PMID- 31638426
OWN - NLM
STAT- MEDLINE
DCOM- 20210913
LR  - 20210913
IS  - 1557-8666 (Electronic)
IS  - 1066-5277 (Linking)
VI  - 27
IP  - 6
DP  - 2020 Jun
TI  - Identification of Marker Genes and Pathways in Patients with Primary Biliary 
      Cholangitis.
PG  - 923-933
LID - 10.1089/cmb.2019.0230 [doi]
AB  - Primary biliary cholangitis (PBC) is an autoimmune liver disease characterized by 
      cholestasis and cirrhosis, and in which hepatic failure may occur. This study 
      explores the changes in the gene expression profiles of liver tissues during the 
      pathogenesis of PBC. Array dataset GSE79850 was downloaded from the Gene 
      Expression Omnibus database. GeneSpring software was used to analyze 
      differentially expressed genes (DEGs) in liver tissues from PBC patients compared 
      with those from controls. Gene ontology (GO) annotation, the Kyoto Encyclopedia 
      of Genes and Genomes (KEGG), and Reactome pathway enrichment analyses were 
      performed by using Database for Annotation, Visualization and Integrated 
      Discovery (DAVID) software. Cytoscape software was used to construct a 
      protein-protein interaction (PPI) network. Plug-ins Molecular Complex Detection 
      and iRegulon were used for clustering analysis and transcription factors related 
      to key genes with PBC. A total of 77 DEGs, including 47 up- and 30 downregulated 
      genes, were identified. The PPI network was established with 74 nodes and 356 
      protein pairs. The C-C motif chemokine ligand 5 (CCL5), interleukin 7 receptor 
      (IL7R), and TNF receptor superfamily member 1A (TNFRSF1A) were identified as hub 
      genes in the PPI network and may, therefore, be marker genes for PBC. Further, 
      the upregulated genes CCL5 and IL7R, and downregulated TNFRSF1A were included in 
      immune system processes as a GO term in the category Biological Processes. In 
      conclusion, CCL5, IL7R, TNFRSF1A, and the immune response pathway may have 
      crucial roles in PBC. These genes and pathways may be potential targets for 
      treating PBC.
FAU - Dong, Xihua
AU  - Dong X
AD  - Department of Laboratory Medicine, The First Affiliated Hospital of China Medical 
      University, Shenyang, China.
FAU - Yu, Xiaoou
AU  - Yu X
AD  - Department of Laboratory Medicine, The First Affiliated Hospital of China Medical 
      University, Shenyang, China.
FAU - Li, Hua
AU  - Li H
AD  - Department of Laboratory Medicine, The First Affiliated Hospital of China Medical 
      University, Shenyang, China.
FAU - Kang, Hui
AU  - Kang H
AD  - Department of Laboratory Medicine, The First Affiliated Hospital of China Medical 
      University, Shenyang, China.
LA  - eng
PT  - Journal Article
DEP - 20191023
PL  - United States
TA  - J Comput Biol
JT  - Journal of computational biology : a journal of computational molecular cell 
      biology
JID - 9433358
RN  - 0 (CCL5 protein, human)
RN  - 0 (Chemokine CCL5)
RN  - 0 (IL7R protein, human)
RN  - 0 (Interleukin-7 Receptor alpha Subunit)
RN  - 0 (Receptors, Tumor Necrosis Factor, Type I)
RN  - 0 (TNFRSF1A protein, human)
SB  - IM
MH  - Chemokine CCL5/*genetics
MH  - Cluster Analysis
MH  - Gene Expression Profiling/*methods
MH  - Gene Expression Regulation
MH  - Gene Ontology
MH  - Gene Regulatory Networks
MH  - Humans
MH  - Interleukin-7 Receptor alpha Subunit/*genetics
MH  - Liver Cirrhosis, Biliary/*genetics
MH  - Protein Interaction Maps
MH  - Receptors, Tumor Necrosis Factor, Type I/*genetics
MH  - Signal Transduction
MH  - Software
OTO - NOTNLM
OT  - GEO
OT  - PBC
OT  - gene expression
OT  - liver tissue
OT  - pathway
EDAT- 2019/10/23 06:00
MHDA- 2021/09/14 06:00
CRDT- 2019/10/23 06:00
PHST- 2019/10/23 06:00 [pubmed]
PHST- 2021/09/14 06:00 [medline]
PHST- 2019/10/23 06:00 [entrez]
AID - 10.1089/cmb.2019.0230 [doi]
PST - ppublish
SO  - J Comput Biol. 2020 Jun;27(6):923-933. doi: 10.1089/cmb.2019.0230. Epub 2019 Oct 
      23.