hematopoietic system
• in pIpC-treated mice
|
• following pIpC treatment, multipotent progenitors transiently expand then are depleted in parallel with hematopoietic stem cells unlike in Stk11tm1Sjm homozygotes
|
• in pIpC-treated mice
|
• in pIpC-treated mice
|
• in pIpC-treated mice
|
• in pIpC-treated mice
|
• 18 days after pIpC treatment; not improved by rapamycin treatment
|
pancytopenia
(
J:165090
)
• by day 24 to 34 of pIpC treatment
|
• starting 2 to 6 days after pIpC treatment
|
• hematopoietic stem cells (HSCs)from pIpC-treated mice exhibit increased cell proliferation compared with cells from Stk11tm1Sjm homozygotes
• 11 days after pIpC-treatment, HSCs exhibit increased apoptosis compared with cells from Stk11tm1Sjm homozygotes
• HSCs from pIpC-treated mice fail to exhibit long-term reconstitution unlike cells from Stk11tm1Sjm homozygotes
• however, mice exhibit normal proliferation of granulocyte macrophage progenitors (GMP) and whole bone marrow (WBM) cells and apoptosis of multipotent progenitor, GMP, and WBM cells
|
cellular
N |
• hematopoietic stem cells from pIpC treated mice exhibit normal reactive oxygen species
|
aneuploidy
(
J:165090
)
• hematopoietic stem cells from pIpC-treated mice become aneuploid unlike similarly treated cells from Stk11tm1Sjm homozygotes
• however, granulocyte macrophage progenitors cells from pIpC-treated mice do not become aneuploid
|
• hematopoietic stem cells from pIpC-treated mice exhibit supernumerary centrosomes and defective mitotic spindle unlike in cells from similarly treated Stk11tm1Sjm homozygotes
|
• in the hematopoietic stem cells of pIpC-treated mice
|
immune system
• in pIpC-treated mice
|
• in pIpC-treated mice
|
endocrine/exocrine glands
• in pIpC-treated mice
|