@article{KuznetsovAlmuzzainiKritikouetal.2017,
  author    = {Kuznetsov, Nikolai V. and Almuzzaini, Bader and Kritikou, Joanna S. and Baptista, Marisa A. P. and Oliveira, Mariana M. S. and Keszei, Marton and Snapper, Scott B. and Percipalle, Piergiorgio and Westerberg, Lisa S.},
  title     = {Nuclear Wiskott-Aldrich syndrome protein co-regulates T cell factor 1-mediated transcription in T cells},
  series = {Genome Medicine},
  volume    = {9},
  journal   = {Genome Medicine},
  doi       = {10.1186/s13073-017-0481-6},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-173486},
  year      = {2017},
  abstract  = {Background The Wiskott-Aldrich syndrome protein (WASp) family of actin-nucleating factors are present in the cytoplasm and in the nucleus. The role of nuclear WASp for T cell development remains incompletely defined. Methods We performed WASp chromatin immunoprecipitation and deep sequencing (ChIP-seq) in thymocytes and spleen CD4\(^+\) T cells. Results WASp was enriched at genic and intergenic regions and associated with the transcription start sites of protein-coding genes. Thymocytes and spleen CD4\(^+\) T cells showed 15 common WASp-interacting genes, including the gene encoding T cell factor (TCF)12. WASp KO thymocytes had reduced nuclear TCF12 whereas thymocytes expressing constitutively active WASp\(^{L272P}\) and WASp\(^{I296T}\) had increased nuclear TCF12, suggesting that regulated WASp activity controlled nuclear TCF12. We identify a putative DNA element enriched in WASp ChIP-seq samples identical to a TCF1-binding site and we show that WASp directly interacted with TCF1 in the nucleus. Conclusions These data place nuclear WASp in proximity with TCF1 and TCF12, essential factors for T cell development.},
  language  = {en}
}
@article{BaptistaKeszeiOliveiraetal.2016,
  author    = {Baptista, Marisa A.P. and Keszei, Marton and Oliveira, Mariana and Sunahara, Karen K.S. and Andersson, John and Dahlberg, Carin I.M. and Worth, Austen J. and Lied{\´e}n, Agne and Kuo, I-Chun and Wallin, Robert P.A. and Snapper, Scott B. and Eidsmo, Liv and Scheynius, Annika and Karlsson, Mikael C.I. and Bouma, Gerben and Burns, Siobhan O. and Forsell, Mattias N.E. and Thrasher, Adrian J. and Nyl{\´e}n, Susanne and Westerberg, Lisa S.},
  title     = {Deletion of Wiskott-Aldrich syndrome protein triggers Rac2 activity and increased cross-presentation by dendritic cells},
  series = {Nature Communications},
  volume    = {7},
  journal   = {Nature Communications},
  doi       = {10.1038/ncomms12175},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-165966},
  pages     = {12175},
  year      = {2016},
  abstract  = {Wiskott-Aldrich syndrome (WAS) is caused by loss-of-function mutations in theWASp gene. Decreased cellular responses in WASp-deficient cells have been interpreted to mean that WASp directly regulates these responses in WASp-sufficient cells. Here, we identify an exception to this concept and show that WASp-deficient dendritic cells have increased activation of Rac2 that support cross-presentation to CD8þ T cells. Using two different skin pathology models, WASp-deficient mice show an accumulation of dendritic cells in the skin and increased expansion of IFNg-producing CD8þ T cells in the draining lymph node and spleen. Specific deletion of WASp in dendritic cells leads to marked expansion of CD8þ T cells at the expense of CD4þ T cells. WASp-deficient dendritic cells induce increased cross-presentation to CD8þ T cells by activating Rac2 that maintains a near neutral pH of phagosomes. Our data reveals an intricate balance between activation of WASp and Rac2 signalling pathways in dendritic cells.},
  language  = {en}
}