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前列腺细胞凋亡反应因子 4 与肿瘤抑制:细胞凋亡不再是唯一机制。

Prostate apoptosis response-4 and tumor suppression: it's not just about apoptosis anymore.

机构信息

Cell Death Signaling Laboratory, Division of Science, Experimental Research Building, New York University Abu Dhabi, PO Box 129188, Saadiyat Island Campus, Abu Dhabi, UAE.

出版信息

Cell Death Dis. 2021 Jan 7;12(1):47. doi: 10.1038/s41419-020-03292-1.

Abstract

The tumor suppressor prostate apoptosis response-4 (Par-4) has recently turned 'twenty-five'. Beyond its indisputable role as an apoptosis inducer, an increasing and sometimes bewildering, new roles for Par-4 are being reported. These roles include its ability to regulate autophagy, senescence, and metastasis. This growing range of responses to Par-4 is reflected by our increasing understanding of the various mechanisms through which Par-4 can function. In this review, we summarize the existing knowledge on Par-4 tumor suppressive mechanisms, and discuss how the interaction of Par-4 with different regulators influence cell fate. This review also highlights the new secretory pathway that has emerged and the likely discussion on its clinical implications.

摘要

肿瘤抑制因子前列腺凋亡反应蛋白 4(Par-4)最近迎来了“二十五岁”生日。除了作为凋亡诱导因子的不可争议的作用外,Par-4 的新作用也在不断被报道,有时甚至令人困惑。这些作用包括调节自噬、衰老和转移的能力。我们对 Par-4 的作用机制的理解不断加深,这反映了 Par-4 反应范围的不断扩大。在这篇综述中,我们总结了 Par-4 肿瘤抑制机制的现有知识,并讨论了 Par-4 与不同调节剂的相互作用如何影响细胞命运。这篇综述还强调了新出现的分泌途径及其可能的临床意义的讨论。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/caf6/7790818/e9dee4fed20b/41419_2020_3292_Fig1_HTML.jpg

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