MCL-1V, a novel mouse antiapoptotic MCL-1 variant, generated by RNA splicing at a non-canonical splicing pair
| Autor: | Nobuko Koshikawa, Akira Nakagawara, Shogo Kojima, Akira Hyakutake, Keizo Takenaga |
|---|---|
| Rok vydání: | 2009 |
| Předmět: |
DNA
Complementary RNA Splicing Cell Molecular Sequence Data Biophysics Exonic splicing enhancer Apoptosis Biology Biochemistry Exon Mice immune system diseases hemic and lymphatic diseases medicine Animals Amino Acid Sequence Cloning Molecular neoplasms Molecular Biology Gene Messenger RNA Protein Stability Cell Biology Exons Molecular biology Mitochondria medicine.anatomical_structure Proto-Oncogene Proteins c-bcl-2 Cancer cell RNA splicing Myeloid Cell Leukemia Sequence 1 Protein Stem cell |
| Zdroj: | Biochemical and biophysical research communications. 391(1) |
| ISSN: | 1090-2104 |
| Popis: | Myeloid cell leukemia-1 (MCL-1) that belongs to BCL-2 family is essential for survival of hematopoietic stem cells. It is upregulated in various types of cancer and promotes cancer cell metastasis. It is known that human MCL-1 gene undergoes differential splicing and yields three mRNAs encoding antiapoptotic MCL-1L and proapoptotic MCL-1S and MCL-1ES. However, no MCL-1 variants have been reported in mouse cells. We report here a new splicing variant of mouse Mcl-1, Mcl-1V, that is expressed in a variety of mouse normal and tumor cell lines and tissues. Comparative sequence analysis of the full-length Mcl-1 and Mcl-1V cDNAs suggested that Mcl-1V mRNA results from splicing within the first coding exon of Mcl-1 gene at a non-canonical donor–acceptor pair. MCL-1V lacks 46 amino acid residues within the N-terminal region of MCL-1. It localizes in mitochondria and inhibits anoxia- and anticancer drug-induced apoptosis as potent as MCL-1, and decayed less rapidly than MCL-1 in the cells undergoing apoptosis. Collectively, our results show that mouse cells ubiquitously express antiapoptotic MCL-1V that may play a role in mitochondrial cell death. |
| Databáze: | OpenAIRE |
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