Investigating the Effects of SFK and Mek Inhibitors on G-CSF Signaling

Granulocyte-Colony Stimulating Factor (G-CSF) is known as a growth factor that positively regulates neutrophil development. G-CSF supports neutrophil differentiation by binding to the G-CSF Receptor (G-CSFR), leading to the activation of downstream signaling pathways such as the Jak/Stat, Mek/Erk1/2 and Src-Family Kinases (SFKs). However, the molecular mechanisms by which G-CSF acts in myeloid development remain incompletely understood. The SFKs have been shown to play a critical role in monocyte development, but significantly less is known about their roles in neutrophil development. The Dong lab recently showed that tyrosine (Y) 729 in the cytoplasmic domain of G-CSFR controls neutrophil versus monocyte development of myeloid precursors by regulating Mek/Erk1/2 pathway and downstream transcription factors c-Fos/Egr-1. As the SFKs have been shown to activate Mek/Erk1/2 signaling pathway, we examined whether they are involved in the regulation of neutrophil development in response to G-CSF. We show here that SFKs appeared to regulate the different aspects of neutrophil versus monocyte development. Additional studies are needed to further clarify the roles of SFKs in myeloid development.
Download pdf
Abstract/Description: Granulocyte-Colony Stimulating Factor (G-CSF) is known as a growth factor that positively regulates neutrophil development. G-CSF supports neutrophil differentiation by binding to the G-CSF Receptor (G-CSFR), leading to the activation of downstream signaling pathways such as the Jak/Stat, Mek/Erk1/2 and Src-Family Kinases (SFKs). However, the molecular mechanisms by which G-CSF acts in myeloid development remain incompletely understood. The SFKs have been shown to play a critical role in monocyte development, but significantly less is known about their roles in neutrophil development. The Dong lab recently showed that tyrosine (Y) 729 in the cytoplasmic domain of G-CSFR controls neutrophil versus monocyte development of myeloid precursors by regulating Mek/Erk1/2 pathway and downstream transcription factors c-Fos/Egr-1. As the SFKs have been shown to activate Mek/Erk1/2 signaling pathway, we examined whether they are involved in the regulation of neutrophil development in response to G-CSF. We show here that SFKs appeared to regulate the different aspects of neutrophil versus monocyte development. Additional studies are needed to further clarify the roles of SFKs in myeloid development.
Subject(s):


Date Created: 2018-08-31
Title: Investigating the Effects of SFK and Mek Inhibitors on G-CSF Signaling.
Name(s): Grim, Allison, author
Dr. Fan Dong, advisor
Type of Resource: text
Genre: poster
Date Created: 2018-08-31
Other Date: 2018
Physical Form: application/pdf
Extent: 1 p.
Abstract/Description: Granulocyte-Colony Stimulating Factor (G-CSF) is known as a growth factor that positively regulates neutrophil development. G-CSF supports neutrophil differentiation by binding to the G-CSF Receptor (G-CSFR), leading to the activation of downstream signaling pathways such as the Jak/Stat, Mek/Erk1/2 and Src-Family Kinases (SFKs). However, the molecular mechanisms by which G-CSF acts in myeloid development remain incompletely understood. The SFKs have been shown to play a critical role in monocyte development, but significantly less is known about their roles in neutrophil development. The Dong lab recently showed that tyrosine (Y) 729 in the cytoplasmic domain of G-CSFR controls neutrophil versus monocyte development of myeloid precursors by regulating Mek/Erk1/2 pathway and downstream transcription factors c-Fos/Egr-1. As the SFKs have been shown to activate Mek/Erk1/2 signaling pathway, we examined whether they are involved in the regulation of neutrophil development in response to G-CSF. We show here that SFKs appeared to regulate the different aspects of neutrophil versus monocyte development. Additional studies are needed to further clarify the roles of SFKs in myeloid development.
Identifier(s): 2018-EOS-Grim-Investigating-The-Effiects-of-SFK (IID)
Subject(s):


Held by: The University of Toledo
Location: University of Toledo Digital Repository
Rights Statement: IN COPYRIGHT
Related Title:
In Collections: