HBV Mutation Detail Information

Virus Mutation HBV Mutation S31A


Basic Characteristics of Mutations
Mutation Site S31A
Mutation Site Sentence By performing Co-IP assay in HBV-free Huh7 cells expressing wild-type HBx, mutant HBx-S31A, or HBx-S31D (serine(31) was mutated into alanine(31) or aspartic acid(31) ), we found that the phosphorylated serine(31) with its near amino acid residues constituted a RPLphosphoS(31) GP (R, arginine; P, proline; L, leucine; S, serine; G, glycine) motif in HBx for 14-3-3zeta docking.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region X
Standardized Encoding Gene X  
Genotype/Subtype -
Viral Reference -
Functional Impact and Mechanisms
Disease -
Immune -
Target Gene -
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location China
Literature Information
PMID 30358169
Title 14-3-3zeta binds to hepatitis B virus protein X and maintains its protein stability in hepatocellular carcinoma cells
Author Tang Y,Zhang Y,Wang C,Sun Z,Li L,Dong J,Zhou W
Journal Cancer medicine
Journal Info 2018 Nov;7(11):5543-5553
Abstract 14-3-3zeta, a phosphopeptide-binding molecule, is reportedly overexpressed in the cancerous tissues of patients with hepatocellular carcinoma (HCC). Hepatitis B virus (HBV) protein X (HBx) draws intensive attention in HBV-related HCC because it not only regulates HBV replication, but also promotes carcinogenesis by interacting with various tumor or antitumor molecules. This study is performed to investigate whether and how 14-3-3zeta interacts with HBx. The coimmunoprecipitation (Co-IP) results showed that 14-3-3zeta bond to HBx in HBV-infected Hep3B HCC cells and CSQT-2 portal vein tumor thrombosis (PVTT) cells. By performing Co-IP assay in HBV-free Huh7 cells expressing wild-type HBx, mutant HBx-S31A, or HBx-S31D (serine(31) was mutated into alanine(31) or aspartic acid(31) ), we found that the phosphorylated serine(31) with its near amino acid residues constituted a RPLphosphoS(31) GP (R, arginine; P, proline; L, leucine; S, serine; G, glycine) motif in HBx for 14-3-3zeta docking. This 14-3-3zeta-HBx interaction was partly impaired when Akt signaling transduction was blocked by LY294002. Furthermore, 14-3-3zeta silencing augmented HBx ubiquitination and decreased its expression in cancer cells and xenograft tumor. The migratory and invasive abilities of CSQT-2 cells were inhibited upon 14-3-3zeta silencing, whereas partly restored by HBx overexpression. Additionally, 14-3-3zeta positively correlated with HBx to be overexpressed in the primary HCC tissues (r = 0.344) and metastatic PVTT (r = 0.348). In summary, findings of this study reveal a novel 14-3-3zeta-HBx interaction in HCC cells and suggest 14-3-3zeta as a candidate target for treating HBV-related HCC.
Sequence Data -
Mutation Information
Note
Basic Characteristics of Mutations
  • Mutation Site: The specific location in a gene or protein sequence where a change occurs.
  • Mutation Level: The level at which a mutation occurs, including the nucleotide or amino acid level.
  • Mutation Type: The nature of the mutation, such as missense mutation, nonsense mutation, synonymous mutation, etc.
  • Gene/Protein/Region: Refers to the specific region of the virus where the mutation occurs. Including viral genes, viral proteins, or a specific viral genome region. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main
  • Gene/Protein/Region studied in the article is marked.
  • Genotype/Subtype: Refers to the viral genotype or subtype where the mutation occurs. If the article does not specifically indicate the relationship between the mutation and its correspondence, the main Genotype/Subtype studied in the article is marked.
  • Viral Reference: Refers to the standard virus strain used to compare and analyze viral sequences.
Functional Impact and Mechanisms
  • Disease: An abnormal physiological state with specific symptoms and signs caused by viral infection.
  • Immune: The article focuses on the study of mutations and immune.
  • Target Gene: Host genes that viral mutations may affect.
Clinical and Epidemiological Correlations
  • Clinical Information: The study is a clinical or epidemiological study and provides basic information about the population.
  • Treatment: The study mentioned a certain treatment method, such as drug resistance caused by mutations. If the study does not specifically indicate the relationship between mutations and their correspondence treatment, the main treatment studied in the article is marked.
  • Location: The source of the research data.
Literature Information
  • Sequence Data: The study provides the data accession number.