Dysregulated epidermal growth factor and tumor growth factor-beta receptor signaling through GFAP-ACTA2 protein interaction in liver fibrosis

Viral hepatitis is associated with high morbidity and mortality. Identification of biological pathways involved in hepatic fibrosis resulting from chronic hepatitis C are essential for better management of patients. Constructing the -human protein interaction network through bioinformatics may enabl...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Pakistan journal of medical sciences 2020-06, Vol.36 (4), p.782-787
Hauptverfasser: Hassan, Sobia, Zil-E-Rubab, Shah, Hussain, Shawana, Summayya
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Viral hepatitis is associated with high morbidity and mortality. Identification of biological pathways involved in hepatic fibrosis resulting from chronic hepatitis C are essential for better management of patients. Constructing the -human protein interaction network through bioinformatics may enable us to discover diagnostic biological pathways. We investigated to identify dysregulated pathways and gene enrichment based on actin alpha 2 ( and glial fibrillar acidic protein ( interaction network analysis in hepatic fibrosis. This is an in-silico study conducted at Ziauddin University from March,2019 to September 2019. Enrichment and protein-protein interaction (PPI) network analysis of the identified proteins: and along with their mapped gene data sets was performed using FunRich version 3.1.3. Biological pathway grouping showed enrichment of proteins (85.7%) in signalling pathway by epidermal growth factor receptor ( ) and Tumor growth factor ( -beta Receptor followed by signaling by and (71.4%) (p < 0.001). were enriched in both and -beta Signalling pathways. and signalling pathways were enriched in liver fibrosis. were enriched and differentially expressed in both and -beta signalling pathways.
ISSN:1682-024X
1681-715X
DOI:10.12669/pjms.36.4.1845