What is it about?
MC survival, proliferation, differentiation, and migration are all maintained by a MC growth factor, stem cell factor (SCF) via its receptor, KIT. SCF activates PKCα and PKCβ isoforms, which in turn modulates KIT phosphorylation and internalization, and activates p38 MAPK and this axis subsequently regulates SCF-induced MC cell proliferation. Downregulation of neither PKCα nor PKCβ affected MC viability and proliferation. In contrast, blocking both attenuated SCF-induced cell viability and proliferation, suggesting that PKCα and PKCβ compensate for each other downstream of SCF signaling
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Why is it important?
Our results not only suggest that PKC classical isoforms are novel therapeutic targets for SCF/MC-mediated inflammatory and allergic diseases, but they also emphasize the importance of inhibiting both PKCα and β isoforms simultaneously to prevent MC proliferation.
Perspectives
I hope this article can provide a better understanding of the SCF mediated signaling in mast cells through its KIT receptor which can help to provide better treatments for SCF/MC-mediated inflammatory and allergic diseases
Yasmine Elshoweikh
University of Akron
Read the Original
This page is a summary of: Protein Kinase C α and β compensate for each other to promote stem cell factor‐mediated KIT phosphorylation, mast cell viability and proliferation, The FASEB Journal, March 2022, Wiley,
DOI: 10.1096/fj.202101838rrr.
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