Characterization of a nonstructural phosphoprotein of two orbiviruses

Devaney, M A; Kendall, Joe; Grubman, Marvin J.

doi:10.1016/0168-1702(88)90040-8

Cited by 45 publications

(26 citation statements)

References 23 publications

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“…Previous ®ndings have indicated that eIF4G is susceptible to rapid cleavage and disappearance of the full length protein, not only in picornavirusinfected cells Devaney et al, 1988;Kirchweger et al, 1994;Ziegler et al, 1995a) but also in uninfected HeLa cells following antisense RNAmediated down-regulation of eIF4E (De Benedetti et al, 1991), in brain following ischaemia and reperfusion (DeGracia et al, 1996), in erythroleukaemia cells induced to di erentiate with haemin (Benton et al, 1996) and in yeast subjected to nutritional deprivation (Berset et al, 1998). Thus eIF4G seems particularly susceptible to degradation, probably by a number of di erent proteolytic pathways depending on the cell type and stimulus.…”

Section: Discussionmentioning

confidence: 99%

Degradation of eukaryotic polypeptide chain initiation factor (eIF) 4G in response to induction of apoptosis in human lymphoma cell lines

1998

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We have investigated the e ect of inducing apoptosis in BJAB and Jurkat cells on the cellular content of several polypeptide chain initiation factors. Serum deprivation results in inhibition of protein synthesis and induction of apoptosis in BJAB cells; at early times, there is selective degradation of polypeptide initiation factor eIF4G but no major losses of other key initiation factors. The disappearance of full length eIF4G is accompanied by the appearance of smaller forms of the protein, including a major product of approximately 76 kDa. Apoptosis induced by cycloheximide results in similar e ects. Both total cytoplasmic eIF4G and eIF4G associated with eIF4E are degraded with a half-life of 2 ± 4 h under these conditions. Treatment of serum-starved or cycloheximide-treated cells with Z-VAD.FMK or Z-DEVD.FMK, which inhibit caspases required for apoptosis, protects eIF4G from degradation and blocks the appearance of the ca. 76 kDa product. Exposure of BJAB cells to rapamycin rapidly inhibits protein synthesis but does not lead to acute degradation of eIF4G. In both BJAB and Jurkat cells induction of apoptosis with anti-Fas antibody or etoposide also results in the selective loss of eIF4G, which is inhibitable by Z-VAD.FMK. These data suggest that eIF4G is selectively targeted for cleavage as cells undergo apoptosis and is a substrate for proteases activated during this process.

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Section: Discussionmentioning

confidence: 99%

Degradation of eukaryotic polypeptide chain initiation factor (eIF) 4G in response to induction of apoptosis in human lymphoma cell lines

1998

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“…VP2 is the protein that has most responsibility for antigenic variation [21,72,130]. At least three non-structural proteins have been identified in infected cells (NS1, 2 and 3/3a) [28,60,69].…”

Section: Aetiologymentioning

confidence: 99%

African horse sickness

2004

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-African horse sickness virus (AHSV) causes a non-contagious, infectious insect-borne disease of equids and is endemic in many areas of sub-Saharan Africa and possibly Yemen in the Arabian Peninsula. However, periodically the virus makes excursions beyond its endemic areas and has at times extended as far as India and Pakistan in the east and Spain and Portugal in the west. The vectors are certain species of Culicoides biting midge the most important of which is the AfroAsiatic species C. imicola. This paper describes the effects that AHSV has on its equid hosts, aspects of its epidemiology, and present and future prospects for control. The distribution of AHSV seems to be governed by a number of factors including the efficiency of control measures, the presence or absence of a long term vertebrate reservoir and, most importantly, the prevalence and seasonal incidence of the major vector which is controlled by climate. However, with the advent of climatechange the major vector, C. imicola, has now significantly extended its range northwards to include much of Portugal, Spain, Italy and Greece and has even been recorded from southern Switzerland. Furthermore, in many of these new locations the insect is present and active throughout the entire year. With the related bluetongue virus, which utilises the same vector species of Culicoides this has, since 1998, precipitated the worst outbreaks of bluetongue disease ever recorded with the virus extending further north in Europe than ever before and apparently becoming endemic in that continent. The prospects for similar changes in the epidemiology and distribution of AHSV are discussed.

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“…Three non-structural proteins, NS1, NS2 and NS3/NS3a, have also been identified in BTVinfected cells (Mertens et al, 1984;Van Dijk & Huismans, 1988). NS2 is the only virus protein that is phosphorylated (Huismans et al, 1987;Devaney et al, 1988) and has also been reported to be associated with the outer capsid layer of purified virus particles (Mertens The nucleotide sequence data reported in this paper will appear in the DDBJ, EMBL and GenBank Nucleotide Sequence Databases under accession number D10905. et al, 1987).…”

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confidence: 99%