TY - JOUR
T1 - ZFAT is an antiapoptotic molecule and critical for cell survival in MOLT-4 cells
AU - Fujimoto, Takahiro
AU - Doi, Keiko
AU - Koyanagi, Midori
AU - Tsunoda, Toshiyuki
AU - Takashima, Yasuo
AU - Yoshida, Yasuhiro
AU - Sasazuki, Takehiko
AU - Shirasawa, Senji
N1 - Funding Information:
We thank T. Danno and Y. Tanaka for their technical assistance. This work was supported by a grant from the Genome Network Project; a Grant-in-Aid for Scientific Research on Priority Areas “Applied Genomics” from the Ministry of Education, Culture, Sports, Science, and Technology; and a Grant-in-Aid for Scientific Research (B) from the Japan Society for the Promotion of the Science.
PY - 2009/2/4
Y1 - 2009/2/4
N2 - ZFAT (also known as ZNF406), originally identified as a candidate gene for autoimmune thyroid disease, encodes a zinc-finger protein, however, its function has not been elucidated. Here, we report that human ZFAT protein is expressed in peripheral B and T lymphocytes and a human acute T lymphoblastic leukaemia cell line, MOLT-4 cells. Intriguing is that mouse ZFAT expression in CD4+ lymphocytes is increased during blast formation. Furthermore, ZFAT-knockdown in MOLT-4 induces apoptosis via activation of caspases. These results suggested that ZFAT protein is a critical regulator involved in apoptosis and cell survival for immune-related cells.
AB - ZFAT (also known as ZNF406), originally identified as a candidate gene for autoimmune thyroid disease, encodes a zinc-finger protein, however, its function has not been elucidated. Here, we report that human ZFAT protein is expressed in peripheral B and T lymphocytes and a human acute T lymphoblastic leukaemia cell line, MOLT-4 cells. Intriguing is that mouse ZFAT expression in CD4+ lymphocytes is increased during blast formation. Furthermore, ZFAT-knockdown in MOLT-4 induces apoptosis via activation of caspases. These results suggested that ZFAT protein is a critical regulator involved in apoptosis and cell survival for immune-related cells.
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U2 - 10.1016/j.febslet.2008.12.063
DO - 10.1016/j.febslet.2008.12.063
M3 - Article
C2 - 19162026
AN - SCOPUS:58649107862
VL - 583
SP - 568
EP - 572
JO - FEBS Letters
JF - FEBS Letters
SN - 0014-5793
IS - 3
ER -
