineage Tracing of Inducible Fluorescently-Labeled Stem Cells in the Adult Mouse Brain

Published on: May 20, 2022

Related Experiment Videos

Last Updated: May 21, 2026

Direct Lineage Reprogramming of Adult Mouse Fibroblast to Erythroid Progenitors
11:46

Direct Lineage Reprogramming of Adult Mouse Fibroblast to Erythroid Progenitors

Published on: December 14, 2018

Lineage Tracing of Inducible Fluorescently-Labeled Stem Cells in the Adult Mouse Brain
09:44

Lineage Tracing of Inducible Fluorescently-Labeled Stem Cells in the Adult Mouse Brain

Published on: May 20, 2022

Area of Science:

  • Hematology
  • Molecular Biology
  • Cancer Research

Background:

  • FMS-like tyrosine kinase 3 (FLT3) is crucial for normal hematopoietic stem and progenitor cell (HSPC) differentiation.
  • FLT3 expression in lymphoid precursors correlates with multilineage differentiation potential.
  • FLT3 activating mutations can cooperate with Nup98-HoxD13 to induce aggressive acute leukemia.

Purpose of the Study:

  • To investigate the role of FLT3 in lineage plasticity within a leukemia model.
  • To determine the differentiation capacity of leukemic initiating cells with mixed lymphoid and myeloid properties.
  • To understand FLT3's role in the inhibition of myeloid differentiation.

Main Methods:

  • Utilized a mouse model of acute leukemia induced by FLT3 and Nup98-HoxD13 mutations.
  • Employed various assays to characterize the leukemic initiating population.
  • Analyzed gene expression patterns to assess lymphoid and myeloid differentiation potential.

Main Results:

  • The leukemic initiating population, despite exhibiting lymphoid and myeloid precursor properties, was restricted to myeloid differentiation.
  • B-lineage characteristics were attributed to primed lymphoid transcription programs, not true B-cell maturation capacity.
  • The model demonstrated the development of undifferentiated myeloid leukemia, implicating FLT3 in differentiation inhibition.

Conclusions:

  • FLT3 mutations contribute to acute leukemia by influencing lineage plasticity and differentiation.
  • Leukemic cells may mimic multipotency through transcriptional priming rather than inherent plasticity.
  • Insights from this model advance understanding of FLT3's complex role in hematopoiesis and leukemia development.