| Name | caspases (protein family or complex) |
|---|---|
| Synonyms | caspase; caspases |
| Name | acrolein |
|---|---|
| CAS | 2-propenal |
| PubMed | Abstract | RScore(About this table) | |
|---|---|---|---|
| 19596284 | Roy J, Pallepati P, Bettaieb A, Tanel A, Averill-Bates DA: Acrolein induces a cellular stress response and triggers mitochondrial apoptosis in A549 cells. Chem Biol Interact. 2009 Oct 7;181(2):154-67. Epub 2009 Jul 9. Acrolein (10-50microM) triggered later stage processes such as activation of caspases-3, -7 and -6, externalization and cleavage of poly (ADP) polymerase after longer times (2h). |
81(1,1,1,1) | Details |
| 15843039 | Tanel A, Averill-Bates DA: The acrolein induces apoptosis via activation of the mitochondrial pathway. Biochim Biophys Acta. 2005 Apr 15;1743(3):255-67. Epub 2005 Jan 5. The activation of caspases-9 and -7 was confirmed by the cleavage of their pro-enzyme form by acrolein. |
31(0,1,1,1) | Details |
| 11803030 | Kern JC, Kehrer JP: Acrolein-induced cell death: a caspase-influenced decision between apoptosis and oncosis/necrosis. Chem Biol Interact. 2002 Jan 22;139(1):79-95. |
15(0,0,2,5) | Details |
| 16040627 | Finkelstein EI, Ruben J, Koot CW, Hristova M, van der Vliet A: Regulation of constitutive neutrophil apoptosis by the alpha,beta-unsaturated aldehydes acrolein and Am J Physiol Lung Cell Mol Physiol. 2005 Dec;289(6):L1019-28. Epub 2005 Jul 22. However, procaspase-3 processing was also prevented, because of inhibited activation of caspases-9 and -8 under similar conditions, suggesting that ACR (and to a lesser extent HNE) can inhibit both intrinsic (mitochondria dependent) and extrinsic mechanisms of neutrophil apoptosis at initial stages. |
2(0,0,0,2) | Details |
| 16381661 | Desmeules P, Devine PJ: Characterizing the ovotoxicity of cyclophosphamide metabolites on cultured mouse ovaries. Toxicol Sci. 2006 Apr;90(2):500-9. Epub 2005 Dec 28. Furthermore, the cell death pathway is likely caspase-independent. Tissues were cultured up to d8, and then follicle counts and immunohistochemistry were performed. 4-Hydroperoxy-CPA (4-HC), a precursor of an activated form of CPA, and PM depleted primordial and primary follicles (> or =1 microM and > or =3 microM, respectively, p < 0.05); acrolein had effects on follicle numbers only under continuous exposure (> =30 microM); carboxycyclophosphamide and 4-ketocyclophosphamide reduced primordial and small primary follicles only at high concentrations (100 microM). |
1(0,0,0,1) | Details |
| 11723234 | Schwartz PS, Waxman DJ: Cyclophosphamide induces caspase 9-dependent apoptosis in 9L tumor cells. . Mol Pharmacol. 2001 Dec;60(6):1268-79. Cyclophosphamide (CPA), a widely used oxazaphosphorine anti-cancer prodrug, is inactive until it is metabolized by cytochrome P450 to yield phosphoramide mustard and acrolein, which alkylate DNA and proteins, respectively. Caspase 9 was identified as the regulatory upstream caspase activated in 9L cells treated with CPA, MFA, or 4OOH-IFA, implicating the mitochondrial apoptotic pathway in oxazaphosphorine-induced tumor cell death. |
1(0,0,0,1) | Details |
| 19635456 | Gan FF, Chua YS, Scarmagnani S, Palaniappan P, Franks M, Poobalasingam T, Bradshaw TD, Westwell AD, Hagen T: Structure-activity analysis of 2'-modified analogues as potential anticancer agents. Biochem Biophys Res Commun. 2009 Oct 2;387(4):741-7. Epub 2009 Jul 25. Exposure to BCA induced cell death via caspase-dependent and -independent pathways. |
1(0,0,0,1) | Details |