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Related Experiment Video

Updated: May 9, 2026

Analysis of the c-KIT Ligand Promoter Using Chromatin Immunoprecipitation

Analysis of the c-KIT Ligand Promoter Using Chromatin Immunoprecipitation

Published on: June 27, 2017

Genetic interaction between Kit and Scl.

Julie Lacombe¹, Gorazd Krosl, Mathieu Tremblay

¹Institute for Research in Immunology and Cancer, Montréal, QC, Canada.

|July 10, 2013

Summary

This summary is machine-generated.

Stem cell leukemia (SCL) transcription factor and c-Kit receptor signaling form a positive feedback loop crucial for hematopoietic stem cell survival and expansion. This loop regulates erythroid progenitor development and survival.

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Last Updated: May 9, 2026

Analysis of the c-KIT Ligand Promoter Using Chromatin Immunoprecipitation

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Published on: June 27, 2017

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Published on: January 31, 2025

Visualization of the Interstitial Cells of Cajal (ICC) Network in Mice

Visualization of the Interstitial Cells of Cajal (ICC) Network in Mice

Published on: July 27, 2011

Area of Science:

Hematopoiesis
Molecular Biology
Stem Cell Biology

Background:

Stem cell leukemia (SCL/TAL1) and c-Kit signaling are vital for hematopoietic stem cell (HSC) survival and quiescence.
SCL is a transcription factor, and c-Kit is a tyrosine kinase receptor involved in hematopoiesis.

Purpose of the Study:

To investigate the regulatory relationship between SCL and c-Kit in hematopoietic stem and progenitor cells.
To determine the role of SCL in Kit-dependent signaling pathways controlling cell survival and proliferation.

Main Methods:

Analysis of SCL expression levels in Kit-positive multipotent and erythroid progenitors.
Assessment of progenitor sensitivity to steel factor (KIT ligand) and interleukin-3.
Studies in mice with a hypomorphic Kit allele (W41/41) and SCL overexpression.
Gene expression profiling to identify common targets of SCL and c-Kit signaling.

Main Results:

SCL levels are limiting for the clonal expansion of Kit-positive multipotent and erythroid progenitors.
Increased SCL enhances progenitor sensitivity to steel factor, while a mutant SCL induces apoptosis.
SCL overexpression in W41/41 mice corrects hematocrit and erythroid progenitor deficiencies.
SCL and c-Kit signaling regulate a common gene expression signature, including apoptosis-associated genes.

Conclusions:

SCL functions downstream of c-Kit to promote megakaryocyte/erythroid progenitor (MEP) survival.
SCL also acts upstream of c-Kit, upregulating Kit expression and enhancing bone marrow chimerism.
SCL and c-Kit form a positive feedback loop essential for multipotent and MEP regulation.