PTB-ASSOCIATED SPLICING FACTOR (PSF) FUNCTIONS AS A REPRESSOR OF STAT6-MEDIATED Ig GENE TRANSCRIPTION BY RECRUITMENT OF HDAC1

نویسندگان

  • Lijie Dong
  • Xinyu Zhang
  • Xiao Fu
  • Xianzhi Zhang
  • Xingjie Gao
  • Mengyu Zhu
  • Xinting Wang
  • ZhenXia Yang
  • Ole Nørregaard Jensen
  • Zhi Yao
  • Olli Silvennoinen
  • Jie Yang
چکیده

Tianjin Medical University, Heping District Qixiangtai Road No.22, Tianjin 300070, P. R. China, Institute of Medical Technology 5 , University of Tampere, Tampere University Hospital, Biokatu 8, FI-33014, Tampere, Finland Running title: PSF represses STAT6-mediated gene transcription Department of Biochemistry & Molecular Biology 6 , University of Southern Denmark, DK-5230 Odense M, Denmark Address correspondence to: Jie Yang, MD, PhD, Department of Immunology, Tianjin Medical University, Heping District Qixiangtai Road No.22, Tianjin 300070, P.R. China, tel. +8622 23542520; fax +862223542581; E-mail: [email protected], Olli Silvennoinen, MD, PhD, Institute of Medical Technology, University of Tampere, Biokatu 8, FI-33014, Tampere, Finland, tel. +358335517845; fax. +358335517332; Email: [email protected]

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Transcriptional activity of androgen receptor is modulated by two RNA splicing factors, PSF and p54nrb.

Nuclear receptors regulate gene activation or repression through dynamic interactions with coregulators. The interactions between nuclear receptors and RNA splicing factors link gene transcription initiation with pre-mRNA splicing, providing a coordinated control of the products of gene transcription. Here we report that two RNA splicing factors, PTB-associated splicing factor (PSF) and p54nrb,...

متن کامل

BNIP3 (Bcl-2 19 kDa interacting protein) acts as transcriptional repressor of apoptosis-inducing factor expression preventing cell death in human malignant gliomas.

The Bcl-2 19 kDa interacting protein (BNIP3) is a pro-cell-death BH3-only member of the Bcl-2 family. We previously found that BNIP3 is localized to the nucleus in the majority of glioblastoma multiforme (GBM) tumors and fails to induce cell death. Herein, we have discovered that nuclear BNIP3 binds to the promoter of the apoptosis-inducing factor (AIF) gene and represses its expression. BNIP3 ...

متن کامل

A RUNX2-HDAC1 co-repressor complex regulates rRNA gene expression by modulating UBF acetylation.

The osteogenic and oncogenic transcription factor RUNX2 downregulates the RNA polymerase I (RNA Pol I)-mediated transcription of rRNAs and changes histone modifications associated with the rDNA repeat. However, the mechanisms by which RUNX2 suppresses rRNA transcription are not well understood. RUNX2 cofactors such as histone deacetylases (HDACs) play a key role in chromatin remodeling and regu...

متن کامل

Fli1 Represses Transcription of the Human α2(I) Collagen Gene by Recruitment of the HDAC1/p300 Complex

Fli1, a member of the Ets transcription factor family, is a key repressor of the human α2(I) collagen (COL1A2) gene. Although our previous studies have delineated that TGF-β induces displacement of Fli1 from the COL1A2 promoter through sequential post-translational modifications, the detailed mechanism by which Fli1 functions as a potent transcriptional repressor of the COL1A2 gene has not been...

متن کامل

Protein kinase Ciota enhances the transcriptional activity of the porcine P-450 side-chain cleavage insulin-like response element.

IGF-I enhances steroidogenesis in granulosa cells by stimulating the expression of the rate-limiting steroidogenic enzyme, cytochrome P-450 side-chain cleavage (P-450(scc)). This effect is mediated through an IGF response element (IGFRE) that binds polypyrimidine tract-binding protein (PTB)-associated splicing factor (PSF) and Sp1. Sp1 is essential for activation of the IGFRE, and PSF functions...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:

دوره   شماره 

صفحات  -

تاریخ انتشار 2010