NF-κB activation with aging: Characterization and therapeutic inhibition

Jing Zhao, Xuesen Li, Sara McGowan, Laura J. Niedernhofer, Paul D. Robbins

Research output: Contribution to journalArticle

9 Scopus citations


Aging is a condition characterized by progressive decline in tissue homeostasis due, at least in part, to the accumulation of replicative, oxidative, and genotoxic stress over time. The activity of the transcription factor NF-κB is upregulated in both naturally aged mice and multiple progeroid mouse models of accelerated aging. Suppressing NF-κB activity genetically or pharmacologically has been shown to delay the onset and progression of aging pathology and therefore prolong the healthspan in progeroid mouse models. Here, we describe the methods for measuring aging endpoints along with NF-κΒ activation in mice, as well as after pharmacologic intervention to prevent NF-κB activation using a NEMO-binding domain (NBD)–protein transduction domain (PTD) fusion peptide.

Original languageEnglish (US)
Pages (from-to)543-557
Number of pages15
JournalMethods in Molecular Biology
StatePublished - Jan 1 2015
Externally publishedYes


  • Aging
  • Aging endpoints
  • Mouse model of aging
  • NF-κB
  • Progeria
  • Stress response

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