HUSCAP logo Hokkaido Univ. logo

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

The nuclear isoform of protein-tyrosine phosphatase TC-PTP regulates interleukin-6-mediated signaling pathway through STAT3 dephosphorylation.

Files in This Item:
BBRC297-4.pdf398.04 kBPDFView/Open
Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/28124

Title: The nuclear isoform of protein-tyrosine phosphatase TC-PTP regulates interleukin-6-mediated signaling pathway through STAT3 dephosphorylation.
Authors: Yamamoto, Tetsuya Browse this author
Sekine, Yuichi Browse this author
Kashima, Keiichi Browse this author
Kubota, Atsuko Browse this author
Sato, Noriko Browse this author
Aoki, Naohito Browse this author
Matsuda, Tadashi Browse this author
Keywords: IL-6
T-cell protein-tyrosine phosphatase (TC-PTP)
Signal transducer and activator of transcription (STAT3)
Leukemia inhibitory factor (LIF)
Issue Date: 4-Oct-2002
Publisher: Elsevier
Journal Title: Biochemical and Biophysical Research Communications
Volume: 297
Issue: 4
Start Page: 811
End Page: 817
Publisher DOI: 10.1016/S0006-291X(02)02291-X
PMID: 12359225
Abstract: In the previous study, we demonstrated that the nuclear isoform of T-cell protein-tyrosine phosphatase (TC-PTP) dephosphorylated and deactivated signal transducer and activator of transcription 5a (STAT5a) and STAT5b, thereby negatively regulating prolactin (PRL)-mediated signaling pathway. In this study, we examined the involvement of the nuclear isoform of TC-PTP in interleukin-6 (IL-6)-mediated signaling pathway. IL-6 is a multifunctional cytokine that plays important roles in the immune system, hematopoiesis, and acute phase reactions, and has also implicated in IL-6-related diseases. Here, we demonstrate that IL-6-induced tyrosine-phosphorylation and activation of STAT3 were suppressed by overexpression of the nuclear isoform of TC-PTP in 293T cells. Tyrosine-phosphorylated STAT3 directly interacted with a substrate-trapping mutant of TC-PTP. Furthermore, retrovirus-mediated overexpression of the nuclear isoform of TC-PTP suppressed the IL-6-induced growth arrest of myeloid leukemia M1 cells. Endogenous TC-PTP complexed with STAT3 in the nucleus of M1 cells. These results strongly suggest that the nuclear isoform of TC-PTP may serve as a negative regulator of IL-6-mediated signaling pathway.
Relation: http://www.sciencedirect.com/science/journal/0006291X
Type: article (author version)
URI: http://hdl.handle.net/2115/28124
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_1.0 )

MathJax is now OFF:


 

 - Hokkaido University