한빛사논문
Abstract
The Biomedical Research Centre, University of British Columbia, Vancouver,
BC, Canada
Department of Pathology and Laboratory Medicine, University of
British Columbia, Vancouver, BC, Canada
* Corresponding author.
The sialomucin CD43 is highly expressed on most hematopoietic cells. Here we show that the CD43 ectodomain is shed from murine granulocytes, mast cells and T cells but not from macrophages. To study the significance of CD43 shedding we constructed two CD43/34 chimeras where the CD43 membrane proximal or transmembrane domain was swapped with the corresponding domain from CD34 that is not shed from cells. Viability of cells that normally shed CD43 was negatively affected when forced to express either of the two CD43/34 chimeras and toxicity was reduced when cells co-expressed wild-type CD43. The CD43 cytoplasmic tail (CD43ct) was found to translocate into the nucleus and inhibition of either its nuclear translocation or its release by {gamma}-secretase was pro-apoptotic. Involvement of CD43 in regulation of apoptosis is consistent with our findings that CD43ct was modified by Small Ubiquitin-like Modifier-1 (SUMO-1) and was co-localized with PML nuclear bodies. CD43 deficient cells exhibited reduced levels of PML nuclear bodies and increased sensitivity to apoptosis induced by growth factor withdrawal or Treg suppression. Taken together, our data indicate an essential function of CD43 processing and nuclear localization of CD43ct in cell homeostasis and apoptosis.
논문정보
관련 링크
연구자 키워드
관련분야 연구자보기
소속기관 논문보기
관련분야 논문보기
해당논문 저자보기