Attenuated and Dominant Negative Variant cDNAs of STAT6: STAT6b and STAT6c
Description of Invention:
This patent relates to signal transduction pathways. In particular, the patent relates to transcription factors. The transcription factors described in the patent are members of the family of transcription factors known as Signal Transducers and Activators of Transcription (STATs). More particularly, the patent discloses the identification, isolation, sequencing and cloning of cDNAs that encode naturally occurring variants, Stat6b and Stat6c, of the protein STAT6.
The Stat6b variant contains an NH2 terminal deletion of naturally occurring Stat6 The Stat6c variant contains an internal deletion, within the SH2 domain, of naturally occurring Stat6. The naturally occurring variants exhibit different properties. Stat6b acts as an attenuated variant, with respect to IL-4 induced MHC class II and Fc receptor cell surface expression, promoter binding and transcriptional activation when compared to Stat6. Stat6c acts as a dominant negative variant with respect to IL-4 mediated up-regulation of the cell surface antigens CD16/CD32 and CD23. The role of both variants in mediating IL-4 activity suggests that either could be useful in developing drugs for targeting diseases involving inflammatory and cell-mediated immune responses such as asthma.
The patent includes claims to the Stat6 variant polypeptides, the nucleic acids, vectors for expression of the variants, cells into which the variants have been introduced and methods of producing the Stat6 variant polypeptides.
Inventors:
William LaRochelle (NCI) Bharvin K.R. Patel (NCI) Jacalyn H. Pierce (NCI)
Relevant Publication: BKR Patel et al. Regulation of interleukin 4-mediated signaling by naturally occurring dominant negative and attenuated forms of human Stat6. Proc Nat Acad Sci USA. 1998 Jan 6;95(1):172-177. [PubMed abs]
For Additional Information Please Contact: Susan S. Rucker J.D.
NIH Office of Technology Transfer
6011 Executive Blvd, Suite 325
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Phone: (301) 435-4478
Email: ruckersu@mail.nih.gov
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