加拿大渥太華大學(xué)心臟研究所研究人員最近發(fā)現(xiàn)了一種可以影響心臟發(fā)展及老化過程的新基因，為治療心臟老化及病變帶來新希望。
渥太華大學(xué)分子生物學(xué)家伯爾更（Patrick Burgon）帶隊(duì)的研究團(tuán)隊(duì)從胎兒心臟研究開始,，了解心臟老化、成長及衰竭過程中所發(fā)生的各種變化,，發(fā)現(xiàn)了存在于肌肉及腦細(xì)胞的細(xì)胞核中的基因可能掌控著其它對心臟發(fā)展有重要關(guān)聯(lián)的基因,。研究人員將這一基因命名為MLIP（Muscle enriched A-type Lamin Interacting Protein），相信這種基因的突變,，與肌肉營養(yǎng)失調(diào)及其他心臟退化疾病有關(guān),。這一發(fā)現(xiàn)在6月的《生物化學(xué)期刊》（Journal of Biological Chemistry）上發(fā)表,。研究人員將通過進(jìn)一步了解MLIP基因的功能，弄清楚心臟如何失去功能,。伯爾更教授表示,，這次發(fā)現(xiàn)為了解心臟發(fā)展過程中的各個特性開啟了新道路。（生物谷Bioon.com）
生物谷推薦原文出處：
Journal of Biological Chemistry
Identification of a Novel Muscle A-type Lamin-interacting Protein (MLIP)*
Elmira Ahmady, Shelley A. Deeke, Seham Raba, Lara Kouri, Laura Kenney, Alexandre F. R. Stewart and Patrick G. Burgon
Mutations in the A-type lamin (LMNA) gene are associated with age-associated degenerative disorders of mesenchymal tissues, such as dilated cardiomyopathy, Emery-Dreifuss muscular dystrophy, and limb-girdle muscular dystrophy. The molecular mechanisms that connect mutations in LMNA with different human diseases are poorly understood. Here, we report the identification of a Muscle-enriched A-type Lamin-interacting Protein, MLIP (C6orf142 and 2310046A06rik), a unique single copy gene that is an innovation of amniotes (reptiles, birds, and mammals). MLIP encodes alternatively spliced variants (23–57 kDa) and possesses several novel structural motifs not found in other proteins. MLIP is expressed ubiquitously and most abundantly in heart, skeletal, and smooth muscle. MLIP interacts directly and co-localizes with lamin A and C in the nuclear envelope. MLIP also co-localizes with promyelocytic leukemia (PML) bodies within the nucleus. PML, like MLIP, is only found in amniotes, suggesting that a functional link between the nuclear envelope and PML bodies may exist through MLIP. Down-regulation of lamin A/C expression by shRNA results in the up-regulation and mislocalization of MLIP. Given that MLIP is expressed most highly in striated and smooth muscle, it is likely to contribute to the mesenchymal phenotypes of laminopathies.
