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פותח על ידי קלירמאש פתרונות בע"מ -
Spodoptera littoralis caspase-1, a Lepidopteran effector caspase inducible by apoptotic signaling
Year:
2005
Source of publication :
apoptosis (source)
Authors :
צ'חנובסקי, נור
;
.
Volume :
10
Co-Authors:
Liu, Q., Entomology Department, Institute of Plant Protection, Volcani Center, POB 6, Bet Dagan, 50250, Israel, College of Life Sciences, Wuhan University, Wuhan 430072, China
Qi, Y., College of Life Sciences, Wuhan University, Wuhan 430072, China
Chejanovsky, N., Entomology Department, Institute of Plant Protection, Volcani Center, POB 6, Bet Dagan, 50250, Israel
Facilitators :
From page:
787
To page:
795
(
Total pages:
9
)
Abstract:
The baculovirus Autographa californica multiple nucleopolyhedrovirus (AcMNPV) can successfully infect Spodoptera frugiperda SF9 cells, but in contrast, in Spodoptera littoralis SL2 cells it induces apoptosis aborting the infection. To understand better the mechanism of induction and execution of apoptosis in SL2 cells, we identified and characterized the first Spodoptera littoralis caspase, Sl-caspase-1. Sl-caspase-1 is an effector caspase that cleaves DEVD but not IETD and LEHD substrates, and the caspase-3 inhibitor DQMD-CHO inhibited this activity. It was involved in two apoptotic pathways induced by UV irradiation and virus infection. Moreover processing of Sl-caspase-1 was a determinant factor for baculovirus induction of apoptosis in SL2 cells. Since very little is known on the regulation of expression of Lepidopteran caspases, we studied Sl-caspase-1 expression after exposure to apoptosis stimuli. We found that triggering apoptosis in SL2 cells increased the steady-state level of Sl-caspase-1 without changing the level of sl-caspase-1 mRNA, suggesting that Sl-caspase-1 was post-transcriptionally up regulated. This regulation might occur as an early event in transduction of the apoptotic signal. © 2005 Springer Science + Business Media, Inc.
Note:
Related Files :
Animals
ultraviolet radiation
עוד תגיות
תוכן קשור
More details
DOI :
10.1007/s10495-005-0365-x
Article number:
0
Affiliations:
Database:
סקופוס
Publication Type:
מאמר
;
.
Language:
אנגלית
Editors' remarks:
ID:
32064
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 01:07
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Scientific Publication
Spodoptera littoralis caspase-1, a Lepidopteran effector caspase inducible by apoptotic signaling
10
Liu, Q., Entomology Department, Institute of Plant Protection, Volcani Center, POB 6, Bet Dagan, 50250, Israel, College of Life Sciences, Wuhan University, Wuhan 430072, China
Qi, Y., College of Life Sciences, Wuhan University, Wuhan 430072, China
Chejanovsky, N., Entomology Department, Institute of Plant Protection, Volcani Center, POB 6, Bet Dagan, 50250, Israel
Spodoptera littoralis caspase-1, a Lepidopteran effector caspase inducible by apoptotic signaling
The baculovirus Autographa californica multiple nucleopolyhedrovirus (AcMNPV) can successfully infect Spodoptera frugiperda SF9 cells, but in contrast, in Spodoptera littoralis SL2 cells it induces apoptosis aborting the infection. To understand better the mechanism of induction and execution of apoptosis in SL2 cells, we identified and characterized the first Spodoptera littoralis caspase, Sl-caspase-1. Sl-caspase-1 is an effector caspase that cleaves DEVD but not IETD and LEHD substrates, and the caspase-3 inhibitor DQMD-CHO inhibited this activity. It was involved in two apoptotic pathways induced by UV irradiation and virus infection. Moreover processing of Sl-caspase-1 was a determinant factor for baculovirus induction of apoptosis in SL2 cells. Since very little is known on the regulation of expression of Lepidopteran caspases, we studied Sl-caspase-1 expression after exposure to apoptosis stimuli. We found that triggering apoptosis in SL2 cells increased the steady-state level of Sl-caspase-1 without changing the level of sl-caspase-1 mRNA, suggesting that Sl-caspase-1 was post-transcriptionally up regulated. This regulation might occur as an early event in transduction of the apoptotic signal. © 2005 Springer Science + Business Media, Inc.
Scientific Publication
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