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BCL2 — PAWR

Pathways - manually collected, often from reviews:

• OpenBEL Selventa BEL large corpus: BCL2 → PAWR (decreases) Cheema et al., J Biol Chem 2003*
  Evidence: The decrease in the Bcl-2 protein and transcript following all-trans-retinoic acid treatment was accompanied by changes in localization of Par-4 and an induction in the expression of WT1 protein. In stable clones expressing ectopic Par-4 and in ATRA-treated cells, we observed decreased Bcl-2 protein and transcript.

Text-mined interactions from Literome

Chendil et al., Cancer Biol Ther 2002 (Prostatic Neoplasms) : Par-4 , a pro-apoptotic gene, inhibits radiation induced NF kappa B activity and Bcl-2 expression leading to induction of radiosensitivity in human prostate cancer cells PC-3
Cheema et al., J Biol Chem 2003 (Prostatic Neoplasms) : Par-4 transcriptionally regulates Bcl-2 through a WT1 binding site on the bcl-2 promoter ... We conclude that Par-4 regulates Bcl-2 through a WT1 binding site on the bcl-2 promoter
Boehrer et al., Leukemia & lymphoma 2004 (Leukemia, Erythroblastic, Acute) : We further demonstrate that -- in contrast to previous reports in non-AML cells -- Par-4 expression in HEL cells leads to an upregulation of Bcl-2
Qiu et al., Oncogene 1999 (Prostatic Neoplasms) : Constitutive- or regulated- overexpression of Par-4 caused a reduction in the levels of the anti-apoptotic protein Bcl-2