KSHV Mutation Detail Information

Virus Mutation KSHV Mutation K152E


Basic Characteristics of Mutations
Mutation Site K152E
Mutation Site Sentence Previously, we identified an RTA mutant, RTA-K152E, which has a defect in its direct DNA-binding activity.
Mutation Level Amino acid level
Mutation Type Nonsynonymous substitution
Gene/Protein/Region RTA
Standardized Encoding Gene ORF50  
Genotype/Subtype -
Viral Reference -
Functional Impact and Mechanisms
Disease Cell line    
Immune -
Target Gene RBPJ    NOTCH1   
Clinical and Epidemiological Correlations
Clinical Information -
Treatment -
Location -
Literature Information
PMID 17850910
Title The interaction between KSHV RTA and cellular RBP-Jkappa and their subsequent DNA binding are not sufficient for activation of RBP-Jkappa
Author Papugani A,Coleman T,Jones C,Zhang L
Journal Virus research
Journal Info 2008 Jan;131(1):1-7
Abstract Kaposi's sarcoma-associated herpesvirus (KSHV) replication and transcription activator (RTA) is necessary and sufficient for the switch from KSHV latency to lytic replication. RTA activates promoters by several mechanisms. RTA can bind to sequences in viral promoters and activate transcription. In addition, RTA interacts with the cellular recombination signal sequence-binding protein-J kappa (RBP-Jkappa), a transcriptional repressor, converts the repressor into an activator and activates viral promoters via RBP-Jkappa. Because RBP-Jkappa is required for RTA to activate lytic replication, it is important to understand how RTA cooperates with RBP-Jkappa protein to activate KSHV lytic replication program. Previously, we identified an RTA mutant, RTA-K152E, which has a defect in its direct DNA-binding activity. In this report, the effect of the mutant RTA on KSHV activation via RBP-Jkappa protein is examined. We demonstrate that RTA-K152E interacts with RBP-Jkappa physically and the mutant RTA and RBP-Jkappa complex binds to target DNA properly in vivo and in vitro. However, the complex of RTA-K152E and RBP-Jkappa does not activate transcription. Furthermore, the RTA mutant (RTA-K12E) inhibits cellular Notch-mediated RBP-Jkappa activation. These data collectively suggest that the complex between KSHV RTA and cellular RBP-Jkappa and the subsequent DNA binding by the complex are not sufficient for the activation of RBP-Jkappa protein. Other factor(s) whether additional cofactor(s) in the complex or the intrinsic conformation of RTA, are predicted to be required for the activation of RBP-Jkappa protein by RTA.
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.