Mouse Monoclonal EBV Nuclear Antigen/EBNA1 antibody. Suitable for ICC, ELISA, IHC-P and reacts with Epstein-Barr virus samples. Cited in 9 publications. Immunogen corresponding to Synthetic Peptide within Epstein-Barr Virus (Strain B95-8) EBNA1.
pH: 7.4
Preservative: 0.097% Sodium azide
Constituents: PBS
| ICC | ELISA | IHC-P | |
|---|---|---|---|
| Epstein-Barr virus | Expected | Expected | Expected |
| Species | Dilution info | Notes |
|---|---|---|
Species Epstein-Barr virus | Dilution info Use at an assay dependent concentration. | Notes - |
| Species | Dilution info | Notes |
|---|---|---|
Species Epstein-Barr virus | Dilution info Use at an assay dependent concentration. | Notes - |
| Species | Dilution info | Notes |
|---|---|---|
Species Epstein-Barr virus | Dilution info Use at an assay dependent concentration. | Notes - |
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Responsible for the origin of replication (oriP) dependent replication and maintenance of viral episomes during latent infection (PubMed:15479791, PubMed:2996781). EBNA1 dimer interacts with the DS (dyad symmetry) element within the origin of replication oriP and with a host mitotic chromosome to initiate viral DNA replication during latency (PubMed:24067969, PubMed:2996781, PubMed:31142669, PubMed:8551585). EBNA1 binding to DS recruits the host origin recognition complex (ORC) (PubMed:12953058). Governs the faithful mitotic segregation of the viral episomes by binding both the FR (family of repeats) element within oriP and the host mitotic chromosomes (PubMed:11172042, PubMed:15479791, PubMed:24067969). Forms a cell cycle-dependent tyrosine-dependent DNA cross-link and single-strand cleavage at oriP required for terminating replication and maintaining viral episomes (PubMed:33482082). Counteracts the stabilization of host p53/TP53 by host USP7, thereby decreasing apoptosis and increasing host cell survival (PubMed:15808506). Induces degradation of host PML through the ubiquitin-proteasome system, which promotes lytic reactivation and may impair the host cell DNA repair (PubMed:18833293). Increases the association of CK2 with PML proteins which increases the phosphorylation of PML proteins by CK2, triggering the polyubiquitylation and degradation of PML (PubMed:20719947). Displays inhibitory effects on a SUMO2-modified complex that includes STUB1, KAP1 and USP7 (PubMed:32176739). This inhibitory effect possibly participates to the maintenance of latency linked to PML silencing (PubMed:32176739).
EBV Nuclear Antigen/EBNA1
BKRF1, EBNA1, Epstein-Barr nuclear antigen 1, EBNA-1, EBV nuclear antigen 1
Mouse Monoclonal EBV Nuclear Antigen/EBNA1 antibody. Suitable for ICC, ELISA, IHC-P and reacts with Epstein-Barr virus samples. Cited in 9 publications. Immunogen corresponding to Synthetic Peptide within Epstein-Barr Virus (Strain B95-8) EBNA1.
pH: 7.4
Preservative: 0.097% Sodium azide
Constituents: PBS
Recognizes repetitive gly-ala region of the nuclear antigen 1 of Epstein Barr virus (EBNA-1).
EBV Nuclear Antigen 1 (EBNA1) is a protein expressed by the Epstein-Barr Virus (EBV) also known as Human Herpesvirus 4. It has a molecular weight of approximately 80 kDa and shows expression in latently infected cells. EBNA1 acts as a viral episome-maintenance protein that binds to the EBV genome ensuring viral DNA replication and partitioning during cell division. This protein facilitates the persistent infection of EBV in host cells. Occasionally it is also referred to as EBV EBNA or EBNA-1 protein.
EBNA1 functions as an EBV-specific DNA-binding protein essential for maintaining the viral episome within infected cells. EBNA1 plays a role in gene regulation by interacting with specific DNA sequences called oriP to assist in the replication and maintenance of the viral DNA. It does not form part of a larger protein complex but strongly influences cellular processes through these interactions. EBNA1 ensures the survival and propagation of the virus without immediate cytopathic effects contributing to its long-term persistence.
EBNA1 is central to viral latency and replication pathways in host cells. EBNA1 influences both the EBV lytic and latent cycles maintaining the latency by stabilizing the viral episome within the nucleus of host cells and regulating viral gene expression. It interacts with cellular proteins like USP7 a deubiquitinase important for the regulation of EBNA1 stability and function. These pathways highlight EBNA1's role in the balance between viral latency and active replication.
EBNA1 is closely associated with several EBV-related cancers such as Burkitt's lymphoma and nasopharyngeal carcinoma. The persistent expression of EBNA1 contributes to oncogenic processes by disrupting normal cellular control mechanisms. EBNA1's interaction with p53 a tumor suppressor protein can interfere with the host's cell-cycle regulation and apoptosis allowing for malignant transformation. These interactions illustrate EBNA1's significant role in the pathogenesis of disorders linked to EBV infection.
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