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Updated: Jul 15, 2026
08:01
Stimulation of Notch Signaling in Mouse Osteoclast Precursors
Published on: February 28, 2017
The notch pathway positively regulates programmed cell death during erythroid differentiation.
A Robert-Moreno1, L Espinosa, M J Sanchez
1Centre Oncologia Molecular, IDIBELL-Institut de Recerca Oncològica, Hospitalet, Barcelona, Spain.
Leukemia
|May 4, 2007
Summary
The Notch signaling pathway, involving RBPjkappa, induces programmed cell death in red blood cells. Blocking this pathway increases red blood cell numbers, revealing Notch
Area of Science:
- Hematology
- Cell Biology
- Molecular Biology
Background:
- Programmed cell death is crucial for erythropoiesis.
- The role of Notch signaling in erythroid apoptosis is not fully understood.
Purpose of the Study:
- To investigate the role of the Notch/RBPjkappa signaling pathway in regulating erythroid apoptosis.
- To determine how Notch signaling impacts erythroid homeostasis.
Main Methods:
- Utilized RBPjkappa knockout mice models.
- Employed gamma-secretase inhibitors (DAPT, L685,458) to block Notch activity.
- Co-cultured erythroid cells with Jagged1-expressing cells.
- Expressed activated Notch1 in murine erythroleukemia cells.
Main Results:
- Notch/RBPjkappa signaling induces erythroid apoptosis in various hematopoietic tissues and cell lines.
- RBPjkappa deficiency or Notch inhibition reduces erythroid cell death, increasing Ter119(+) cell counts.
- Jagged1 stimulation promotes erythroid apoptosis, which is blocked by inhibiting Notch activity.
- Activated Notch1 expression is sufficient to induce apoptosis in differentiating erythroleukemia cells.
Conclusions:
- The Notch signaling pathway is a key regulator of erythroid homeostasis.
- Notch signaling induces apoptosis in erythroid cells, controlling their population.
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