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SNIP1在疾病中的临床应用及其病理生理机制。

The clinical utilization of SNIP1 and its pathophysiological mechanisms in disease.

作者信息

Chen Yinzhong, Guo Wei, Guo Xiucheng, Wanqing Qiao, Yin Zongsheng

机构信息

Department of Orthopedics, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, China.

Department of Orthopedics, the Second Affiliated Hospital of Shandong First Medical University, Tai'an, Shandong, China.

出版信息

Heliyon. 2024 Jan 17;10(2):e24601. doi: 10.1016/j.heliyon.2024.e24601. eCollection 2024 Jan 30.

DOI:10.1016/j.heliyon.2024.e24601
PMID:38304835
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10831730/
Abstract

Smad intranuclear binding protein 1 (SNIP1), a highly conserved nuclear protein, functions as a transcriptional regulator and exerts a significant influence on disease progression. In addition, the N-terminal domain of SNIP1 facilitates its interaction with Smad4, a signaling protein associated with the TGF-β family, and RelA/p65, a transcription factor connected to NF-κB. This interaction further enhances the transcriptional activation of c-Myc-dependent genes. Presently, the primary emphasis in research is directed towards targeting the catalytic domain of SNIP1, as it holds promise as a potential therapeutic target for various diseases. While the significance of SNIP1 in pathological mechanisms remains uncertain, this review aims to comprehensively examine the existing literature on the association between SNIP1 and proteins implicated in the regulation of diverse clinical conditions, including cancer, inflammation, and related diseases.

摘要

Smad核内结合蛋白1(SNIP1)是一种高度保守的核蛋白,作为转录调节因子发挥作用,并对疾病进展产生重大影响。此外,SNIP1的N端结构域促进其与Smad4(一种与TGF-β家族相关的信号蛋白)和RelA/p65(一种与NF-κB相关的转录因子)相互作用。这种相互作用进一步增强了c-Myc依赖性基因的转录激活。目前,研究的主要重点是靶向SNIP1的催化结构域,因为它有望成为各种疾病的潜在治疗靶点。虽然SNIP1在病理机制中的重要性仍不确定,但本综述旨在全面审视现有文献中关于SNIP1与参与调节多种临床病症(包括癌症、炎症及相关疾病)的蛋白质之间关联的研究。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc4/10831730/49b1177e71ec/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc4/10831730/6472b055a11e/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc4/10831730/e1c3e47a411d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc4/10831730/aae463119f07/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc4/10831730/40d5af0d9345/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc4/10831730/49b1177e71ec/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc4/10831730/6472b055a11e/ga1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc4/10831730/e1c3e47a411d/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc4/10831730/aae463119f07/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc4/10831730/40d5af0d9345/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc4/10831730/49b1177e71ec/gr4.jpg

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本文引用的文献

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SNIP1 reduces extracellular matrix degradation and inflammation via inhibiting the NF-κB signaling pathway in osteoarthritis.SNIP1 通过抑制 NF-κB 信号通路减少骨关节炎中的细胞外基质降解和炎症。
Arch Biochem Biophys. 2023 Oct 1;747:109764. doi: 10.1016/j.abb.2023.109764. Epub 2023 Sep 20.
2
LncRNA BCAN-AS1 stabilizes c-Myc via N-methyladenosine-mediated binding with SNIP1 to promote pancreatic cancer.长链非编码 RNA BCAN-AS1 通过 N6-甲基腺苷介导与 SNIP1 结合稳定 c-Myc,从而促进胰腺癌。
Cell Death Differ. 2023 Oct;30(10):2213-2230. doi: 10.1038/s41418-023-01225-x. Epub 2023 Sep 19.
3
Correction: MKRN1 promotes colorectal cancer metastasis by activating the TGF-β signalling pathway through SNIP1 protein degradation.
更正:MKRN1通过降解SNIP1蛋白激活TGF-β信号通路促进结直肠癌转移。
J Exp Clin Cancer Res. 2023 Sep 15;42(1):240. doi: 10.1186/s13046-023-02825-8.
4
SNIP1 and PRC2 coordinate cell fates of neural progenitors during brain development.SNIP1 和 PRC2 在大脑发育过程中协调神经祖细胞的命运。
Nat Commun. 2023 Aug 8;14(1):4754. doi: 10.1038/s41467-023-40487-4.
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A molecular brake that modulates spliceosome pausing at detained introns contributes to neurodegeneration.一种调节内含子滞留时剪接体暂停的分子刹车,有助于神经退行性变。
Protein Cell. 2023 May 8;14(5):318-336. doi: 10.1093/procel/pwac008.
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MiR-138-5p suppresses the progression of lung cancer by targeting SNIP1.miR-138-5p 通过靶向 SNIP1 抑制肺癌的进展。
Thorac Cancer. 2023 Feb;14(6):612-623. doi: 10.1111/1759-7714.14791. Epub 2023 Jan 3.
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Isosteviol attenuates DSS-induced colitis by maintaining intestinal barrier function through PDK1/AKT/NF-κB signaling pathway.异甜菊醇通过PDK1/AKT/NF-κB信号通路维持肠道屏障功能,从而减轻右旋糖酐硫酸钠诱导的结肠炎。
Int Immunopharmacol. 2023 Jan;114:109532. doi: 10.1016/j.intimp.2022.109532. Epub 2022 Dec 9.
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