2003
DOI: 10.1099/vir.0.19163-0
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Dengue virus M protein contains a proapoptotic sequence referred to as ApoptoM

Abstract: The induction of apoptotic cell death is a prominent cytopathic effect of dengue (DEN) viruses. One of the key questions to be addressed is which viral components induce apoptosis in DEN virus-infected cells. This study investigated whether the small membrane (M) protein was involved in the induction of apoptosis by DEN virus. This was addressed by using a series of enhanced green fluorescent protein-fused DEN proteins. Evidence is provided that intracellular production of the M ectodomains (residues M-1 to M-… Show more

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Cited by 75 publications
(67 citation statements)
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“…Analyses of the amino acid sequences revealed a substitution at residue prM29 (Ala→Val) in various strains of the study, suggesting that this position may be a hot spot for mutations. dos Santos et al (2002) also identified changes at this position.Furthermore, Catteau et al (2003) reported that the M ectodomain is involved in the induction of apoptosis by the four DENV serotypes, suggesting that exporting the M ectodomain from the Golgi apparatus to the plasma membrane is essential for the initiation of apoptosis by the Fig. 1: differences of amino acids among the gene E sequences of Brazilian dengue virus serotype 1 (DENV-1) compared among themselves and with the FGA/89 DENV-1 strain (French Guiana).…”
mentioning
confidence: 99%
“…Analyses of the amino acid sequences revealed a substitution at residue prM29 (Ala→Val) in various strains of the study, suggesting that this position may be a hot spot for mutations. dos Santos et al (2002) also identified changes at this position.Furthermore, Catteau et al (2003) reported that the M ectodomain is involved in the induction of apoptosis by the four DENV serotypes, suggesting that exporting the M ectodomain from the Golgi apparatus to the plasma membrane is essential for the initiation of apoptosis by the Fig. 1: differences of amino acids among the gene E sequences of Brazilian dengue virus serotype 1 (DENV-1) compared among themselves and with the FGA/89 DENV-1 strain (French Guiana).…”
mentioning
confidence: 99%
“…En el presente trabajo, la infección con el DENV-2 causó un evidente efecto citopático en los cultivos de neuroblastoma, así como pérdida de viabilidad, la cual fue más evidente cuando se usó una mayor multiplicidad de infección. La evaluación morfológica y las pruebas TUNEL evidenciaron el proceso de muerte celular por apoptosis desde una fase muy temprana de la infección, lo cual se corroboró con el patrón de degradación del ADN y la marcación con anexina V, en concordancia con lo reportado en modelos de ratón con neuroinfección por dengue (13) y en otras líneas neuronales (34)(35)(36)(37)(38). Aunque anteriormente Lee, et al (39) reportaron que en células de neuroblastoma de ratón la infección con el DENV activaba un mecanismo anti-apoptótico dependiente de la vía PI3K/Akt, al parecer esto no sucede en las células SH-SY5Y.…”
Section: Discussionunclassified
“…Esto sugiere que la participación del TNF-α autocrino en la mortalidad celular observada sería solo parcialmente responsable de la apoptosis, lo cual indicaría la participación de otros mecanismos inductores de muerte presentes durante la infección in vitro. En este sentido, se han reportado nueve aminoácidos del extremo C-terminal de la proteína M del DENV como necesarios y suficientes para la inducción de apoptosis en células de neuroblastoma en el ratón por la acción de un mecanismo dependiente de la vía mitocondrial (34). La ausencia de la caspasa 8 en el modelo indica una tendencia hacia un débil efecto apoptótico dependiente del TNF-α endógeno producido por los cultivos infectados, y hacia una mayor relevancia de otros mecanismos inductores de muerte que deben ser investigados.…”
Section: Discussionunclassified
“…The flavivirus prM/M protein was also shown to interact with mammalian and mosquito host factors (36)(37)(38)(39)(40)(41), thus indicating that this small protein may be involved in additional nonstructural aspects of the flavivirus infectious cycle. Notably, a peptide identified in flavivirus M proteins was shown to potently trigger apoptosis in mammalian cells (42,43). This proapoptotic phenotype could be alleviated once the residue located at position 36 in the M protein (M-36) of wild-type yellow fever virus (YFV) or DV serotype 2 (DV2), i.e., a leucine or an isoleucine (Fig.…”
mentioning
confidence: 99%
“…This proapoptotic phenotype could be alleviated once the residue located at position 36 in the M protein (M-36) of wild-type yellow fever virus (YFV) or DV serotype 2 (DV2), i.e., a leucine or an isoleucine (Fig. 1B), respectively, was mutated to a phenylalanine (42). The residue M-36 lies on the hydrophobic side of the amphipathic helix (Fig.…”
mentioning
confidence: 99%