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Ubiquitin Specific Peptidase 16 ( USP16 ) has been reported to contribute to somatic stem-cell defects in Down syndrome. However, how this gene being regulated is largely unknown. To study the mechanism underlying  USP16  gene expression,  USP16  gene promoter was cloned and analyzed by luciferase assay. We identified that the 5′ flanking region (− 1856 bp ~ + 468 bp) of the human  USP16  gene contained the functional promotor to control its transcription. Three bona fide NFκB binding sites were found in  USP16  promoter. We showed that p65 overexpression enhanced endogenous  USP16  mRNA level. Furthermore, LPS and TNFα, strong activators of the NFκB pathway, upregulated the  USP16  transcription. Our data demonstrate that  USP16  gene expression is tightly regulated at transcription level. NFκB signaling regulates the human  USP16  gene expression through three  cis -acting elements. The results provide novel insights into a potential role of dysregulation of  USP16  expression in Alzheimer’s dementia in Down Syndrome.

Transcriptional activation of USP16 gene expression by NFκB signaling