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SR蛋白家族在细胞凋亡过程中的作用及机制

Role and mechanism of serine/arginine protein family in the process of apoptosis
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摘要 细胞凋亡是多基因严格控制的程序性细胞死亡方式,与多种疾病的发生发展密切相关,目前,凋亡调控的确切机制尚不完全清楚。参与细胞凋亡外源性或内源性调控的相关基因在转录水平可被选择性剪接产生不同的亚型,从而增加了细胞凋亡调控的复杂性。丝氨酸/精氨酸(SR)蛋白是前体信使RNA(pre-mRNA)剪接所需的基本剪接因子,作为选择性剪接的关键调节器,在细胞凋亡调控过程中具有重要的作用。人类SR蛋白家族根据被发现的时间顺序分别命名为富丝氨酸/精氨酸剪接因子1-12(SRSF1-12),由于其自身的特殊结构域,它们在细胞凋亡中的调控作用及机制不尽相同。本文主要综述SR蛋白家族成员在细胞凋亡中的作用和调控机制. Apoptosis is a programmed cell death mode strictly controlled by multiple genes,which is closely related to the occurrence and development of a variety of diseases.At present,the exact mechanism of apoptosis regulation is not fully understood.The related genes involved in the exogenous or endogenous regulation of apoptosis can be alternatively spliced at the transcriptional level to produce different isoforms,thus increasing the complexity of apoptosis regulation.The serine/arginine(SR)proteins are essential splicing factors required for precursor messenger RNA(premRNA)splicing.As key regulators of alternative splicing,SR proteins play an important role in the regulation of apoptosis.The human SR protein family is named serine/arginine-rich splicing factor 1-12(SRSF1-12)according to the chronological order of discovery.Due to their special structural domains,their regulatory effects and mechanisms in apoptosis are different.This review focuses on the roles and regulatory mechanisms of SR protein family members in apoptosis.
作者 罗鸿 张飞 任超 王涛 谢志鸿 彭吾训 Luo Hong;Zhang Fei;Ren Chao;Wang Tao;Xie Zhihong;Peng Wuxun(School of Clinical Medicine,Guizhou Medical University,Guiyang 550004,China;Department of Orthopedics,the Affiliated Hospital of Guizhou Medical University,Guiyang 550004,China)
出处 《中华实验外科杂志》 CAS 北大核心 2023年第7期1428-1434,共7页 Chinese Journal of Experimental Surgery
基金 国家自然科学基金(82060397、81860387)。
关键词 丝氨酸/精氨酸蛋白 凋亡 选择性剪接 Serine/arginine proteins Apoptosis Alternative splicing
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  • 1李长有,宋今丹,原银栋,范广宇.血管内皮生长因子及其受体在鼠成骨细胞分化中的作用[J].中华实验外科杂志,2004,21(7):852-854. 被引量:13
  • 2Plotorak Z, Cohen T, Sivan R, et al. VEGF145, a secreted vascular endothelial growth factor isoform that binds to extracellular matrix. J Biom Chem, 1997, 272:7151-7158.
  • 3Eckart L, Ban J, Ballaun C. Reverse transcription-polymerase chain reaction products of alternatively spliced mRNAs form heteroduplexes and heteroduplex complexes. J Biol Chem, 1999, 274: 2613-2615.
  • 4Song JH,Wang CX,Song DK,et al. Interferon gamma induces neurite outgrowth by up-regulation of p35 neuron-specific cyclin-dependent kinase 5 activator via activation of ERK1/2 pathway. J Biol Chem, 2005,280 : 12896-12901.
  • 5Ganten TM, Haas TL, Sykora J, et al. Enhanced caspase-8 recruitment to and activation at the DISC is critical for sensitisation of human hepatocellular carcinoma cells to TRAIL-induced apoptosis by chemotherapeutic drugs. Cell Death Differ,2004,11:86-96.
  • 6Shin EC,Seong YR, Kim CH,et al. Human hepatocellular carcinoma cells resist to TRAIL-induced apoptosis, and the resistance is abolished by cisplatin. Exp Mol Med ,2002,34 : 114-122.
  • 7Yamanaka T, Shiraki K, Sugimoto K, et al. Chemotherapeutic agents augment TRAIL-induced apoptosis in human hepatocellular carcinoma cell lines. Hepatology, 2000,32 : 482-490.
  • 8Truneh A, Sharma S, Silverman C, et al. Temperature-sensitive differential affinity of TRAIL for its receptors. DR5 is the highest affinity receptor. J Biol Chem ,2000,275:23319-23325.
  • 9Gura T. How TRAIL kills cancer cells ,but not normal cells. Science, 1997,277:768.
  • 10Irmler M,Thome M,Hahne M,et al. Inhibition of death receptor signals by cellular FLIP. Nature, 1997,388:190-195.

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