Related Experiment Video
Updated: May 24, 2026

Stimulation of Notch Signaling in Mouse Osteoclast Precursors
Published on: February 28, 2017
Myeloproliferation and hematopoietic stem cell dysfunction due to defective Notch receptor modification by O-fucose
1Department of Pathology, Case Western Reserve University, Cleveland, OH 44106, USA. lan.zhou@case.edu
Abstract:
O-fucosylglycans on Notch extracellular domain epidermal growth factor (EGF) repeats are critical in modulating Notch signaling by altering the sensitivity of Notch receptors to activation by Notch ligands. Mice lacking Notch O-fucosylglycans display granulo-monocytic myeloproliferation, hematopoietic stem cell dysfunction and aberrant stem cell niche occupancy. The inability of the stem cells/progenitors that lack Notch O-fucosylglycans to transcribe Notch signaling activation is attributed by a loss of effective Notch-ligand interaction. These findings, in conjunction with myeloproliferation identified in mouse models with defective Notch cleavage or ligand endocytosis, reveal emerging new roles of Notch in hematopoietic stem cell biology and myeloid homeostasis.
Related Concept Videos
Notch Signaling Pathway
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 until 1985...
Notch Signaling Pathway
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 until 1985...
Role Of Notch Signalling In Intestinal Stem Cell Renewal
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...
Regulation of Hematopoietic Stem Cells
Proteoglycans
Differentiation of Common Myeloid Progenitor Cells
