Sustained Expression of the Novel EBV-Induced Zinc Finger Gene, <i>ZNF</i>
                  <i>EB</i>, Is Critical for the Transition of B Lymphocyte Activation to Oncogenic Growth Transformation

Tune, Cathryn E.; Pilon, Marc; Saiki, Yuriko; Hm, Dosch

doi:10.4049/jimmunol.168.2.680

Cited by 8 publications

(5 citation statements)

References 64 publications

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“…ZNF24 may be down-regulated to promote VEGF expression during tumor progression and other angiogenesis-dependent diseases characterized by aberrant VEGF expression. Furthermore, ZNF24 is localized to a chromosomal locus (18q12) that is mutated in a number of human cancers, such as colorectal carcinomas (17,18), head and neck cancer (27), invasive breast cancer (21), gastric cardia adenocarcinomas (28), testicular germ cell tumors (29), and a number of hematopoietic malignancies (30). The high incidence of mutations within this chromosomal locus strongly suggests the presence of potential tumor suppressor genes within this region.…”

Section: Discussionmentioning

confidence: 99%

Repression of Vascular Endothelial Growth Factor Expression by the Zinc Finger Transcription Factor ZNF24

Harper

Li²,

Loureiro

et al. 2007

Cancer Research

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Section: Discussionmentioning

confidence: 99%

Repression of Vascular Endothelial Growth Factor Expression by the Zinc Finger Transcription Factor ZNF24

Harper

Li²,

Loureiro

et al. 2007

Cancer Research

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“…ZNF EB maps to human chromosome 18q12 (62). The 18q12 region is known to be a hot spot for structural cytogenetic changes in numerous different malignancies (37). The mRNA expression of ZNF EB , a human homolog of Zfp35, is transiently induced upon activation of human B cells by anti-IgM F(abЈ) 2 or a phorbol ester plus calcium ionophore (37).…”

Section: Discussionmentioning

confidence: 99%

“…Zfp35 belongs to C 2 H 2 -type Zfp family and contains 18 continuous typical C 2 H 2 zinc fingers in its C-terminal and contains one acidic region with a numbers of glutamic and aspartic acid domain in its N terminus (36). A human homolog of Zfp35, ZNF EB , was identified in EBV-positive B cells and shows ϳ79% homology at the amino acid level compared with mice (37). The rat homolog Zfp239 was identified in the cDNA library of the spleen by the Mammalian Gene Collection Program and shows ϳ84% homology at the amino acid level compared with mice (38).…”

mentioning

confidence: 99%

Enhanced Th2 Cell Differentiation and Allergen-Induced Airway Inflammation in Zfp35-Deficient Mice

Kitajima

Iwamura

Miki-Hosokawa

et al. 2009

The Journal of Immunology

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Studies of human asthma and of animal models of allergic airway inflammation revealed a crucial role for Th2 cells in the pathogenesis of allergic asthma. Kruppel-type zinc finger proteins are the largest family of a regulatory transcription factor for cellular development and function. Zinc finger protein (Zfp) 35 is an 18-zinc finger motif-containing Kruppel-type zinc finger protein, while its function remains largely unknown. The aim of this study was to clarify the role of Zfp35 in the pathogenesis of Th2-dependent allergic inflammation, such as allergic asthma. We examined airway eosinophilic inflammation and hyperresponsiveness in two mouse models, which use our newly generated Zfp35-deficient (Zfp35−/−) mice and adoptive transfer of cells. In Zfp35−/− mice, Th2 cell differentiation, Th2 cytokine production, eosinophilic inflammation, and airway hyperresponsiveness were substantially enhanced. Furthermore, adoptive transfer of Ag-sensitized Zfp35−/− CD4 T cells into the asthmatic mice resulted in enhanced airway inflammation and airway hyperresponsiveness. These results indicate that Zfp35 controls Th2 cell differentiation, allergic airway inflammation, and airway hyperresponsiveness in a negative manner. Thus, Zfp35 may control Th2-dependent diseases, such as allergic asthma.

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“…In addition, interferon-stimulated genes serve as enhancers of antiviral innate immunity [15]. The novel EBV-induced Zinc Finger Gene (ZNFEB) including its intronless locus and human protein variants, controls entry and exit from cell cycling in activated lymphocytes [16].…”

Section: Zinc-finger Proteinmentioning

confidence: 99%

Virucidal Activities of Zinc-Finger Antiviral Proteins and Zinc-Binding Domains for Virus Entry, DNA/RNA Replication and Spread

Ishida¹

2020

EJBMR

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The novel EBV (Epstein-Barr virus)-induced ZNFEB including its intronless locus and human protein variants, controls virus entry and exit from cell cycling in activated lymphocytes. ZNF ZCCHC3 binds RNA and facilitates viral RNA that is critical for RLR-mediated innate immune response to RNA virus. ZAP (Zinc-Finger Antiviral Protein) inhibits entry, replication and spread of certain viruses and promotes viral RNA degradation. ZAP may regulate DNA and RNA virus replication that ZAP inhibits Retroviral RNA production and HIV-1(Human Immuno-Deficiency Virus Type 1) infection by promoting the degradation of specific viral mRNAs. Futhermore, ZAP could regulate RNA virus degradation of SARS-CoV's (SARS Corona Virus) and MERS-CoV's (MERS Corona Virus) RNA virus. Replication of SARS-CoV requires proteolytic processing of the replicase polyprotein by a PLpro (Papain-Like Protease) that zinc conjugate inhibits SARSCoV PLpro protease activity. Zinc conjugated complexes as SARS-CoV 3C-like protease inhibitors play important role for this Zn2+-centered coordination pattern that the zinc-coordinating inhibitor is tetrahedrally coordinated. ZBD (Zinc-Binding Domain) is essential for formation of the functional Junin virus envelope glycoprotein complex. Complex ZBD regulates replicative arterivirus helicase and controls mRNA decay helicase. Viral inhibitor p53 down-regulates SARS-CoV replications that p53 inhibits replication of infectious SARS-CoV as well as of replicons and HCoV-NL63 (Human Coronavirus NL63). ZAP-70 kinase regulates HIV cell-to-cell spread that HIV usurps components of the immunological synapse machinery to ensure its own spread through cell-to-cell contacts. Enveloped viruses enter cells and initiate disease-causing cycles of replication that in all cases virus-cell fusion is executed by one or more viral surface glycoproteins denoted as the fusion protein. Virucidal activities of ZNF, ZAP and ZBD are recognised by which Zn2+ ions bind RNA and facilitates viral RNA that is critical for RLR (RIG-1 Like Receptor)-mediated innate immune response to RNA virus and highly diverse fusion proteins have converged on the same overall strategy to mediate a common pathway of membrane fusion, causing to lead enhancement of the anti-viral activity. Zinc ions become used as Zn-coordinated inhibitors for viral regulation of virucidal activities.

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Sustained Expression of the Novel EBV-Induced Zinc Finger Gene, ZNF EB, Is Critical for the Transition of B Lymphocyte Activation to Oncogenic Growth Transformation

Cited by 8 publications

References 64 publications

Repression of Vascular Endothelial Growth Factor Expression by the Zinc Finger Transcription Factor ZNF24

Repression of Vascular Endothelial Growth Factor Expression by the Zinc Finger Transcription Factor ZNF24

Enhanced Th2 Cell Differentiation and Allergen-Induced Airway Inflammation in Zfp35-Deficient Mice

Virucidal Activities of Zinc-Finger Antiviral Proteins and Zinc-Binding Domains for Virus Entry, DNA/RNA Replication and Spread

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