@Article{biocell.2022.020109,
AUTHOR = {LIANGYING ZHANG, SHAOTING ZHANG, ZHAOYANG FAN, ZONGYING JIANG, ANBU LIU, SHUJING LI, JIANMIN SUN},
TITLE = {PI3 kinase isoform p110δ is more important than p110α in KIT signaling in hematopoietic cells},
JOURNAL = {BIOCELL},
VOLUME = {46},
YEAR = {2022},
NUMBER = {9},
PAGES = {2081--2087},
URL = {http://www.techscience.com/biocell/v46n9/47739},
ISSN = {1667-5746},
ABSTRACT = {PI3 kinases are important for KIT signaling and KIT mutants mediated cell transformation. In order to know the
difference of PI3 kinase isoforms p110α and p110δ in the signaling of wild-type KIT and the often occurred KIT mutation
D816V in hematopoietic malignancy mastocytosis, the predominant PI3 kinase isoform p110δ in hematopoietic tissues was
knocked out in hematopoietic cells. We found that loss of p110δ expression dramatically inhibits PI3 kinase activation
mediated by both wild-type KIT and KIT/D816V. By over expression of p110α in p110δ knock out cells, wild-type KIT
mediated PI3 kinase activation was not changed while over expression of p110δ increased PI3 kinase activation.
Similarly, in KIT/D816V expressing cells without p110δ expression, over expression of p110δ but not p110α restored
PI3 kinase activation. In agreement with the signaling results, cell proliferation, cell survival and cell cycle assay further
showed that over expression of p110δ but not p110α in p110δ knock out cells increases both wild-type KIT and KIT/
D816V mediated cell survival and proliferation. These results suggested that p110δ plays a more important role than
p110α in KIT signaling and KIT mutant mediated cell transformation in hematopoietic cells.},
DOI = {10.32604/biocell.2022.020109}
}