Kim Jae-Hong, Sim Se-Hoon, Ha Hye-Jeong, Ko Jeong-Jae, Lee Kangseok, Bae Jeehyeon
Department of Biomedical Science, College of Life Science, CHA University, Seongnam, Republic of Korea.
FEBS Lett. 2009 Sep 3;583(17):2758-64. doi: 10.1016/j.febslet.2009.08.006. Epub 2009 Aug 14.
Myeloid cell leukemia-1 (MCL-1L) is a pro-survival member of the BCL-2 family that promotes cell survival. In this study, we identify a new splicing variant of human MCL-1 that encodes MCL-1ES (extra short). Sequence analysis indicates that this variant results from splicing within the first coding exon of MCL-1 at a non-canonical GC-AG donor-acceptor pair. The deduced sequence of MCL-1ES encodes a protein of 197 amino acids, and the PEST (proline, glutamic acid, serine, and threonine) motifs present in MCL-1L are absent. MCL-1ES interacts with MCL-1L and induces mitochondrial cell death, suggesting that alternative splicing of MCL-1 may control the fate of cells.
髓样细胞白血病-1（MCL-1L）是BCL-2家族中促进细胞存活的一个促存活成员。在本研究中，我们鉴定出一种人类MCL-1的新剪接变体，其编码MCL-1ES（超短型）。序列分析表明，该变体是由于MCL-1第一个编码外显子内一个非典型GC-AG供体-受体对处的剪接所致。MCL-1ES的推导序列编码一个197个氨基酸的蛋白质，且不存在MCL-1L中存在的PEST（脯氨酸、谷氨酸、丝氨酸和苏氨酸）基序。MCL-1ES与MCL-1L相互作用并诱导线粒体细胞死亡，这表明MCL-1的可变剪接可能控制细胞的命运。
