Protein kinase clk/STY is differentially regulated during erythroleukemia cell differentiation: a bias toward the skipped splice variant characterizes postcommitment stages

作     者：Ana GARCíA-SACRISTáN■,María J. FERNáNDEZ-NESTOSA,Pablo HERNáNDEZ,Jorge B.SCHVARTZMAN,Dora B. KRIMER 

作者机构：Department of Cell and Developmental Biology Centro de Investigaciones Biológicas Consejo Superior de InvestigacionesCientíficas Ramiro de Maeztu 9 Madrid 28040 Spain Instiute of Molecular Medicine 1649-028 Lisbon Medical School Lisbon Portugal Department of Cell and Developmental Biology Centro de Investigaciones Biológicas Consejo Superior de InvestigacionesCientíficas Ramiro de Maeztu 9 Madrid 28040 Spain Department of Cell and Developmental Biology Centro de Investigaciones Biológicas Consejo Superior de InvestigacionesCientíficas Ramiro de Maeztu 9 Madrid 28040 Spain Department of Cell and Developmental Biology Centro de Investigaciones Biológicas Consejo Superior de InvestigacionesCientíficas Ramiro de Maeztu 9 Madrid 28040 Spain Department of Cell and Developmental Biology Centro de Investigaciones Biológicas Consejo Superior de InvestigacionesCientíficas Ramiro de Maeztu 9 Madrid 28040 Spain 

出 版 物：《Cell Research》 (细胞研究(英文版))

年 卷 期：2005年第15卷第7期

页      面：495-503页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：Comunidad de Madrid (CAM)(grantSAF2001-1740) Spanish Ministerio de Ciencia y Tecnología MJFN is recipient of a graduate fellowship Comunidad de Madrid (CAM) 

主　　题：clk/STY LAMMER kinase alternative splicing erythroleukemia cells. 

摘      要：Clk/STY is a LAMMER protein kinase capable to phosphorylate serine/arginine-rich (SR) proteins that modulate pre-mRNA splicing. Clk/STY alternative splicing generates transcripts encoding a full-length kinase and a truncated catalyti-cally inactive protein. Here we showed that clk/STY, as well as other members of the family (e.g. clk2, clk3 and clk4),are up-regulated during HMBA-induced erythroleukemia cell differentiation. mRNAs coding for the full-length and thetruncated forms were responsible for the overall increased expression. In clk/STY, however, a switch was observed forthe ratio of the two alternative spliced products. In undifferentiated cells the full-length transcript was more abundantwhereas the transcript encoding for the truncated form predominated at latter stages of differentiation. Surprisingly,overexpression of clk/STY did not alter the splicing switch upon differentiation in MEL cells. These results suggest thatclk/STY might contribute to control erythroid differentiation by a mechanism that implicates a balance between thesetwo isoforms.