hnRNP U enhances caspase-9 splicing and is modulated by AKT-dependent phosphorylation of hnRNP L

Vu, NT; Park, MA; Shultz, JC; Goehe, RW; Hoeferlin, LA; Shultz, MD; Smith, SA; Lynch, KW; Chalfant, CE

HERO ID

2901861

Reference Type

Journal Article

Year

2013

Language

English

PMID

23396972

HERO ID 2901861
In Press No
Year 2013
Title hnRNP U enhances caspase-9 splicing and is modulated by AKT-dependent phosphorylation of hnRNP L
Authors Vu, NT; Park, MA; Shultz, JC; Goehe, RW; Hoeferlin, LA; Shultz, MD; Smith, SA; Lynch, KW; Chalfant, CE
Journal Journal of Biological Chemistry
Volume 288
Issue 12
Page Numbers 8575-8584
Abstract Caspase-9 has two splice variants, pro-apoptotic caspase-9a and anti-apoptotic caspase-9b, which are regulated by RNA trans-factors associated with exon 3 of caspase-9 pre-mRNA (C9/E3). In this study, we identified hnRNP U as an RNA trans-factor associated with C9/E3. Down-regulation of hnRNP U led to a decrease in the caspase-9a/9b mRNA ratio, demonstrating a novel enhancing function. Importantly, hnRNP U bound specifically to C9/E3 at an RNA cis-element previously reported as the binding site for the splicing repressor, hnRNP L. Phosphorylated hnRNP L interfered with hnRNP U binding to C9/E3, and our results demonstrate the importance of the phosphoinositide 3-kinase/AKT pathway in modulating the association of hnRNP U to C9/E3. Taken together, these findings show that hnRNP U competes with hnRNP L for binding to C9/E3 to enhance the inclusion of the four-exon cassette, and this splice-enhancing function is blocked by the AKT pathway via phosphorylation of hnRNP L.
Doi 10.1074/jbc.M112.443333
Pmid 23396972
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English