Please use this identifier to cite or link to this item: https://doi.org/10.3390/ijms23095127
Title: Phosphoproteomics Unravel HBV Triggered Rewiring of Host Phosphosignaling Events
Authors: Lim, ZiJie
Mohd-Ismail, Nur Khairiah Binte
Png, Evelyn
Sze, Ching Wooen 
Lin, Qifeng 
Hong, Wanjin
Lim, Seng Gee 
Tan, Yee-Joo 
Gunaratne, Jayantha 
Keywords: Science & Technology
Life Sciences & Biomedicine
Physical Sciences
Biochemistry & Molecular Biology
Chemistry, Multidisciplinary
Chemistry
hepatitis B virus
phosphoproteomics
phosphosignaling
kinases
kinase inhibitor
kinome
HEPATITIS-B-VIRUS
CLOSED CIRCULAR DNA
CORE PROTEIN
KINASES
CLK
PHOSPHORYLATION
IDENTIFICATION
PATHWAY
REPLICATION
INHIBITORS
Issue Date: 1-May-2022
Publisher: MDPI
Citation: Lim, ZiJie, Mohd-Ismail, Nur Khairiah Binte, Png, Evelyn, Sze, Ching Wooen, Lin, Qifeng, Hong, Wanjin, Lim, Seng Gee, Tan, Yee-Joo, Gunaratne, Jayantha (2022-05-01). Phosphoproteomics Unravel HBV Triggered Rewiring of Host Phosphosignaling Events. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES 23 (9). ScholarBank@NUS Repository. https://doi.org/10.3390/ijms23095127
Abstract: Hepatitis B virus (HBV) infection persists as a major global health problem despite the availability of HBV vaccines for disease prevention. However, vaccination rates remains low in some regions of the world, driving the need for novel strategies to minimise infections and prevent disease progression. Thus, understanding of perturbed molecular signaling events during early phases of HBV infection is required. Phosphosignaling is known to be involved in the HBV infection processes, yet systems-level changes in phosphosignaling pathways in the host during infection remain unclear. To this end, we performed phosphoproteome profiling on HBV-infected HepG2NTCP cells. Our results showed that HBV infection drastically altered the host phosphoproteome and its associated proteins, including kinases. Computational analysis of this phosphoproteome revealed dysregulation of the pathways involved in immune responses, cell cycle processes, and RNA processing during HBV infection. Kinase Substrate Enrichment Analysis (KSEA) identified the dysregulated activities of important kinases, including those from CMGC (CDK, MAPK, GSK, and CLK), AGC (protein kinase A, G, and C), and TK (Tyrosine Kinase) families. Of note, the inhibition of CLKs significantly reduced HBV infection in HepG2-NTCP cells. In all, our study unravelled the aberrated phosphosignaling pathways and the associated kinases, presenting potential entry points for developing novel therapeutic strategies for HBV treatment.
Source Title: INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
URI: https://scholarbank.nus.edu.sg/handle/10635/228580
ISSN: 16616596
14220067
DOI: 10.3390/ijms23095127
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