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Drug-Target Interaction

Drug

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PubChem ID:1701
Structure:
Synonyms:
34284-75-8
35452-30-3
4-(2-Aminoethyl)benzenesulfonyl fluoride
4-(2-Aminoethyl)benzenesulfonyl fluoride hydrochloride
4-(2-Aminoethyl)benzenesulfonylfluoride
4-beta-Aminoethylbenzolsulfofluoride
AC1L1C1L
AC1Q4OX1
AEBSF
AES
AIDS-122624
AIDS122624
AR-1F5821
Benzenesulfonyl fluoride, 4-(2-aminoethyl)-
C002010
C8H10FNO2S
CCG-204227
CHEBI:40582
CHEMBL1096339
DB07347
Lopac-A-8456
Lopac0_000132
LS-174460
NCGC00015097-01
NCGC00015097-02
NCGC00015097-03
NCGC00162071-01
Pefabloc
[4-(2-Aminoethyl)-benzenesulphonyl fluoride]

Target

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Uniprot ID:ICE_DROME
Synonyms:
Caspase
drICE
EC-Numbers:3.4.22.-
Organism:Drosophila melanogaster
Fruit fly
PDB IDs:-

Binding Affinities:

Ki: Kd:Ic 50:Ec50/Ic50:
----

References:

14502243
A serine protease is involved in the initiation of DNA damage-induced apoptosis.. E C de Bruin; D Meersma; J de Wilde; I den Otter; E M Schipper; J P Medema; L T C Peltenburg (2003) Cell death and differentiation display abstract
Caspases are considered to be the key effector proteases of apoptosis. Initiator caspases cleave and activate downstream executioner caspases, which are responsible for the degradation of numerous cellular substrates. We studied the role of caspases in apoptotic cell death of a human melanoma cell line. Surprisingly, the pancaspase inhibitor zVAD-fmk was unable to block cleavage of poly(ADP-ribose) polymerase (PARP) after treatment with etoposide, while it did prevent DEVDase activity. It is highly unlikely that caspase-2, which is a relatively zVAD-fmk-resistant caspase, is mediating etoposide-induced PARP cleavage, as a preferred inhibitor of this caspase could not prevent cleavage. In contrast, caspase activation and PARP degradation were blocked by pretreatment of the cells with the serine protease inhibitor 4-(2-aminoethyl)benzenesulfonyl fluoride (AEBSF). We therefore conclude that a serine protease regulates an alternative initiation mechanism that leads to caspase activation and PARP cleavage. More importantly, while zVAD-fmk could not rescue melanoma cells from etoposide-induced death, the combination with AEBSF resulted in substantial protection. This indicates that this novel pathway fulfills a critical role in the execution of etoposide-induced programmed cell death.