ライフサイエンスコーパス: NF-kappaB2

1 NF-kappaB2 is the principal protein involved in the nonc

2 NF-kappaB2-deficient mice have impaired T and B cell res

3 NF-kappaB2/p100 cleavage was abrogated in B cells from A

4 g of NF-kappaB2 p100 to p52, which activates NF-kappaB2 signaling.

5 precursor protein p100 generates the active NF-kappaB2 subunit p52, which in turn transcriptionally

6 or complex and activation of the alternative NF-kappaB2 pathway.

7 Markedly increased cytosolic p100, an NF-kappaB2-inhibitory form, and reduced nuclear NF-kappa

8 inhibit pre-BCR signals through the ATM- and NF-kappaB2-dependent induction of SPIC, a hematopoietic-

9 V on NIK complex formation with IKKalpha and NF-kappaB2 were determined by coimmunoprecipitation assa

10 t BAFF-R results in increased NF-kappaB1 and NF-kappaB2 activity and increased immunoglobulin product

11 NF-kappaB1 and NF-kappaB2 also play a role during the earlier transitio

12 Although NF-kappaB1 and NF-kappaB2 are not absolutely required for survival and

13 ned the relative roles of the NF-kappaB1 and NF-kappaB2 pathways in TCR/CD28 costimulation.

14 ors, IkappaBs, as well as the NF-kappaB1 and NF-kappaB2 precursor proteins, p105 and p100.

15 esting redundant functions of NF-kappaB1 and NF-kappaB2 proteins in the development of this cell line

16 Using mice deficient in both NF-kappaB1 and NF-kappaB2, which are thus partially compromised in both

17 s or the unprocessed forms of NF-kappaB1 and NF-kappaB2.

18 se findings demonstrate that NF-kappaB1- and NF-kappaB2-mediated signaling pathways differentially re

19 xpel infection, NF-kappaB1 knockout (KO) and NF-kappaB2 KO mice developed chronic infections associat

20 of progrowth genes, such as c-MYC, MDR1, and NF-kappaB2.

21 NF-kappaB1 (p50 and its precursor p105), and NF-kappaB2 (p52 and its precursor p100), plays a central

22 clude Rel-A, c-Rel, Rel-B, NF-kappaB/p50 and NF-kappaB2/p52 .

23 transcriptional factors NF-kappaB1 (p50) and NF-kappaB2 (p52), affecting their biological activities.

24 elA), c-Rel (Rel), RelB, NF-kappaB1/p50, and NF-kappaB2/p52.

25 tic factor acts downstream of the BAFF-R and NF-kappaB2 pathway to promote peripheral B cell survival

26 by inducing anti-apoptotic genes, BAFF-R and NF-kappaB2, an essential component for BAFF-R survival s

27 The transcription factors RELB and NF-kappaB2 (p100/p52) are the downstream mediators of th

28 le for the combined activity of the RELB and NF-kappaB2 subunits in B cell homeostasis that cannot be

29 e here report that ablation of both RELB and NF-kappaB2, but not of the single transcription factors,

30 factors of the alternative pathway, RELB and NF-kappaB2, in late B-cell development is incompletely u

31 e novel splicing variants of relA, relB, and NF-kappaB2 in the lungs of CD14 knockout but not wild-ty

32 xpression, and expression of RelA, RelB, and NF-kappaB2 in their spleens.

33 lex, which resulted in NIK stabilization and NF-kappaB2-p100 processing.

34 d expression of p80HT, a lymphoma-associated NF-kappaB2 mutant, in lymphocytes.

35 ralizing BR3-Fc protein showed reduced basal NF-kappaB2 activation.

36 However, a causal relationship between NF-kappaB2 mutation and lymphomagenesis has not been est

37 Loss of both NF-kappaB2 and Bcl-3, but not either one alone, led to a

38 hanism underlying lymphomagenesis induced by NF-kappaB2 mutations, which occur recurrently in a varie

39 nuclear translocation, or the non-canonical (NF-kappaB2) pathway, which involves NF-kappaB-induced ki

40 hages and neutrophils exhibited constitutive NF-kappaB2 activation.

41 entially detrimental effects of constitutive NF-kappaB2 signaling in lymphocytes.

42 ted through its interaction with cytoplasmic NF-kappaB2/p100.

43 ptor induces the processing of the cytosolic NF-kappaB2/p100 precursor to yield the mature p52 subuni

44 observe that TNF stimulation induces delayed NF-kappaB2/p100 processing and investigate the coupling

45 These findings demonstrate NF-kappaB2 mutation as an oncogenic event in vivo and su

46 ir counterparts expressing the tumor-derived NF-kappaB2 mutant p80HT, which develop predominantly B c

47 motes processing of the transcription factor NF-kappaB2/p100 to p52.

48 These studies identify a novel role for NF-kappaB2 in the negative regulation of RelB-induced DC

49 175H with small interfering RNA specific for NF-kappaB2 made these cells more sensitive to etoposide.

50 The gene NF-kappaB2 is a prominent member of this group, whose ov

51 Here we show that mice deficient in NF-kappaB2, a member of the NF-kappaB family, display a

52 uman CD4+ T cells resulted in an increase in NF-kappaB2/p100 expression with no appreciable increase

53 -13 responses and resistance to infection in NF-kappaB2 KO, but not NF-kappaB1 KO mice.

54 velop a fatal lupus-like syndrome, inhibited NF-kappaB2 processing and attenuated the disease process

55 hesis-dependent processing of the inhibitory NF-kappaB2 p100 precursor protein to the p52 form and re

56 investigated the requirement for NF-kappaB1, NF-kappaB2, and c-Rel in the expression of Th2 cytokine

57 us Rel/NF-kappaB proteins c-Rel, NF-kappaB1, NF-kappaB2, and RelA.

58 icient embryos exhibit levels of NF-kappaB1, NF-kappaB2, RelA, c-Rel, and IkappaBbeta similar to thos

59 in the expression of nuclear factor kappaB2 (NF-kappaB2) gene coding for p100/p52 subunit of NF-kappa

60 pathway, that releases RelB from the 100-kDa NF-kappaB2 complex.

61 KKalpha to mediate processing of the 100-kDa NF-kappaB2 precursor into its 52-kDa DNA binding isoform

62 ated with an endogenous approximately 50-kDa NF-kappaB2 substrate.

63 ing also inhibited p100 processing to 52-kDa NF-kappaB2 ("p52"), suggesting that RIG-I was functional

64 NIK, IKKalpha, and both 100 kDa- and 52-kDa NF-kappaB2 isoforms strongly complex 15 h after exposure

65 IK "knock-down" blocked RSV-inducible 52-kDa NF-kappaB2 processing and interfered with the early acti

66 cates into the nucleus complexed with 52-kDa NF-kappaB2.

67 esented in this report show that DCs lacking NF-kappaB2 have dramatically enhanced RelB activity, ass

68 Moreover, NF-kappaB2(-/-) mice manifest autoimmunity characterized

69 noncanonical NF-kappaB-inducing kinase (NIK)-NF-kappaB2 pathway is not well understood in obesity.

70 ires the parallel engagement of noncanonical NF-kappaB2 signaling leading to p52 recruitment to the I

71 The function of the 'nonclassical' NF-kappaB2-RelB pathway is less clear, although T cells

72 was also largely abolished in the absence of NF-kappaB2.

73 l distinct signaling pathways for actions of NF-kappaB2 mutants and p52 and suggest a causal role for

74 This activation of NF-kappaB2 requires NIK and IKKalpha, while NEMO/IKKgamm

75 IAP antagonists depends on the activation of NF-kappaB2 signaling, a mechanism paralleling that respo

76 t APRIL, also induced CLL-cell activation of NF-kappaB2.

77 indings identify a physiological function of NF-kappaB2 in the development of medullary thymic epithe

78 -deficient B cells produce reduced levels of NF-kappaB2 (p100) basally and in response to stimulation

79 light reduction in the cytoplasmic levels of NF-kappaB2 p100 protein, an additional precursor inhibit

80 recursors in the GC expressed high levels of NF-kappaB2 relative to surrounding lymphocytes.

81 onger IkappaB phosphorylation, processing of NF-kappaB2 (p100/p52), and activation of JNK, ERK, and p

82 mune system requires regulated processing of NF-kappaB2 p100 to p52, which activates NF-kappaB2 signa

83 s NF-kappaB via signal-induced processing of NF-kappaB2 p100.

84 Processing of NF-kappaB2 precursor protein p100 to generate p52 is tig

85 non-canonical pathway based on processing of NF-kappaB2 precursor protein p100 to generate p52 plays

86 athway relies on the inducible processing of NF-kappaB2 precursor protein, p100, as opposed to the de

87 is a mechanism regulating the processing of NF-kappaB2/p100.

88 tion of the COOH-terminal ankyrin repeats of NF-kappaB2 (p100(-/-)) had marked gastric hyperplasia, r

89 ( *)7), in NFKB2 affecting the C terminus of NF-kappaB2 (also known as p100/p52 or p100/p49).

90 promiscuous gene expression in the thymus of NF-kappaB2(-/-) mice.

91 B cell population and have constitutive p100 NF-kappaB2 processing.

92 the proteasome-mediated proteolysis of p100 NF-kappaB2 resulting in the generation of active p52, wh

93 categories characterized by selective p100 (NF-kappaB2) and p105 (NF-kappaB1) signaling.

94 al BAFF-R and its downstream substrate p100 (NF-kappaB2).

95 lpha, inhibiting the processing of the p100 (NF-kappaB2) subunit, which also plays a critical role in

96 n-canonical NF-kappaB pathway in which p100 (NF-kappaB2) is processed to p52.

97 ed here, we found that EBV LMP1 induced p100/NF-kappaB2 processing in human lymphoblasts and HEK293 c

98 LTbetaR and CD40 activation of p100/NF-kappaB2 is now known to be NIK/IKKalpha-dependent and

99 IFNalpha/beta-induced processing of the p100/NF-kappaB2 precursor into p52.

100 IFNalpha/beta-induced processing of the p100/NF-kappaB2 precursor into p52.

101 rmore, the abundance of NF-kappaB1 p105/p50, NF-kappaB2 p100/p52, and TRAF2 was increased in UAKD.

102 ied the expression of p50 (NF-kappaB1), p52 (NF-kappaB2), p65 (RelA) and IkappaB-alpha inhibitor as w

103 ia association with p50 (NF-kappaB1) or p52 (NF-kappaB2) homodimers.

104 /nuclear factor-kappaB1 (NF-kappaB1) and p52/NF-kappaB2 homodimers in nuclei where it modulates trans

105 e more divergent RHDs of p50/NF-kappaB1, p52/NF-kappaB2, or RelB.

106 n via interaction with p50/NF-kappaB1 or p52/NF-kappaB2 homodimers.

107 s via association with p50/NF-kappaB1 or p52/NF-kappaB2 homodimers.

108 hen it associates with p50/NF-kappaB1 or p52/NF-kappaB2, the precise molecular mechanisms through whi

109 IKKalpha preferentially phosphorylates NF-kappaB2, and this activity requires its phosphorylati

110 ternary complex with IKKalpha and processed NF-kappaB2.

111 kappaB activation pathway based on regulated NF-kappaB2 processing rather than IkappaB degradation.

112 hown that BCR signaling positively regulates NF-kappaB2, suggesting BCR regulation of BR3 signaling.

113 RELB/NF-kappaB2 deficiency in GC B cells was associated with

114 nuclear factor kappa B (NF-kappaB) subunit (NF-kappaB2) is aberrantly expressed in many tumour types

115 p52 and suggest a causal role for sustained NF-kappaB2 activation in the pathogenesis of autoimmunit

116 We further demonstrated that NF-kappaB2 was required for thymic Aire gene transcripti

117 or dependency of p100 induction suggest that NF-kappaB2/p100 acts as a late-acting negative-feedback

118 The NF-kappaB2 gene is recurrently mutated in human lymphoid

119 otoxin-beta receptor (LTbetaR) activates the NF-kappaB2 transcription factors, p100 and RelB, by regu

120 orylation in HC11 cells without altering the NF-kappaB2 pathway.

121 view of the genes that are regulated by the NF-kappaB2 pathway in DCs.

122 F-kappaB target genes, and processing of the NF-kappaB2 (p100) precursor.

123 monstrate the physiological relevance of the NF-kappaB2 p100 precursor protein in limiting the potent

124 We have also observed activation of the NF-kappaB2 pathway in mutant p53-expressing cells.

125 ediate these functions via activation of the NF-kappaB2 pathway.

126 Processing of the NF-kappaB2 precursor protein p100 to generate p52 is an

127 gradation, thus preventing processing of the NF-kappaB2 precursor protein p100 to release p52.

128 nuclear translocation and DNA binding of the NF-kappaB2-Rel B complex.

129 This effect involved activation of the NF-kappaB2-RelB signaling pathway and inhibition of the

130 signaling pathway based on processing of the NF-kappaB2/p100 precursor protein, which associates with

131 C-terminal, partially truncated forms of the NF-kappaB2/p52 precursor p100, p100DeltaCs, manifest con

132 y induce loss of drug sensitivity is via the NF-kappaB2 pathway.

133 Thus NF-kappaB2 downstream of LTbetaR plays an important role

134 Two NF-kappaB2 variants acquired only minor changes in their

135 ement of a cell-intrinsic mechanism in which NF-kappaB2 (p100) limits nuclear translocation of NF-kap

136 amine the interactions of TRAF1 and NIK with NF-kappaB2/p100 processing, we mathematically modeled TR

137 In parallel with NF-kappaB2, Bcl-3 functions within stroma to generate me

138 enhancer in the c-myb promoter together with NF-kappaB2/p52 and this binding activity was enhanced by