BZLF1 Antibody

1. position C189 in Zta impacts sequence-specific binding to DNA containing modified and unmodified cytosine. PMID: 29772230
2. ERK/c-Jun recruits Tet1 to Induce Zta expression and Epstein-Barr virus reactivation through DNA demethylation. PMID: 27708396
3. HIF-1alpha directly bound the promoter of the EBV primary latent-lytic switch BZLF1 gene, Zp, activating transcription via a consensus hypoxia-response element (HRE) located at nt -83 through -76 relative to the transcription initiation site. PMID: 28617871
4. By CRISPR/Cas9-induced inactivation of TLR9, MyD88, IRAK4 and IRAK1 we confirm that BZLF1 repression is dependent on functional TLR9 and MyD88 signaling, and identify IRAK4 as an essential element for TLR9-induced repression of BZLF1 expression upon BCR cross-linking PMID: 29088270
5. Comparison of how AP-1 (Jun/Jun dimer) and Epstein-Barr virus Zta recognize methyl groups within their cognate response elements PMID: 28158710
6. Binding of PARP1 at the BZLF1 lytic switch promoter restricts Epstein Barr Virus reactivation. PMID: 28456021
7. These results suggest that lytic Epstein-Barr virus infection attenuates the transmission of inflammatory paracrine senescence through BZLF1 downregulation of TNF-alpha secretion and alters the inflammatory microenvironment to allow virus propagation and persistence. PMID: 27334596
8. The dimerization region of Epstein-Barr virus Zta is not required to mediate host CIITA repression. PMID: 26653871
9. These results suggest that Epstein-Barr Virus BZLF1 attenuates the proinflammatory responses to facilitate viral replication. PMID: 26537683
10. Presented is a model of DNA damage responses activation during the EBV lytic cycle in which ZEBRA induces ATM kinase phosphorylation, in a DNA binding dependent manner, to modulate gene expression. PMID: 25950714
11. RanBPM was found to enhance Zta-dependent transcriptional activity via the inhibition of Zta sumoylation. PMID: 25900136
12. Studied the effects of BZLF1 on cellular response to DNA damage in nasopharyngeal carcinoma cells. PMID: 26006018
13. This is the first report to characterize BZLF1 gene polymorphisms in paediatric patients from our geographical region and to suggest the association of these polymorphisms with malignant lymphomas. PMID: 24666405
14. ZEBRA and BGLF5 each function as viral host shutoff factors. PMID: 24705134
15. these results indicate a critical role for MCAF1 in AP-1-dependent Rta activation of BZLF1 transcription. PMID: 24598729
16. Performed the recombinant production of a biologically active Epstein-Barr virus BZLF1 trans-activator, i.e., Z-encoded broadly reactive activator (ZEBRA), that recognized specific DNA motifs. PMID: 24291446
17. B-cell specific transcription factor, Oct-2, inhibits the function of the viral immediate-early protein, BZLF1, and prevents lytic viral reactivation. PMID: 22346751
18. the genetic characteristics of BZLF1 gene and its promoter Zp of the epidemic strains in children with primary Epstein-Barr virus (EBV)-associated diseases PMID: 24772891
19. TAF-Ibeta promotes BZLF1 expression and subsequent lytic infection by affecting chromatin at the BZLF1 promoter PMID: 23691099
20. Mutation of MEF2 sites severely impaired both spontaneous and induced expression of not only BZLF1, but also BRLF1 in comparison to wild-type or revertant virus cases. PMID: 23843637
21. The B-cell-specific transcription factor and master regulator Pax5 promotes Epstein-Barr virus latency by negatively regulating the viral immediate early protein BZLF1. PMID: 23678172
22. Zta drives cell migration and invasion through MMPs PMID: 23409137
23. BZLF1 is a pioneer factor that reverses epigenetic silencing of viral DNA to allow escape from latency. PMID: 22969425
24. Genome-wide analyses of Zta binding to the Epstein-Barr virus genome reveals interactions in both early and late lytic cycles and an epigenetic switch leading to an altered binding profile. PMID: 23015699
25. The mechanism of p53-mediated Epstein-Barr viral Zta protein activation requires the cooperative action of another cellular factor, Sp1. PMID: 22711357
26. Herpes simplex virus type 1 induces the reactivation of latent EBV by triggering BZLF1 expression. PMID: 22188237
27. Epigenetic modification of the BZLF1 promoter in latent Raji cells by histone H3 lysine 27 trimethylation (H3K27me3), H3K9me2/me3, and H4K20me3. PMID: 22357272
28. The s show that expression of the Epstein-Barr virus immediate-early protein BZLF1 is restricted to Blimp1-positive epithelial cells in oral hairy leukoplakia. PMID: 22278826
29. The abundance of Zta protein coupled with the methylation status of the Epstein-Barr virus (EBV) genome act together to co-ordinate the expression of lytic cycle genes at the majority of EBV promoters. PMID: 22022468
30. conclude that TGF-beta induces EBV lytic reactivation via the canonical Smad pathway by activating BZLF1 gene expression through multiple SBEs acting in concert PMID: 21593157
31. study reports that specific single missense mutations within the basic domain of ZEBRA induce the formation of nuclear aggresomes, which strongly sequester the mutant protein PMID: 21233201
32. The s conclude that the ZIIR element is a potent silencing element in the BZLF1 promoter Zp and plays a key role in establishment and maintenance of virus latency by inhibiting activation of Zp through the PKC signal transduction pathway. PMID: 21389123
33. This study also reveals that the interaction between Zta and Ku80 involves the C-terminal region of Zta and the 425 aa N-terminal region of Ku80. PMID: 21123545
34. Data show that Daudi cells express glucocorticoid receptors that mediate Dex-dependent up-regulation of BZLF1 mRNA levels. PMID: 20466055
35. By a chromatin immunoprecipitation (ChIP) assay, the s show that Ubn-1 blocks EB1-human herpesvirus 4 DNA interaction. PMID: 21084479
36. These observations indicate that the EBV lytic transactivator protein Zta displays activity consistent with a pathogenic role in pulmonary fibrosis associated with herpesvirus infection. PMID: 20817778
37. Results strongly suggest that oxidative stress contributes to the reactivation of EBV lytic cycle, through induction of BZLF-1 gene expression. PMID: 19898754
38. Enhanced binding of ZEBRA to the origin of lytic DNA replication is crucial for lytic viral DNA replication. PMID: 20808903
39. Data propose that EBV protein Zta activates SOCS3 protein as an immune escape mechanism that both suppresses optimal IFNalpha secretion by human monocytes and favors a state of type I IFN irresponsiveness in these cells. PMID: 20689596
40. sumoylation of BZLF1 regulates its transcriptional activity through histone modification during Epstein-Barr virus productive replication PMID: 20516063
41. Study renders ZEBRA-MD a promising candidate for therapeutic protein delivery applications. PMID: 20385549
42. These data suggest that Zta acts by inducing and/or stabilizing a DNA hairpin structure during productive infection. PMID: 20444899
43. viral BZLF1 protein is crucial both to establish latency and to escape from it; Epstein Barr virus has evolved to its host mode of dna methylation. PMID: 20080764
44. Our work implies that the balance of promyelocytic leukemia protein and BZLF1 levels in cells may affect how each protein functions. PMID: 16307818
45. there are three phosphorylation sites on the Epstein-Barr virus ZEBRA protein PMID: 16321978
46. Results describe the crystal structure of ZEBRA's DNA binding domain bound to an Epstein-Barr virus lytic gene promoter element. PMID: 16483937
47. Comparison among viral orthologues of Zta suggest that a conserved N-terminal extension of the consensus B-ZIP domain is required for this multivalent DNA recognition capacity of Zta and is essential for viral reactivation.[Zta] PMID: 16971443
48. BZLF1 is expressed as an immediate-early gene following primary EBV infection of B lymphocytes. PMID: 17079287
49. We report that the plasma cell differentiation factor, XBP-1s, activates the expression of the master regulator of EBV lytic activation, BZLF1. PMID: 17898050
50. HHV8-RTA and EBV-BZLF1 are co-localized and physically interact with each other in dually-infected PELs, required for the mutual inhibition of the two molecules PMID: 18253508

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KEGG: vg:3783744