Apoptosis induced by Semliki Forest virus is RNA replication dependent and mediated via Bak. (Q39844204)

15 September 2017

Apoptosis induced by Semliki Forest virus is RNA replication dependent and mediated via Bak. (English)

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15 September 2017

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C Urban

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C Rhême

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S Maerz

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B Berg

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R Pick

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R Nitschke

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C Borner

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language of work or name

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25 April 2008

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Cell Death & Differentiation

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15

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1396-1407

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https://scigraph.springernature.com/pub.10.1038/cdd.2008.61

15 September 2017

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Neurovirulent strains of Alphavirus induce apoptosis in bcl-2-expressing cells: role of a single amino acid change in the E2 glycoprotein

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Sindbis virus: an efficient, broad host range vector for gene expression in animal cells

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Death receptor-induced cell killing

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Life in the balance: how BH3-only proteins induce apoptosis.

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Proapoptotic Bak is sequestered by Mcl-1 and Bcl-xL, but not Bcl-2, until displaced by BH3-only proteins

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Cell death provoked by loss of interleukin-3 signaling is independent of Bad, Bim, and PI3 kinase, but depends in part on Puma

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BH3 domains of BH3-only proteins differentially regulate Bax-mediated mitochondrial membrane permeabilization both directly and indirectly

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The pathophysiology of mitochondrial cell death

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Bid, a Bcl2 interacting protein, mediates cytochrome c release from mitochondria in response to activation of cell surface death receptors

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Viral proteins targeting mitochondria: controlling cell death

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Near death experiences: poxvirus regulation of apoptotic death

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Sendai virus infection induces apoptosis through activation of caspase-8 (FLICE) and caspase-3 (CPP32).

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bcl-2 acts early to restrict Semliki Forest virus replication and delays virus-induced programmed cell death

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Protection against fatal Sindbis virus encephalitis by beclin, a novel Bcl-2-interacting protein

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Induction of Bad-mediated apoptosis by Sindbis virus infection: involvement of pro-survival members of the Bcl-2 family

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Alphaviruses induce apoptosis in Bcl-2-overexpressing cells: evidence for a caspase-mediated, proteolytic inactivation of Bcl-2.

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vFLIP protects PC-12 cells from apoptosis induced by Sindbis virus: implications for the role of TNF-alpha

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Induction of apoptosis by Sindbis virus occurs at cell entry and does not require virus replication.

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Protein kinase PKR plays a stimulus- and virus-dependent role in apoptotic death and virus multiplication in human cells

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A single amino acid change in the nuclear localization sequence of the nsP2 protein affects the neurovirulence of Semliki Forest virus

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The combined functions of proapoptotic Bcl-2 family members bak and bax are essential for normal development of multiple tissues

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7 January 2021

Caspase-6 is the direct activator of caspase-8 in the cytochrome c-induced apoptosis pathway: absolute requirement for removal of caspase-6 prodomain

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7 January 2021

Apoptosis induction by caspase-8 is amplified through the mitochondrial release of cytochrome c.

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7 January 2021

Mitochondria as the central control point of apoptosis

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VDAC2 inhibits BAK activation and mitochondrial apoptosis

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The mitochondrial protein Bak is pivotal for gliotoxin-induced apoptosis and a critical host factor of Aspergillus fumigatus virulence in mice

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Bak but not Bax is essential for Bcl-xS-induced apoptosis

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Inhibition of virus-induced neuronal apoptosis by Bax.

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A single amino acid change in the E2 spike protein of a virulent strain of Semliki Forest virus attenuates pathogenicity

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7 January 2021

Sindbis virus nonstructural protein nsP2 is cytotoxic and inhibits cellular transcription

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7 January 2021

Rapid turnover of mcl-1 couples translation to cell survival and apoptosis

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7 January 2021

Intracellular pattern recognition receptors in the host response

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7 January 2021

Serine proteases mediate apoptosis-like cell death and phagocytosis under caspase-inhibiting conditions.

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7 January 2021

Identifiers

DOI

10.1038/CDD.2008.61

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Dimensions Publication ID

15 September 2017

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