Akirin2-Mediated Transcriptional Control by Recruiting SWI/SNF Complex in B Cells

Crit Rev Immunol. 2016;36(5):395-406. doi: 10.1615/CritRevImmunol.2017019629.


Extensive studies in last decade have demonstrated that dynamic control of gene transcription is key in the regulation of inflammatory responses. Although signaling pathways and transcription factors have a central role, growing evidence for the involvement of chromatin in the regulation of gene expression in immune cells has uncovered an evolutionarily conserved role of pathogen recognition and epigenetic regulation. The substantial potential of these responses to drive pathological inflammation and tissue damage highlights the need for rigorous control of these responses. Recently, an evolutionarily conserved nuclear factor, Akirin2, has been identified as an essential link between nuclear factor-κB and chromatin remodelers for transcriptional regulation in macrophages and B cells. In this review, we discuss current understanding of the molecular mechanisms that have instrumental roles in governing the inflammatory response with special emphasis on Akirin2 in B cells.

Publication types

  • Review

MeSH terms

  • Animals
  • B-Lymphocytes / immunology*
  • Chromatin / metabolism*
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / metabolism*
  • Epigenesis, Genetic
  • Gene Expression Regulation
  • Humans
  • Inflammation / immunology*
  • NF-kappa B / metabolism
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • Signal Transduction
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*


  • ARID1B protein, human
  • Chromatin
  • DNA-Binding Proteins
  • NF-kappa B
  • Transcription Factors
  • ZBTB7A protein, human
  • SNF1-related protein kinases
  • Protein Serine-Threonine Kinases