Potter and Patron in Classical Athens. By T. B. L. Webster. 8½ × 5½. Pp. xvi + 312 + 16 pls. London: Methuen, 1972. £5.

Cook, B. F.

doi:10.1017/s0003581500030158

Cited by 2 publications

(2 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…45). The E1A gene product of adenovirus sensitizes infected cells to NK cell killing (46,47), further supporting the hypothesis discussed above that a role for the E3 complex may be to compensate for the increased sensitivity of infected cells to apoptosis induced by other viral genes. Taken together, these data indicate that the inhibition of TRAIL killing by E3-10.4K/14.5K/6.7K may be critical for adenovirus to evade several host cytotoxic effector mechanisms in vivo.…”

Section: Discussionsupporting

confidence: 71%

Three Adenovirus E3 Proteins Cooperate to Evade Apoptosis by Tumor Necrosis Factor-related Apoptosis-inducing Ligand Receptor-1 and -2

Benedict¹,

Norris²,

Prigozy³

et al. 2001

Journal of Biological Chemistry

119

106

View full text Add to dashboard Cite

Adenovirus encodes multiple gene products that regulate proapoptotic cellular responses to viral infection mediated by both the innate and adaptive immune systems. The E3-10.4K and 14.5K gene products are known to modulate the death receptor Fas. In this study, we demonstrate that an additional viral E3 protein, 6.7K, functions in the specific modulation of the two death receptors for tumor necrosis factor-related apoptosisinducing ligand (TRAIL). The 6.7K protein is expressed on the cell surface and forms a complex with the 10.4K and 14.5K proteins, and this complex is sufficient to induce down-modulation of TRAIL receptor-1 and -2 from the cell surface and reverse the sensitivity of infected cells to TRAIL-mediated apoptosis. Down-modulation of TRAIL-R2 by the E3 complex is dependent on the cytoplasmic tail of the receptor, but the death domain alone is not sufficient. These results identify a mechanism for viral modulation of TRAIL receptor-mediated apoptosis and suggest the E3 protein complex has evolved to regulate the signaling of selected cytokine receptors.

show abstract

Section: Discussionsupporting

confidence: 71%

Three Adenovirus E3 Proteins Cooperate to Evade Apoptosis by Tumor Necrosis Factor-related Apoptosis-inducing Ligand Receptor-1 and -2

Benedict¹,

Norris²,

Prigozy³

et al. 2001

Journal of Biological Chemistry

119

106

View full text Add to dashboard Cite

show abstract

“…Our recently published data suggest that the major mechanism through which E1A induces cytolytic susceptibility involves a postrecognition stage in the interaction with killer lymphocytes rather than an E1A effect on target cell recognition (7). Killer cells use two major types of mechanisms to lyse their targets (reviewed in refs.…”

Section: Immunology: Cook Et Almentioning

confidence: 99%

Role of p300-family proteins in E1A oncogene induction of cytolytic susceptibility and tumor cell rejection

Cook

Krantz

Routes

1996

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

The mechanism by which the adenoviral (Ad) E1A oncogene induces cellular susceptibility to lysis by killer lymphocytes involves interactions between its first exon and different second-exon accessory regions. Mutational analysis showed that two first-exon regions-one in the N terminus and one in the conserved region 1 (CR1) domain-are necessary for this activity. E1A complex formation with cellular p300 protein through these first-exon-encoded regions correlated with induction of the cytolytic susceptible phenotype but was only effective in the context of E1A second-exon expression. An E1A first-exon deletion that prevented p300 binding eliminated both oncoprotein-induced cytolytic susceptibility and rejection of transfected sarcoma cells by immunocompetent animals. These results suggest that the E1A oncogene induces cytolytic susceptibility and tumor rejection by interactions with cellular proteins of the p300 family that affect transcription of genes involved in the cellular response to injury inf licted by host killer cells.

show abstract

Potter and Patron in Classical Athens. By T. B. L. Webster. 8½ × 5½. Pp. xvi + 312 + 16 pls. London: Methuen, 1972. £5.

Cited by 2 publications

References 0 publications

Three Adenovirus E3 Proteins Cooperate to Evade Apoptosis by Tumor Necrosis Factor-related Apoptosis-inducing Ligand Receptor-1 and -2

Three Adenovirus E3 Proteins Cooperate to Evade Apoptosis by Tumor Necrosis Factor-related Apoptosis-inducing Ligand Receptor-1 and -2

Role of p300-family proteins in E1A oncogene induction of cytolytic susceptibility and tumor cell rejection

Contact Info

Product

Resources

About