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利用下一代测序数据破译靶向内质网的蛋白质及其在前列腺癌发病机制中的意义。

To Decipher the Proteins Targeting into the Endoplasmic Reticulum and Their Implications in Prostate Cancer Etiology Using Next-Generation Sequencing Data.

机构信息

Research Center, College of Computer and Information Science, King Saud University, Riyadh 11451, Saudi Arabia.

Nanomedicine & Biotechnology Research Unit, Department of Pharmaceutics, College of Pharmacy, P.O. Box 2457, King Saud University, Riyadh 11451, Saudi Arabia.

出版信息

Molecules. 2018 Apr 24;23(5):994. doi: 10.3390/molecules23050994.

Abstract

Cancer was initially considered a genetic disease. However, recent studies have revealed the connection between bacterial infections and growth of different types of cancer. The enteroinvasive strain of alters the normal behavior of host cells that may result in the growth of prostate cancer. The role of in the growth and development of prostate cancer still remains unclear. The infection may regulate several factors that influence prostate cancer growth in susceptible individuals. The aim of this study was to predict proteins targeted into the endoplasmic reticulum (ER) of the host cell, and their potential role in the induction of prostate cancer. From the whole proteome of , 19 proteins were predicted to be targeted into the ER of host cells. The results of our study predict that several proteins of may be targeted to the host cell ER, and possibly alter the normal pattern of protein folding. These predicted proteins can modify the normal function of the host cell. Thus, the intercellular infection of in host cells may serve as a potential factor in prostate cancer etiology.

摘要

癌症最初被认为是一种遗传疾病。然而,最近的研究揭示了细菌感染与不同类型癌症生长之间的联系。肠侵袭性菌株改变了宿主细胞的正常行为,可能导致前列腺癌的生长。在前列腺癌的生长和发展中,的作用尚不清楚。感染可能调节了几种影响易感个体前列腺癌生长的因素。本研究的目的是预测宿主细胞内质网(ER)中靶向的蛋白及其在诱导前列腺癌中的潜在作用。从整个基因组中,预测有 19 种蛋白被靶向到宿主细胞的 ER 中。我们的研究结果预测,可能有几种的蛋白被靶向到宿主细胞 ER,并可能改变蛋白质折叠的正常模式。这些预测的蛋白可以改变宿主细胞的正常功能。因此,在宿主细胞中的细胞间感染可能是前列腺癌病因学中的一个潜在因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7ce8/6099661/021f0595c3d0/molecules-23-00994-g001.jpg

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