FYN and CD247: Key Genes for Septic Shock Based on Bioinformatics and Meta-Analysis

FYN公司 生物 基因 感染性休克 基因表达 计算生物学 小桶 败血症 遗传学 转录组 免疫学 信号转导 原癌基因酪氨酸蛋白激酶Src
作者
Yingchun Hu,Ye Tian,Yue Jiang,Miao Qian,Lin Hu,Tingyan Zhou
出处
期刊:Combinatorial Chemistry & High Throughput Screening [Bentham Science]
卷期号:25 (10): 1722-1730 被引量:12
标识
DOI:10.2174/1386207324666210816123508
摘要

Background: Septic shock is sepsis accompanied by hemodynamic instability and high clinical mortality. Material and Methods: GSE95233, GSE57065, GSE131761 gene-expression profiles of healthy control subjects and septic shock patients were downloaded from the Gene-Expression Omnibus (GEO) database, and differences of expression profiles and their intersection were analysed using GEO2R. Function and pathway enrichment analysis was performed on common differentially expressed genes (DEG), and key genes for septic shock were screened using a protein-protein interaction network created with STRING. Also, data from the GEO database were used for survival analysis for key genes, and a meta-analysis was used to explore expression trends of core genes. Finally, high-throughput sequencing using the blood of a murine sepsis model was performed to analyse the expression of CD247 and FYN in mice. Results: A total of 539 DEGs were obtained (p < 0.05). Gene ontology analysis showed that key genes were enriched in functions, such as immune response and T cell activity, and DEGs were enriched in signal pathways, such as T cell receptors. FYN and CD247 are in the centre of the protein-protein interaction network, and survival analysis found that they are positively correlated with survival from sepsis. Further, meta-analysis results showed that FYN could be useful for the prognosis of patients, and CD247 might distinguish between sepsis and systemic inflammatory response syndrome patients. Finally, RNA sequencing using a mouse septic shock model showed low expression of CD247 and FYN in this model. Conclusion: FYN and CD247 are expected to become new biomarkers of septic shock.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
程逸晨发布了新的文献求助10
刚刚
田田田田完成签到,获得积分10
刚刚
小晴天发布了新的文献求助10
刚刚
MIMI完成签到,获得积分10
刚刚
不摇头的向日葵完成签到,获得积分10
刚刚
SciGPT应助1111采纳,获得10
刚刚
跳跃的凌文完成签到 ,获得积分10
1秒前
1秒前
香蕉诗蕊应助青枫采纳,获得10
2秒前
2秒前
2秒前
思源应助K先生采纳,获得10
2秒前
JOSIELO完成签到 ,获得积分10
2秒前
黄柒柒发布了新的文献求助10
3秒前
Li应助仁爱的秋天采纳,获得10
3秒前
香蕉诗蕊应助muzi采纳,获得10
3秒前
4秒前
万能图书馆应助小铭同学采纳,获得80
4秒前
Ricky发布了新的文献求助10
4秒前
neverlost6发布了新的文献求助10
4秒前
wuran发布了新的文献求助30
5秒前
rnanoda完成签到,获得积分10
5秒前
6秒前
天天快乐应助棉花糖采纳,获得10
6秒前
tianliangjie9712完成签到,获得积分10
7秒前
科研通AI6应助sunyanghu369采纳,获得10
7秒前
CNS关闭了CNS文献求助
7秒前
金雪发布了新的文献求助10
7秒前
英勇的飞扬完成签到,获得积分10
7秒前
星辰大海应助低调的涵内采纳,获得10
8秒前
青阳完成签到,获得积分10
8秒前
8秒前
9秒前
EatFish发布了新的文献求助10
9秒前
9秒前
白衣卿相完成签到 ,获得积分10
9秒前
卡卡滴滴发布了新的文献求助10
10秒前
10秒前
10秒前
上官若男应助neverlost6采纳,获得10
10秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Encyclopedia of Reproduction Third Edition 3000
《药学类医疗服务价格项目立项指南(征求意见稿)》 1000
花の香りの秘密―遺伝子情報から機能性まで 800
1st Edition Sports Rehabilitation and Training Multidisciplinary Perspectives By Richard Moss, Adam Gledhill 600
Chemistry and Biochemistry: Research Progress Vol. 7 430
Biotechnology Engineering 400
热门求助领域 (近24小时)
化学 材料科学 生物 医学 工程类 计算机科学 有机化学 物理 生物化学 纳米技术 复合材料 内科学 化学工程 人工智能 催化作用 遗传学 数学 基因 量子力学 物理化学
热门帖子
关注 科研通微信公众号,转发送积分 5629869
求助须知:如何正确求助?哪些是违规求助? 4720921
关于积分的说明 14971132
捐赠科研通 4787826
什么是DOI,文献DOI怎么找? 2556570
邀请新用户注册赠送积分活动 1517709
关于科研通互助平台的介绍 1478285