HUSCAP logo Hokkaido Univ. logo

Hokkaido University Collection of Scholarly and Academic Papers >
Faculty of Pharmaceutical Sciences >
Peer-reviewed Journal Articles, etc >

Functional involvement of Daxx in gp130-mediated cell growth and survival in BaF3 cells

Files in This Item:
EJI-Muromoto101007.pdf6.6 MBPDFView/Open
Please use this identifier to cite or link to this item:

Title: Functional involvement of Daxx in gp130-mediated cell growth and survival in BaF3 cells
Authors: Muromoto, Ryuta Browse this author →KAKEN DB
Kuroda, Makoto Browse this author
Togi, Sumihito Browse this author
Sekine, Yuichi Browse this author →KAKEN DB
Nanbo, Asuka Browse this author →KAKEN DB
Shimoda, Kazuya Browse this author →KAKEN DB
Oritani, Kenji Browse this author →KAKEN DB
Matsuda, Tadashi Browse this author →KAKEN DB
Keywords: Cell death
Issue Date: Dec-2010
Publisher: Wiley
Journal Title: European Journal of Immunology
Volume: 40
Issue: 12
Start Page: 3570
End Page: 3580
Publisher DOI: 10.1002/eji.201040688
PMID: 21108476
Abstract: Death domain-associated protein (Daxx) is a multifunctional protein that modulates both cell death and transcription. Several recent studies have indicated that Daxx is a mediator of lymphocyte death and/or growth suppression, although the detailed mechanism is unclear. Previously, we reported that Daxx suppresses IL-6 family cytokine-induced gene expression by interacting with STAT3. STAT3 is important for the growth and survival of lymphocytes; therefore, we here examined the role of Daxx in the gp130/STAT3-dependent cell growth/survival signals. We found that Daxx suppresses the gp130/STAT3-dependent cell growth and that Daxx endogenously interacts with STAT3 and inhibits the DNA-binding activity of STAT3. Moreover, small-interfering RNA-mediated knockdown of Daxx enhanced the expression of STAT3-target genes and accelerated the STAT3-mediated cell cycle progression. In addition, knockdown of Daxx-attenuated lactate dehydrogenase leakage from cells, indicating that Daxx positively regulates cell death during gp130/STAT3-mediated cell proliferation. Notably, Daxx specifically suppressed the levels of Bcl2 mRNA and protein, even in cytokine-unstimulated cells, indicating that Daxx regulates Bcl2 expression independently of activated STAT3. These results suggest that Daxx suppresses gp130-mediated cell growth and survival by two independent mechanisms: inhibition of STAT3-induced transcription and down-regulation of Bcl2 expression.
Rights: This is the pre-peer-reviewed version of the following article: FULL CITE, which has been published in final form at
Type: article (author version)
Appears in Collections:薬学研究院 (Faculty of Pharmaceutical Sciences) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 松田 正

Export metadata:

OAI-PMH ( junii2 , jpcoar )

MathJax is now OFF:


Feedback - Hokkaido University