Apoptosis, or cell death program, can be activated by various mechanisms within the extrinsic and the intrinsic pathway. While activation of cell death receptors leads to the engagement of the extrinsic pathway, the intrinsic pathway is activated by mitochondria during cellular stress, both
resulting in an activation of caspases.
In the present pathway we emphasized the activation of caspases by those two pathways in pancreatic cancer (PDAC) cells. Please notice, that PDAC cells are so called type-II cells. In these cells the activation of cell death receptors is not sufficient to activated caspases. By cleavage of Bid, type-II cells activate the intrinsic pathway as "amplification loop".
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GenMAPP notes
Rأ¼ckert F et al. Examination of Apoptosis Signaling in Pancreatic Cancer by Computational Signal Transduction Analysis.
PLoS ONE, 2010. 5: e12243
GenMAPP remarks
Arrows: activation, broken arrows: inhibtion
HomologyConvert
This pathway was inferred from Homo sapiens pathway WP1772(80459) with a 90.0% conversion rate.
Rأ¼ckert F, Dawelbait G, Winter C, Hartmann A, Denz A, Ammerpohl O, Schroeder M, Schackert HK, Sipos B, Klأ¶ppel G, Kalthoff H, Saeger HD, Pilarsky C, Grأ¼tzmann R; ''Examination of apoptosis signaling in pancreatic cancer by computational signal transduction analysis.''; PLoS One, 2010 PubMedEurope PMCScholia
Mott JL, Kobayashi S, Bronk SF, Gores GJ; ''mir-29 regulates Mcl-1 protein expression and apoptosis.''; Oncogene, 2007 PubMedEurope PMCScholia
PLoS ONE, 2010. 5: e12243
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