Abstract
AbstractEstrogen receptor (ER)-[alpha]46 is known as an important isoform for ER[alpha]. It inhibits the function of full length ER[alpha] in MCF-7 mammary carcinoma cells and associated with cell cycle arrest. On the other hand, the oncogene HMGA1 (formally HMG I/Y) is known to have increased expression in mammary carcinoma correlating with the degree of malignancy. We present here that HMGA1a (HMG I) induces the exon skipped product, ER[alpha]46 mRNA, by tethering U1 snRNP to an upstream pseudo 5' splice site, which is quite analogous to the PSI-mediated splicing regulation of Drosophila P-element.
Highlights
Division of Gene Expression Mechanism, ICMS, *Dept. of Breast Surgery, Fujita Health University, Toyoake, Aichi 470-1192, Japan.
Kenji Ohe, *Toshiaki Utsumi & Akila Mayeda
Division of Gene Expression Mechanism, ICMS, *Dept.
Summary
Division of Gene Expression Mechanism, ICMS, *Dept. of Breast Surgery, Fujita Health University, Toyoake, Aichi 470-1192, Japan.
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
