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银屑病中信号下调模型。

The Model of -Downregulated Signaling in Psoriasis.

作者信息

Sobolev Vladimir, Nesterova Anastasia, Soboleva Anna, Dvoriankova Evgenia, Piruzyan Anastas, Mildzikhova Dzerassa, Korsunskaya Irina, Svitich Oxana

机构信息

I. Mechnikov Research Institute for Vaccines and Sera RAMS, 5 Malyy Kazennyy Pereulok, 105064 Moscow, Russia.

Centre of Theoretical Problems of Physico-Chemical Pharmacology, Russian Academy of Sciences, Russian Academy of Sciences, 4 Kosygin street, 119334 Moscow, Russia.

出版信息

PPAR Res. 2020 Oct 9;2020:6529057. doi: 10.1155/2020/6529057. eCollection 2020.

DOI:10.1155/2020/6529057
PMID:33133175
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7568796/
Abstract

Interactions of genes in intersecting signaling pathways, as well as environmental influences, are required for the development of psoriasis. Peroxisome proliferator-activated receptor gamma () is a nuclear receptor and transcription factor which inhibits the expression of many proinflammatory genes. We tested the hypothesis that low levels of expression promote the development of psoriatic lesions. We combined experimental results and network functional analysis to reconstruct the model of -downregulated signaling in psoriasis. We hypothesize that the expression of , , , and and genes in psoriatic skin is correlated with the level of expression, and they belong to the same signaling pathway that regulates the development of psoriasis lesion.

摘要

银屑病的发生发展需要相互交叉的信号通路中的基因相互作用以及环境影响。过氧化物酶体增殖物激活受体γ(PPARγ)是一种核受体和转录因子,可抑制许多促炎基因的表达。我们检验了PPARγ表达水平低会促进银屑病皮损发展这一假说。我们结合实验结果和网络功能分析来重建银屑病中PPARγ下调信号传导的模型。我们推测,银屑病皮肤中PPARγ、IL-17、IL-23、IFN-γ和TNF-α基因的表达与PPARγ表达水平相关,且它们属于调控银屑病皮损发展的同一信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/8733546fafbd/PPAR2020-6529057.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/5f288bcb6ef8/PPAR2020-6529057.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/535908c5f854/PPAR2020-6529057.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/11bab9dff720/PPAR2020-6529057.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/3d3aed98383a/PPAR2020-6529057.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/d03780a97713/PPAR2020-6529057.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/38f02e448a8f/PPAR2020-6529057.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/8733546fafbd/PPAR2020-6529057.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/5f288bcb6ef8/PPAR2020-6529057.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/535908c5f854/PPAR2020-6529057.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/11bab9dff720/PPAR2020-6529057.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/3d3aed98383a/PPAR2020-6529057.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/d03780a97713/PPAR2020-6529057.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/38f02e448a8f/PPAR2020-6529057.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/156e/7568796/8733546fafbd/PPAR2020-6529057.007.jpg

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