High impact information on AY078069

• IkappaBNS protein intrinsically forces Foxp3 induction during development of regulatory T (Treg) cells via binding to conserved non-coding sequences of the Foxp3 locus. Thus, IkappaBNS-deficient mice develop less Treg cells [1].
• Although their number is reduced, the suppressive function of mature IkappaBNS-deficient Treg cells is not affected [1].
• Thus, IkappaBNS regulates inflammatory responses by inhibiting the induction of a subset of TLR-dependent genes through modulation of NF-kappaB activity [2].
• IkappaBNS-deficient macrophages and dendritic cells show increased TLR-mediated expression of genes such as IL-6 and IL-12p40, which are induced late after TLR stimulation [2].
• IkappaBNS inhibits induction of a subset of Toll-like receptor-dependent genes and limits inflammation [2].
• In contrast, IkappaBNS-deficient cells showed normal induction of genes that are induced early or induced via IRF-3 activation [2].
• These genes included nuclear IkappaB proteins such as Bcl-3 and IkappaBNS [3].

Anatomical context of AY078069

• Thus, IkappaBNS selectively suppresses LPS-induced IL-6 production in macrophages [3].

Physical interactions of AY078069

• 7. IkappaBNS expression led to constitutive and intense DNA binding of NF-kappaB p50/p50 homodimers [3].

Regulatory relationships of AY078069

• The nuclear IkappaB protein IkappaBNS selectively inhibits lipopolysaccharide-induced IL-6 production in macrophages of the colonic lamina propria [3].

Other interactions of AY078069

• Here, we show that IkappaBNS, a TLR-inducible nuclear IkappaB protein, negatively regulates induction of a subset of TLR-dependent genes through inhibition of NF-kappaB activity [2].

References