Rig-g as a key mediator of the antiproliferative activity of interferon-related pathways through enhancing p21 and p27 proteins
文献类型:期刊论文
作者 | Xiao, Shu; Li, Dong; Zhu, Hai-Qing; Song, Man-Gen; Pan, Xiao-Rong; Jia, Pei-Min; Peng, Lin-Ling; Dou, Ai-Xia; Chen, Guo-Qiang; Chen, Sai-Juan |
刊名 | Proceedings of the national academy of sciences of the united states of america
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出版日期 | 2006-10-31 |
卷号 | 103期号:44页码:16448-16453 |
关键词 | Cell growth inhibition Retinoic acid Rig-g Stat1 |
ISSN号 | 0027-8424 |
DOI | 10.1073/pnas.0607830103 |
通讯作者 | Chen, zhu(zchen@stn.sh.cn) |
英文摘要 | The rig-g gene, originally isolated from an acute promyelocytic leukemia cell line nb4, codes for a 60-kda cytoplasmic protein that is induced by all-trans retinoic acid (atra) treatment along with the induction of morphological differentiation of nb4 cells. here, we provide evidence that ectopic expression of rig-g in u937 cells can lead to a significant accumulation of cells at g(1)/s transition. growth arrest seems to occur by modulating several major cell cycle regulatory players. interestingly, rig-g alters jab1 cellular distribution through interacting with this protein and increases the intracellular level of p27 by preventing it from the jab-1-dependent and ubiquitin/proteasome-mediated degradation. furthermore, we demonstrate a role of rig-g for c-myc down-regulation that results in an up-regulation of p21, tightly associated with cell cycle arrest. in addition, our studies reveal that rig-g is a direct target of stat1, a key transcription factor in regulating ifn responses, and may be one of the first experimentally proven molecular mediators for the anti proliferative effect of ifn-alpha. considering that ifn-alpha and atra synergistically inhibit growth along the intracellular pathways triggered by the two compounds in many cell types, we suggest that rig-g may also represent one of the key molecular nodes of signaling cross-talk between atra and ifn-alpha. |
WOS关键词 | CDK INHIBITOR P15(INK4B) ; COP9 SIGNALOSOME ; RETINOIC ACID ; PROMYELOCYTIC LEUKEMIA ; GENE-EXPRESSION ; INDUCED-DIFFERENTIATION ; STIMULATED GENES ; CELLS ; MYC ; COMPLEX |
WOS研究方向 | Science & Technology - Other Topics |
WOS类目 | Multidisciplinary Sciences |
语种 | 英语 |
WOS记录号 | WOS:000241879500069 |
出版者 | NATL ACAD SCIENCES |
URI标识 | http://www.irgrid.ac.cn/handle/1471x/2378547 |
专题 | 中国科学院大学 |
通讯作者 | Chen, Zhu |
作者单位 | 1.Chinese Acad Sci, Shanghai Inst Biol Sci, Hlth Sci Ctr, Rui Jin Hosp,Shanghai Inst Hematol, Shanghai 200025, Peoples R China 2.Chinese Acad Sci, Shanghai Inst Biol Sci, Hlth Sci Ctr, State Key Lab Med Genom, Shanghai 200025, Peoples R China 3.Chinese Acad Sci, Grad Sch, Shanghai 200025, Peoples R China 4.Shanghai Jiao Tong Univ, Sch Med, Shanghai 200025, Peoples R China 5.Shanghai Jiao Tong Univ, Shanghai Ctr Syst Biomed, Shanghai 200240, Peoples R China |
推荐引用方式 GB/T 7714 | Xiao, Shu,Li, Dong,Zhu, Hai-Qing,et al. Rig-g as a key mediator of the antiproliferative activity of interferon-related pathways through enhancing p21 and p27 proteins[J]. Proceedings of the national academy of sciences of the united states of america,2006,103(44):16448-16453. |
APA | Xiao, Shu.,Li, Dong.,Zhu, Hai-Qing.,Song, Man-Gen.,Pan, Xiao-Rong.,...&Tong, Jian-Hua.(2006).Rig-g as a key mediator of the antiproliferative activity of interferon-related pathways through enhancing p21 and p27 proteins.Proceedings of the national academy of sciences of the united states of america,103(44),16448-16453. |
MLA | Xiao, Shu,et al."Rig-g as a key mediator of the antiproliferative activity of interferon-related pathways through enhancing p21 and p27 proteins".Proceedings of the national academy of sciences of the united states of america 103.44(2006):16448-16453. |
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来源:中国科学院大学
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