Divergent transcription of early 35- and 94-kilodalton protein genes encoded by the HindIII K genome fragment of the baculovirus Autographa californica nuclear polyhedrosis virus

Friesen, Paul D.; Miller, Loisk .

doi:10.1128/jvi.61.7.2264-2272.1987

Cited by 130 publications

(61 citation statements)

References 34 publications

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“…Clones with the insert in the two orientations were selected. The sequence of the I'CR product was identical to the p35 seqnence published by Friesen and Miller (1987) (16).…”

Section: Plasmid Constructionsmentioning

confidence: 65%

“…Recent identification of proteins that can block apoptosis may be used as tools to unravel pathways of cell death. The Bcl-2 protooncogene (2,44) is the prototype of these anti-death proteins (1,13,16,24,31,40), and a family of proteins homologous to Bcl-2 is now emerging (for review see reference 49). Among these, the Bcl-X gene is the most homologous to Bcl-2 (6) and encodes two splice variants termed Bcl-X1 and Bcl-Xs.…”

mentioning

confidence: 99%

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Viral proteins E1B19K and p35 protect sympathetic neurons from cell death induced by NGF deprivation.

Martinou¹,

Fernandez²,

Missotten³

et al. 1995

The Journal of Cell Biology

131

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Abstract. To study molecular mechanisms underlying neuronal cell death, we have used sympathetic neurons from superior cervical ganglia which undergo programmed cell death when deprived of nerve growth factor. These neurons have been microinjected with expression vectors containing cDNAs encoding selected proteins to test their regulatory influence over cell death. Using this procedure, we have shown previously that sympathetic neurons can be protected from NGF deprivation by the protooncogene Bcl-2. We now report that the E1B19K protein from adenovirus and the p35 protein from baculovirus also rescue neurons.Other adenoviral proteins, E1A and E1B55K, have no effect on neuronal survival. E1B55K, known to block apoptosis mediated by p53 in proliferative cells, failed to rescue sympathetic neurons suggesting that p53 is not involved in neuronal death induced by NGF deprivation.E1B19K and p35 were also coinjected with Bcl-Xs which blocks Bcl-2 function in lymphoid cells. Although BcI-Xs blocked the ability of Bcl-2 to rescue neurons, it had no effect on survival that was dependent upon expression of E1B19K or p35. p ROGRAMMED cell death plays a key role during development of the nervous system (for review see reference 36), although the molecular mechanisms by which neurons die are unknown. Epigenetic factors, such as neurotrophic factors, seem to promote neuronal survival by blocking an intrinsic cell death program (for review see references 26, 38). Recent identification of proteins that can block apoptosis may be used as tools to unravel pathways of cell death. The Bcl-2 protooncogene (2, 44) is the prototype of these anti-death proteins (1,13,16,24,31,40), and a family of proteins homologous to Bcl-2 is now emerging (for review see reference 49). Among these, the Bcl-X gene is the most homologous to Bcl-2 (6) and encodes two splice variants termed Bcl-X1 and Bcl-Xs. Bcl-Xs lacks a 63-amino acid region that is conserved between different Bel-2 family members. Whereas BcI-X1 has anti-apoptotic function, BclXs inhibits the ability of Bcl-2 to enhance the survival of trophic factor-deprived cells (6).Other anti-apoptotic proteins, with no obvious primary sequence homology with members of the Bcl-2 family, have also been characterized. Among these are the E1B19K and EIB55K proteins from adenovirus and the p35 protein from baculovirus.The first two authors contributed equally to this work.Address all correspondence to Dr. Jean-Claude Martinou, Glaxo Institute for Molecular Biology, 14 Chem des Aulx, 1228 Plan-les-Ouates, Geneva, Switzerland. Tel.: (41) 22 706 The EIB gene encodes two major proteins, the 19-kD and 55-kD proteins which cooperate with E1A proteins to allow transformation (3,5,34,45). Although EIA alone is capable of stimulating cell proliferation, this is accompanied by rapid cell degeneration due to apoptosis. The E1B proteins overcome this effect thereby enhancing cell transformation (47). The 19-kD EIB protein can also block the cytotoxic action of tumor necrosis factor or of anti-FAS antibodies (18...

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“…Clones with the insert in the two orientations were selected. The sequence of the I'CR product was identical to the p35 seqnence published by Friesen and Miller (1987) (16).…”

Section: Plasmid Constructionsmentioning

confidence: 65%

mentioning

confidence: 99%

Viral proteins E1B19K and p35 protect sympathetic neurons from cell death induced by NGF deprivation.

Martinou¹,

Fernandez²,

Missotten³

et al. 1995

The Journal of Cell Biology

131

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“…Insect baculoviruses contain at least two independent genes that promote the survival of the infected host cell, p35 (Friesen and Miller, 1987;Clem et al, 1991;Hershberger et al, 1992Hershberger et al, , 1994Clem and Miller, 1993;Kamita et al, 1993) and iap (Crook et al, 1993;Birnbaum et al, 1994). Recombinant baculoviruses lacking both genes induce accelerated host cell death leading to severely impaired virus production (Clem and Miller, 1994b).…”

Section: Introductionmentioning

confidence: 99%

A conserved family of cellular genes related to the baculovirus iap gene and encoding apoptosis inhibitors.

et al. 1996

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The baculovirus inhibitor of apoptosis gene, iap, can impede cell death in insect cells. Here we show that iap can also prevent cell death in mammalian cells. The ability of iap to regulate programmed cell death in widely divergent species raised the possibility that cellular homologs of iap might exist. Consistent with this hypothesis, we have isolated Drosophila and human genes which encode IAP‐like proteins (dILP and hILP). Like IAP, both dILP and hILP contain amino‐terminal baculovirus IAP repeats (BIRs) and carboxy‐terminal RING finger domains. Human ilp encodes a widely expressed cytoplasmic protein that can suppress apoptosis in transfected cells. An analysis of the expressed sequence tag database suggests that hilp is one of several human genes related to iap. Together these data suggest that iap and related cellular genes play an evolutionarily conserved role in the regulation of apoptosis.

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“…An alternative approach is the engineering of cell lines with genes that code for caspase inhibitors. Three classes of genetic caspase inhibitors dominate: p35 from Autographa californica nuclear polyhedrosis virus, CrmA from cowpox virus, and the diverse IAP family found in numerous organisms, including humans and insects as well as viruses (Clem et al, 1991, Friesen andMiller, 1987;Palumbo et al, 1989, Pickup et al, 1984Ray et al, 1992. This study focuses on CrmA and a prominent member of the inhibitor of apoptosis protein (IAP) family, XIAP.…”

Section: Introductionmentioning

confidence: 99%

Study of caspase inhibitors for limiting death in mammalian cell culture

Sauerwald

Oyler

Betenbaugh

2002

Biotech & Bioengineering

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Apoptosis in mammalian cell culture is associated with decreased bioproduct yields and can be inhibited through altering the intracellular signaling pathways mediating programmed cell death. In this study, we evaluated the capacity to inhibit caspases to maintain high viable cell numbers in CHO and 293 cultures. Two genetic caspase inhibitors, XIAP and CrmA, were examined along with a mutant of each, XIAP-BIR123NC, which contains three BIR domains but lacks the RING finger, and CrmA-DQMD, which has CrmA's pseudosubstrate site replaced with that of another caspase inhibitor, p35. Stable CHO pooled and 293 clonal cell lines expressing each protein were exposed to apoptotic insults, including spent medium, Sindbis virus, and etoposide. For each insult the mutated protein resulted in higher viabilities than its wild-type counterpart. However, the mutants provided different levels of protection, depending on the insult considered. CrmA-DQMD was the preferred inhibitor for spent medium-induced apoptosis, whereas XIAP-BIR123NC conferred better protection for etoposide-induced death. Addition of Z-VAD.fmk to the genetically engineered cells enhanced viabilities in the presence of spent medium or etoposide; however, the largest increases in viability were experienced by the control cells, indicating an overlap in caspase inhibition between the genetic and chemical inhibitors. Finally, parental 293 cells were treated with caspase-8 and -9 inhibitors, Z-IETD.fmk and Z-LEHD.fmk, in concert with spent medium or etoposide exposure. Spent medium-induced death was delayed more readily with the caspase-8 inhibitors, CrmA-DQMD and Z-IETD.fmk, and etoposide-induced death was stalled more so with XIAP-BIR123NC and Z-LEHD.fmk. These results suggest that the apoptosis pathways induced and the level of protection afforded by a particular caspase inhibitor may vary with the insult considered.

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Divergent transcription of early 35- and 94-kilodalton protein genes encoded by the HindIII K genome fragment of the baculovirus Autographa californica nuclear polyhedrosis virus

Cited by 130 publications

References 34 publications

Viral proteins E1B19K and p35 protect sympathetic neurons from cell death induced by NGF deprivation.

Viral proteins E1B19K and p35 protect sympathetic neurons from cell death induced by NGF deprivation.

A conserved family of cellular genes related to the baculovirus iap gene and encoding apoptosis inhibitors.

Study of caspase inhibitors for limiting death in mammalian cell culture

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