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在内质网和高尔基体处的非基因组 STAT5 依赖性效应以及线粒体中的 STAT6-GFP。

Non-genomic STAT5-dependent effects at the endoplasmic reticulum and Golgi apparatus and STAT6-GFP in mitochondria.

作者信息

Sehgal Pravin B

机构信息

Departments of Cell Biology & Anatomy, and Medicine; New York Medical College; Valhalla, NY USA.

出版信息

JAKSTAT. 2013 Oct 1;2(4):e24860. doi: 10.4161/jkst.24860. Epub 2013 Apr 29.

Abstract

STAT protein species are well-known as transcription factors that regulate nuclear gene expression. Recent novel lines of research suggest new non-genomic functions of STAT5A/B and STAT6. It was discovered in human pulmonary arterial endothelial cells that STAT5A, including STAT5A-GFP, constitutively associated with the Golgi apparatus, and both STAT5A and B with the endoplasmic reticulum. Acute siRNA-mediated knockdown of STAT5A/B led to the rapid development of a dramatic cystic change in the endoplasmic reticulum (ER) characterized by deposition of the ER structural protein reticulon-4 (RTN4; also called Nogo-B) and the ER-resident GTPase atlastin-3 (ATL3) along cyst membranes and cyst-zone boundaries, accompanied by Golgi fragmentation. Functional consequences included reduced anterograde trafficking, an ER stress response (increased GRP78/BiP) and eventual mitochondrial fragmentation. This phenotype was "non-genomic" in that it was elicited in enucleated cytoplasts. In cross-immunopanning assays STAT5A and B species associated with ATL3, and the ER-lumen spacer CLIMP63 (also called cytoskeleton-associated protein 4, CKAP4) but not RTN4. From a disease significance perspective we posit that STAT5, which is known to be affected by estradiol-17β and prolactin, represents the gender-sensitive determinant in the pathogenesis of idiopathic pulmonary hypertension (IPAH), a disease which includes ER/Golgi dysfunctions but with a 2- to 4-fold higher prevalence in postpubertal women. A separate line of recent research produced evidence for the association of STAT6-GFP, but not STAT3-GFP, STAT3-DsRed, or STAT3-Flag, with mitochondria in live-cell, immunofluorescence, and immunoelectron microscopy. An N-terminal truncation of STAT6-GFP (1-459), which lacked the SH2 domain and Tyr-phosphorylation site, constitutively associated with mitochondria. Thus, the emergent new of biology STAT proteins includes non-genomic roles-structurally and functionally-in the three closely related membrane organelles consisting of the endoplasmic reticulum, Golgi apparatus, and mitochondria.

摘要

信号转导和转录激活因子(STAT)蛋白家族作为调节核基因表达的转录因子而广为人知。最近新的研究方向揭示了STAT5A/B和STAT6的非基因组新功能。在人肺动脉内皮细胞中发现,包括STAT5A-GFP在内的STAT5A与高尔基体持续相关,而STAT5A和STAT5B均与内质网相关。急性小干扰RNA(siRNA)介导的STAT5A/B敲低导致内质网(ER)迅速发生显著的囊性变化,其特征是内质网结构蛋白网织蛋白-4(RTN4;也称为Nogo-B)和内质网驻留鸟苷三磷酸酶atlastin-3(ATL3)沿囊膜和囊区边界沉积,同时伴有高尔基体碎片化。功能后果包括顺向运输减少、内质网应激反应(葡萄糖调节蛋白78/BiP增加)以及最终的线粒体碎片化。这种表型是“非基因组”的,因为它是在去核的胞质体中引发的。在交叉免疫筛选试验中,STAT5A和STAT5B与ATL3以及内质网腔间隔蛋白CLIMP63(也称为细胞骨架相关蛋白4,CKAP4)相关,但与RTN4不相关。从疾病意义的角度来看,我们认为已知受雌二醇-17β和催乳素影响的STAT5是特发性肺动脉高压(IPAH)发病机制中的性别敏感决定因素,IPAH是一种存在内质网/高尔基体功能障碍的疾病,在青春期后女性中的患病率高出2至4倍。最近另一项研究通过活细胞、免疫荧光和免疫电子显微镜,证实了STAT6-GFP与线粒体相关,但STAT3-GFP、STAT3-DsRed或STAT3-Flag与线粒体不相关。STAT6-GFP的N端截短体(1-459)缺乏SH2结构域和酪氨酸磷酸化位点,与线粒体持续相关。因此,新兴的STAT蛋白生物学新功能包括在内质网、高尔基体和线粒体这三个密切相关的膜细胞器中具有非基因组作用——结构上和功能上的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5e85/3894245/409652700cd7/jkst-2-e24860-g1.jpg

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