Integrated Bioinformatics Analysis Reveals Potential Pathway Biomarkers and Their Interactions for Clubfoot

生物 小桶 生物信息学 表型 遗传学 基因 转录组 基因表达
作者
Jing Ding,Zhenpeng Liang,Weijia Feng,Qixun Cai,Ziming Zhang
出处
期刊:Medical Science Monitor [International Scientific Information, Inc.]
卷期号:26 被引量:7
标识
DOI:10.12659/msm.925249
摘要

BACKGROUND:Congenital talipes equinovarus (clubfoot), one of the most regular pediatric congenital skeletal anomalies, seriously affects the normal growth and development of about 1 in 1000 newborns. Although it has been investigated widely, the etiology and pathogenesis of clubfoot are still controversial. MATERIAL AND METHODS:g: Profiler, NetworkAnalyst and WebGestalt were used to probe the enriched signaling pathways by using the Gene Ontology (GO), Human Phenotype Ontology (HP), Kyoto Encyclopedia of Genes and Genomes (KEGG), Reactome (REAC), and WikiPathways (WP) databases. Large numbers of enriched signaling pathways were identified using the integrated bioinformatics enrichment analyses. RESULTS:Apoptosis or programmed cell death (PCD), disease, muscle contraction, metabolism, and immune system were the top functions. Embryo or organ morphogenesis and development, cell or muscle contraction, and apoptosis were the top biological processes, and cell/muscle contraction and apoptosis were the top molecular functions using enriched GO terms analysis. There were a large number of complex interactions in the genes, enriched pathways, and transcription factor (TF)-miRNA co-regulatory networks. Transcription factors such as FOXN3, GLI3, HOX, and NCOR2 family regulated the gene expression of APAF1, BCL2, BID, CASP, MTHFR, and TPM family. CONCLUSIONS:The results of bioinformatics enrichment analysis not only supported the previously proposed hypotheses, e.g., extracellular matrix (ECM) abnormality, fetal movement reducing, genetic abnormality, muscle abnormality, neurological abnormality, skeletal abnormality and vascular abnormality, but also indicated that cellular or immune responses to external stimulus, molecular transport and metabolism may be new etiological mechanisms in clubfoot.
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
更新
大幅提高文件上传限制,最高150M (2024-4-1)

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
1秒前
天天快乐应助学术辣鸡采纳,获得10
1秒前
2秒前
老肖应助qiu采纳,获得10
3秒前
不配.应助kk123采纳,获得10
4秒前
喵了个酥发布了新的文献求助10
4秒前
嗷嗷嗷完成签到 ,获得积分10
5秒前
科研通AI2S应助dawn采纳,获得10
6秒前
Orange应助轻松的贞采纳,获得10
7秒前
KEHUGE发布了新的文献求助20
8秒前
8秒前
9秒前
畅快不平关注了科研通微信公众号
9秒前
欣慰外绣发布了新的文献求助10
12秒前
不配.应助科研通管家采纳,获得10
13秒前
科研通AI2S应助科研通管家采纳,获得10
13秒前
感性的穆发布了新的文献求助10
13秒前
科研通AI2S应助科研通管家采纳,获得10
13秒前
wanci应助科研通管家采纳,获得10
13秒前
Hello应助科研通管家采纳,获得10
13秒前
打打应助科研通管家采纳,获得10
14秒前
科研通AI2S应助科研通管家采纳,获得30
14秒前
14秒前
14秒前
在水一方应助科研通管家采纳,获得10
14秒前
不配.应助dr0422采纳,获得10
14秒前
14秒前
美好斓发布了新的文献求助10
14秒前
小齐怪发布了新的文献求助10
15秒前
15秒前
16秒前
12345发布了新的文献求助10
17秒前
芋你呀完成签到,获得积分10
18秒前
思源应助eurus采纳,获得10
18秒前
19秒前
BMII发布了新的文献求助10
20秒前
轻松的贞发布了新的文献求助10
21秒前
NIKO完成签到,获得积分20
22秒前
小马甲应助xiguan采纳,获得10
24秒前
望着拥有完成签到,获得积分10
24秒前
高分求助中
The Oxford Handbook of Social Cognition (Second Edition, 2024) 1050
The Young builders of New china : the visit of the delegation of the WFDY to the Chinese People's Republic 1000
юрские динозавры восточного забайкалья 800
English Wealden Fossils 700
Chen Hansheng: China’s Last Romantic Revolutionary 500
Mantiden: Faszinierende Lauerjäger Faszinierende Lauerjäger 500
PraxisRatgeber: Mantiden: Faszinierende Lauerjäger 500
热门求助领域 (近24小时)
化学 医学 生物 材料科学 工程类 有机化学 生物化学 物理 内科学 纳米技术 计算机科学 化学工程 复合材料 基因 遗传学 催化作用 物理化学 免疫学 量子力学 细胞生物学
热门帖子
关注 科研通微信公众号,转发送积分 3141332
求助须知:如何正确求助?哪些是违规求助? 2792381
关于积分的说明 7802238
捐赠科研通 2448574
什么是DOI,文献DOI怎么找? 1302618
科研通“疑难数据库(出版商)”最低求助积分说明 626650
版权声明 601237