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In addition, expression and translocation of BNIP3 to mitochondria have been reported as the cell death regulatory factors for mitochondrial dysfunction (Zhang and Ney, 2009)

SFN promotes the phosphorylative degradation of -catenin while concurrently suppressing downstream targets including c-Myc and cyclin D1, effectively dismantling the transcriptional program that drives CSC self-renewal (71)

Research focuses on its role as a PepT1 ligand and its ability to modulate NF-B activity within specialized laboratory cell lines

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