CASP8-associated protein 2

Definition:

Participates in TNF-alpha-induced blockade of glucocorticoid receptor (GR) transactivation at the nuclear receptor coactivator level, upstream and independently of NF-kappa-B. Suppresses both NCOA2- and NCOA3-induced enhancement of GR transactivation. Involved in TNF-alpha-induced activation of NF-kappa-B via a TRAF2-dependent pathway. Acts as a downstream mediator for CASP8-induced activation of NF-kappa-B. Required for the activation of CASP8 in FAS-mediated apoptosis. Required for histone gene transcription and progression through S phase.

References:

[1]. Tomoshige Kino, et al. Tumor necrosis factor alpha receptor- and Fas-associated FLASH inhibit transcriptional activity of the glucocorticoid receptor by binding to and interfering with its interaction with p160 type nuclear receptor coactivators. J Biol Chem. 2003 Jan 31;278(5):3023-9. [Content Brief]

[2]. D Barcaroli, et al. FLASH is required for histone transcription and S-phase progression. Proc Natl Acad Sci U S A. 2006 Oct 3;103(40):14808-12. [Content Brief]

[3]. Kristijana Milovic-Holm, et al. FLASH links the CD95 signaling pathway to the cell nucleus and nuclear bodies. EMBO J. 2007 Jan 24;26(2):391-401. [Content Brief]

[4]. Tomoshige Kino, et al. FLASH interacts with p160 coactivator subtypes and differentially suppresses transcriptional activity of steroid hormone receptors. J Steroid Biochem Mol Biol. 2004 Dec;92(5):357-63. [Content Brief]

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