NDLI: LPS induces the interaction of a transcription factor, LPS-induced TNF-α factor, and STAT6(B) with effects on multiple cytokines

Content Provider	PubMed Central
Author	Tang, Xiaoren Marciano, Deborah Levy Leeman, Susan E. Amar, Salomon
Copyright Year	2005
Abstract	TNF-α is a pivotal cytokine whose overproduction can be lethal. Previously, we identified a transcription factor, LPS-induced TNF-α factor (LITAF), that regulates TNF-α transcription. We now report the discovery and characterization of a regulatory cofactor that we call signal transducer and activator of transcription (STAT) 6(B) because of its considerable homology to STAT6 [here referred to as STAT6(A)]. The STAT6(B) gene expression was found to be activated by LPS. Furthermore, we show that cotransfection of STAT6(B) and LITAF induces an interaction between the two proteins, consequently forming a complex that subsequently translocates into the nucleus and up-regulates the transcription of cytokines. The effect of the complex on a panel of cytokines was tested. In addition, the specific role of LITAF in this complex was established with experiments, including RNA interference technology. Overall, these findings describe roles for LITAF, STAT6(B), and the LITAF-STAT6(B) complex in the regulation of inflammatory cytokines in response to LPS stimulation in mammalian cells.
Related Links	http://dx.doi.org/10.1073/pnas.0501159102
Ending Page	5137
Page Count	6
Starting Page	5132
File Format	PDF
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	14
Volume Number	102
Language	English
Publisher	National Academy of Sciences
Publisher Date	2005-04-05
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	General Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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LPS induces the interaction of a transcription factor, LPS-induced TNF-alpha factor, and STAT6(B) with effects on multiple cytokines.

LPS-induced TNF-α factor (LITAF)-deficient mice express reduced LPS-induced cytokine: Evidence for LITAF-dependent LPS signaling pathways

Correction for Tang et al., LPS-induced TNF-α factor (LITAF)-deficient mice express reduced LPS-induced cytokine: Evidence for LITAF-dependent LPS signaling pathways

Whole-body deletion of LPS-induced TNF-α factor (LITAF) markedly improves experimental endotoxic shock and inflammatory arthritis

Site-specific ubiquitination is required for relieving the transcription factor Miz1-mediated suppression on TNF-α–induced JNK activation and inflammation

LPS-induced TNF-α factor (LITAF)-deficient mice express reduced LPS-induced cytokine: Evidence for LITAF-dependent LPS signaling pathways

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LPS induces the interaction of a transcription factor, LPS-induced TNF-α factor, and STAT6(B) with effects on multiple cytokines

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LPS induces the interaction of a transcription factor, LPS-induced TNF-alpha factor, and STAT6(B) with effects on multiple cytokines.

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