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Title of Journal: Apoptosis

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Abbravation: Apoptosis

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Springer US

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DOI

10.1002/zamm.19650450621

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1573-675X

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Annexin II receptor induces apoptosis independent

Authors: Yuan Xiong Cuiqing Fan Lijuan Kong Lin Dong Ning Zhu Jiewen Zhang Le Wang Tao Qin Yan Shen Meihong Chen
Publish Date: 2013/05/04
Volume: 18, Issue: 8, Pages: 925-939
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Abstract

Annexin II receptor AXIIR is also known as chromosome 5 open reading frame 39 C5orf39 it was originally identified as a cell surface receptor for Annexin II AXIIR gene is peculiar to human So far the only known function about AXIIR is mediating Annexin II signal In this study we find that overexpression of AXIIR induces apoptosis and this phenomenon is found in multiple human cell types AXIIR is located in cytoplasm binds to and activates proCaspase8 which subsequently activates Caspase3/7 AXIIR also downregulates BCL2 BCLXL and activates Caspase9 which finally activates Caspase3/7 as well Overexpression of BCLXL does not affect AXIIRinduced apoptosis whereas inhibition of Caspase8 partially abolished AXIIRinduced apoptosis AXIIR induces apoptosis independent of Annexin II and FADD AXIIR is neither required for TRAILinduced Caspase8 activation Although the transcriptional level of AXIIR in multiple cell types is considerably high the translational level of AXIIR can hardly be detected And inhibition of protein degradation pathways does not elevate AXIIR expression Taken together our observations reveal that besides being a cell surface receptor of Annexin II AXIIR can also be located in cytoplasm and act as a novel inducer of apoptosis in human cells partially through activating Caspase8 in a manner that is different from conventional apoptotic pathways The translation of AXIIR is generally tightly inhibited in cells The physiological significance of such inhibition might be to prevent cells from apoptosisWe thank Dr Samuel Zhang for kindly providing primary NHDF We also thank the Core Instrument Facility in CAMS/PUMC in flow cytometry analysis This work was supported by Natural Science Foundation of China 31050008 Grant 2007CB946901 from Major State Basic Research Development Program of China 973 Program and the grant to M Chen from Program for New Century Excellent Talents in University of China

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