Apoptosis regulators from DNA viruses. (Q53854543)

21 May 2018

review article

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title

Apoptosis regulators from DNA viruses. (English)

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21 May 2018

author name string

Barry M

series ordinal

1

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21 May 2018

McFadden G

series ordinal

2

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21 May 2018

publication date

1 August 1998

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21 May 2018

Current Opinion in Immunology

published in

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21 May 2018

volume

10

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21 May 2018

issue

4

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21 May 2018

page(s)

422-430

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21 May 2018

Regulation of apoptosis by viral gene products

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Characterization of reaper- and FADD-induced apoptosis in a lepidopteran cell line

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A BIR motif containing gene of African swine fever virus, 4CL, is nonessential for growth in vitro and viral virulence.

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Death effector domain-containing herpesvirus and poxvirus proteins inhibit both Fas- and TNFR1-induced apoptosis

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A novel family of viral death effector domain-containing molecules that inhibit both CD-95- and tumor necrosis factor receptor-1-induced apoptosis

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The adenovirus E3-10.4K/14.5K complex mediates loss of cell surface Fas (CD95) and resistance to Fas-induced apoptosis

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Interaction of the adenovirus 14.7-kDa protein with FLICE inhibits Fas ligand-induced apoptosis

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Distinct domains of M-T2, the myxoma virus tumor necrosis factor (TNF) receptor homolog, mediate extracellular TNF binding and intracellular apoptosis inhibition.

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Latent membrane protein 1 of Epstein-Barr virus mimics a constitutively active receptor molecule.

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The Epstein-Barr virus oncogene product latent membrane protein 1 engages the tumor necrosis factor receptor-associated death domain protein to mediate B lymphocyte growth transformation and activate NF-kappaB

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Activation of a ras-MAPK-dependent pathway by Epstein-Barr virus latent membrane protein 1 is essential for cellular transformation

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Localization of the major NF-kappaB-activating site and the sole TRAF3 binding site of LMP-1 defines two distinct signaling motifs

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Expression of Epstein-Barr virus latent membrane protein 1 protects Jurkat T cells from apoptosis induced by serum deprivation

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Cooperative interaction between Bcl-2 and Epstein-Barr virus latent membrane protein 1 in the growth transformation of human epithelial cells

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Herpesvirus saimiri encodes a functional homolog of the human bcl-2 oncogene

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Epstein-Barr virus BHRF1 protein protects intestine 407 epithelial cells from apoptosis induced by tumor necrosis factor alpha and anti-Fas antibody

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7 January 2021

BHRF1, a viral homologue of the Bcl-2 oncogene, is conserved at both the sequence and functional level in different Epstein-Barr virus isolates

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African swine fever virus gene A179L, a viral homologue of bcl-2, protects cells from programmed cell death

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Bcl-2, Bcl-XL and adenovirus protein E1B19kD are functionally equivalent in their ability to inhibit cell death.

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The adenovirus E4orf6 protein can promote E1A/E1B-induced focus formation by interfering with p53 tumor suppressor function

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The large E1B protein together with the E4orf6 protein target p53 for active degradation in adenovirus infected cells

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7 January 2021

ONYX-015, an E1B gene-attenuated adenovirus, causes tumor-specific cytolysis and antitumoral efficacy that can be augmented by standard chemotherapeutic agents

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7 January 2021

The hepatitis B virus X gene induces p53-mediated programmed cell death

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7 January 2021

Hepatitis B virus HBx protein sensitizes cells to apoptotic killing by tumor necrosis factor alpha

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The hepatitis B virus X protein enhances the DNA binding potential and transcription efficacy of bZip transcription factors

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Destabilization of the RB tumor suppressor protein and stabilization of p53 contribute to HPV type 16 E7-induced apoptosis

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Suppression of interleukin-1beta converting enzyme (ICE)-induced apoptosis by SV40 large T antigen

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Abrogation of a mitotic checkpoint by E2 proteins from oncogenic human papillomaviruses correlates with increased turnover of the p53 tumor suppressor protein.

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Transforming potential of the herpesvirus oncoprotein MEQ: morphological transformation, serum-independent growth, and inhibition of apoptosis.

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Activation of the IFN-inducible enzyme RNase L causes apoptosis of animal cells.

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Interferon action and apoptosis are defective in mice devoid of 2',5'-oligoadenylate-dependent RNase L

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A double-stranded RNA-activated protein kinase-dependent pathway mediating stress-induced apoptosis

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The apoptosis pathway triggered by the interferon-induced protein kinase PKR requires the third basic domain, initiates upstream of Bcl-2, and involves ICE-like proteases

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Complementation of deletion of the vaccinia virus E3L gene by the Escherichia coli RNase III gene

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Even viruses can learn to cope with stress

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Ultraviolet-induced cell death blocked by a selenoprotein from a human dermatotropic poxvirus.

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The herpes simplex virus 1 protein kinase US3 is required for protection from apoptosis induced by the virus

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E4orf4, a novel adenovirus death factor that induces p53-independent apoptosis by a pathway that is not inhibited by zVAD-fmk

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Herpes simplex virus 1 induces and blocks apoptosis at multiple steps during infection and protects cells from exogenous inducers in a cell-type-dependent manner

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Identifiers

DOI

1 reference

21 May 2018

release_q5nezu6mlrgyjpa4qiofq7sej4

Fatcat ID

1 reference

Fatcat

https://api.fatcat.wiki/v0/release/q5nezu6mlrgyjpa4qiofq7sej4

24 November 2022

mapped directly with Wikidata item

PubMed ID

9722918

1 reference

21 May 2018