ライフサイエンスコーパス: anti-IgM

1 L-5 + CD40 ligand, but not to LPS or soluble anti-IgM.

2 ta degradation in the presence or absence of anti-IgM.

3 optosis and accelerated apoptosis induced by anti-IgM.

4 ased expression of Egr-1 upon treatment with anti-IgM.

5 nt increase in ceramide when challenged with anti-IgM.

6 t 50 min and was unaltered by treatment with anti-IgM.

7 lls to about 15 min following treatment with anti-IgM.

8 rwent apoptotic death after stimulation with anti-IgM.

9 ere inhibited in WEHI-231 cells treated with anti-IgM.

10 ression ablated apoptosis induced by TPCK or anti-IgM.

11 ates for c-myc message due to treatment with anti-IgM.

12 level by differential binding to bead-bound anti-IgM.

13 e of lipopolysaccharide (LPS), anti-CD40, or anti-IgM.

14 , Akt, and c-Jun-NH(2)-kinase in response to anti-IgM.

15 is regained, as is B-cell responsiveness to anti-IgM.

16 sponse to treatment with LPS, anti-CD40, and anti-IgM.

17 cessary for proliferation induced by soluble anti-IgM (a prototype for thymus independent-type 2 anti

18 gM transmembrane domain or by treatment with anti-IgM Ab from birth, we asked whether B cells are a c

19 activation of B cells by culture with LPS or anti-IgM Ab increases the expression of CD27L.

20 Treatment of these cells with anti-IgM Abs leads to the recruitment of the kinase from

21 ity comparable to optimal BCR ligation using anti-IgM Abs, it does so with limited activation of inhi

22 apoptosis induction after cross-linking with anti-IgM Abs.

23 Anti-IgM activated B cells expressing either CD22 mutant

24 n was isolated from cytosolic fractions from anti-IgM-activated B-cells (DT40) that lacked endogenous

25 e the subcellular location of activated Syk, anti-IgM-activated B-cells were fractionated into solubl

26 Anti-IgM also increased mRNA translation in normal blood

27 Prolonged (>24 h) exposure to anti-IgM (an antigen surrogate that induces membrane cro

28 cell cycle arrest and apoptosis triggered by anti-IgM and also abrogated down-regulation of cyclin D2

29 cell subpopulations that were activated with anti-IgM and anti-CD40 in the presence or absence of IL-

30 D2(-/-) mice can proliferate in response to anti-IgM and anti-CD40, but the time taken to enter S-ph

31 pulations were identified through the use of anti-IgM and anti-IgD mAbs.

32 inositol-3 kinase (PI3K), and show that both anti-IgM and anti-IgD stimulation results in an increase

33 Bcl-x protein expression was induced by anti-IgM and appeared in a time frame that correlates we

34 l responses to subthreshold stimulation with anti-IgM and C3d and with decreased T-dependent humoral

35 molecule, despite a normal response to both anti-IgM and CpG ODN 1826.

36 te as well as splenic B cells in response to anti-IgM and LPS stimulation in vitro.

37 10delta subunits of PI3K both participate in anti-IgM and mIg/CD19 coligation-induced Ca(2+) flux, al

38 on and cell death following stimulation with anti-IgM and the combination of anti-IgM plus anti-CD95.

39 TLR7.1Tg T1 cells were hyper-responsive to anti-IgM and TLR7 ligand stimulation in vitro and produc

40 in medium with or without F(ab')2 anti-IgM (anti-IgM), and luciferase expression was assayed.

41 hway, were resistant to apoptosis induced by anti-IgM, and showed no significant increase in ceramide

42 Anti-IgM- and anti-CD40 plus anti-Ig-induced B cell prol

43 y reducing proliferative responses to IL-4-, anti-IgM-, and/or anti-CD40 stimulation.

44 Cross-linking of surface Ig receptors with anti IgM (anti-mu heavy chain, anti-mu), but not anti-Ig

45 induce or costimulate proliferation, namely, anti-IgM (anti-Ig), anti-CD40 (CD40L), LPS, and, to a le

46 y cultured in medium with or without F(ab')2 anti-IgM (anti-IgM), and luciferase expression was assay

47 nsduced CLL cells to treatment with F(ab)(2) anti-IgM (anti-mu).

48 CR) on BKS-2, an immature B cell lymphoma by anti-IgM antibodies (Ab) caused apoptosis.

49 Staphylococcus aureus plus interleukin-2 or anti-IgM antibodies and in human T lymphocytes stimulate

50 on of the B-cell antigen receptor (BCR) with anti-IgM antibodies caused marked tyrosine phosphorylati

51 Anti-IgM antibodies induced transient tyrosine phosphory

52 timulate the BCR we incubated CLL cells with anti-IgM antibodies.

53 ease in cyclin D2 mRNAs when challenged with anti-IgM antibodies.

54 Human B cells were stimulated with anti-IgM antibody, and effects of IVIg on several parame

55 ngliosides and BCR in the cells treated with anti-IgM antibody.

56 -4 showed a unique protective effect against anti-IgM apoptotic signals on transitional B cell checkp

57 a more heterogeneous pattern of responses to anti-IgM are observed.

58 identical calcium (Ca(2+)) flux responses to anti-IgM as mCD22-expressing wild-type B cells.

59 l-xL) arrest at G0/G1 following culture with anti-IgM but do not undergo apoptosis.

60 Anti-IgM causes a decline in c-myc mRNA levels in all of

61 d to microtitration wells and anti-IgG- plus anti-IgM-coated indicator erythrocytes as the detection

62 Ca(2+) flux independently of PI3K following anti-IgM cross-linking.

63 n hen egg lysozyme, or surrogate for antigen anti-IgM, demonstrated that lipid rafts are highly dynam

64 These results suggest that anti-IgM destabilizes c-myc mRNA by a process that invol

65 cell-deficient by treatment from birth with anti-IgM develop minimal SAT.

66 B cells pretreated with anti-IgD-dextran or anti-IgM-dextran did not show significant inhibition.

67 type I IL-1R-/- mice activated in vitro with anti-IgM do not proliferate in response to IL-1, but do

68 When stimulated in vitro with anti-IgM, dual kappa surface-positive cells underwent ac

69 However anti-IgM exerts differential effects in EBV-positive and

70 show suboptimal proliferation in response to anti-IgM F(ab)'2 fragments and LPS, and are phenotypical

71 Extensive time course analyses of these anti-IgM + IL-4-stimulated B cells revealed that the G1-

72 ulation of healthy donor B cells with CD40L, anti-IgM, IL-21, CpG, IFN-alpha, IL-6 or BAFF induces mi

73 er, Bcl-xL, is induced maximally by IL-4 and anti-IgM/IL-4 in a Stat6-dependent manner.

74 or do not undergo CSR despite efficient GT (anti-IgM+IL4).

75 lated negatively isolated CLL cells by using anti-IgM, imiquimod, and CpG oligodeoxynucleotide for BC

76 stimulation with human recombinant BAFF and anti-IgM in an assay in which TACI-Fc fusion protein inh

77 Treatment of WEHI-231 cells with anti-IgM in early G1 phase prevents phosphorylation of t

78 inase activity following 24-h treatment with anti-IgM, in contrast to the 2-fold increase in neutral

79 In addition, anti-IgM increased translation of mRNA-encoding MYC, a m

80 n mitogenic responses to LPS, anti-CD40, and anti-IgM, indicating a general defect in the ability to

81 e cell cycle arrest and apoptosis induced by anti-IgM, indicating that down-regulation of cyclin D2 i

82 -/- transgenic mice also responded poorly to anti-IgM, indicating that the xid mutation does not crea

83 Anti-IgM induced IkappaB alpha degradation followed by i

84 , we showed that exogenous ceramide mimicked anti-IgM-induced apoptosis and that apoptosis was potent

85 Inhibition of anti-IgM-induced apoptosis by K13 may contribute to the

86 at CpG DNA protection of WEHI-231 cells from anti-IgM-induced apoptosis may be mediated by specific a

87 that ERK2 plays an active role in mediating anti-IgM-induced apoptosis of WEHI 231 B cells.

88 s gene expression and the protection against anti-IgM-induced apoptosis of WEHI-231 cells.

89 B cells are significantly more resistant to anti-IgM-induced apoptosis than their normal counterpart

90 otected the mature B-cell line Ramos against anti-IgM-induced apoptosis through NF-kappaB activation.

91 HI cells with bcl-xL conferred resistance to anti-IgM-induced apoptosis, whereas transfection with bc

92 reated mice are resistant to spontaneous and anti-IgM-induced apoptosis.

93 ity of CpG DNA to rescue WEHI-231 cells from anti-IgM-induced apoptosis.

94 line WEHI 231 from both TGF-beta-induced and anti-IgM-induced apoptosis.

95 ved DCs (iBMDCs) have been shown to suppress anti-IgM-induced B cell activation.

96 In CLL, anti-IgM-induced BIM phosphorylation correlated with unm

97 ed receptor signalling activity, measured by anti-IgM-induced calcium mobilization, and with increase

98 eotides (CpG DNA) rescue WEHI-231 cells from anti-IgM-induced cell cycle arrest and apoptosis.

99 ether CpG DNA can rescue WEHI-231 cells from anti-IgM-induced cell cycle arrest and apoptosis.

100 rs pocket proteins, including p130, overcame anti-IgM-induced cell cycle arrest in WEHI-bcl-xL.

101 dent kinases (CDKs), and their inhibitors in anti-IgM-induced cell cycle arrest to better understand

102 We show that anti-IgM-induced cell death in a human B lymphoma cell l

103 Prevention of anti-IgM-induced cell death in B104 cells by the calcine

104 Full-length Bcl-2 was unable to prevent anti-IgM-induced cell death of the immature B cell line

105 se inhibitor p21(WAF1/CIP1) were involved in anti-IgM-induced cell death.

106 induced apoptosis and were without effect on anti-IgM-induced cell death.

107 The anti-IgM-induced changes of pH(i) were associated with d

108 on of NF-kappaB subunit RelB and blocked the anti-IgM-induced decline in c-Myc and rise in p27(Kip1)

109 CpG DNA reversed anti-IgM-induced down-regulation of c-myc expression in

110 on of apoptosis occurs without alteration in anti-IgM-induced down-regulation of c-myc mRNA, suggesti

111 frame that correlates well with the onset of anti-IgM-induced Fas resistance.

112 ory protein (vFLIP) K13 in the modulation of anti-IgM-induced growth arrest and apoptosis in B cells.

113 s WEHI 231, an immature B-cell line, against anti-IgM-induced growth arrest and apoptosis.

114 ontrast, Syk expression did not reconstitute anti-IgM-induced inositol phosphate production.

115 Anti-IgM-induced mRNA translation was associated with in

116 VacA inhibited both T cell-induced and PMA/anti-IgM-induced proliferation of purified B cells.

117 2,4,6-trinitrophenyl-Ficoll response, anti-IgM-induced proliferation, B1 cell development, and

118 LL and other B-cell malignancies, to inhibit anti-IgM-induced signalling was reduced following IL-4 p

119 cally immature B cell lymphoma WEHI-231 with anti-IgM induces G1 arrest followed by apoptotic cell de

120 body against their surface immunoglobulin M (anti-IgM) induces apoptosis and has been studied extensi

121 with an Ab against the surface IgM protein (anti-IgM) induces apoptosis that can be rescued by engag

122 ostimulated B-cell proliferation with either anti-IgM, interleukin-2 (IL-2), IL-4, or CD40 and trigge

123 an antibody against the surface IgM chains (anti-IgM) is preceded by dramatic changes in Nuclear Fac

124 (Daudi) because its response to anti-Id (or anti-IgM) is similar to that of a BCL1 cell line, more r

125 onse of X-linked immunodeficiency B cells to anti-IgM ligation.

126 ses in vivo and proliferation in response to anti-IgM, LPS, and anti-CD40 stimulation in vitro.

127 an conjugates consisting of affinity-diverse anti-IgM mAb, with and without anti-CD21 mAb, were synth

128 The anti-IgM-mediated activation-induced cell death inductio

129 ion of CpG DNA protected WEHI-231 cells from anti-IgM-mediated apoptosis as well as growth arrest.

130 The increased susceptibility to anti-IgM-mediated apoptosis was associated with increase

131 Lastly, a significant decrease in anti-IgM-mediated apoptosis was seen upon downregulation

132 l transduction events, including a defect in anti-IgM-mediated calcium flux.

133 duced CD69 up-regulation in Jurkat cells, on anti-IgM-mediated CD69 up-regulation in B cells, or on t

134 es not affect the ability of CD40 to inhibit anti-IgM-mediated ERK2 activation and apoptosis.

135 fied a 122-bp enhancer element necessary for anti-IgM-mediated induction of the CD5 promoter.

136 al B cells in these mice exhibit a defect in anti-IgM-mediated proliferation.

137 -/-) mice with EAE showed elevation in serum anti-IgM MOG Ab levels over that seen in WT mice, along

138 h receptors by treatment of splenocytes with anti-IgM or anti-CD3 plus anti-CD28 also leads to E2A de

139 Incubating MDSCs with B cells activated by anti-IgM or anti-CD40 Abs inhibited the proliferation of

140 ced by stimulation of the BCR and CD40 using anti-IgM or anti-CD40 Abs were unaffected by the absence

141 bility to flux calcium in response to either anti-IgM or anti-IgD cross-linking and contain a signifi

142 primarily costimulated B cells activated by anti-IgM or anti-IgM plus anti-CD40.

143 urface activation markers was assessed after anti-IgM or CpG stimulation by using flow cytometry on B

144 Stimulation of CLL cells with anti-IgM or CXCL12 caused decreased priming that could b

145 Stimulation of mouse B cells with anti-IgM or IgD antibodies, bacterial lipopolysaccharide

146 he nucleus following stimulation with either anti-IgM or ionomycin.

147 mpared with Spib(-/-) B cells in response to anti-IgM or LPS stimulation.

148 ependent (anti-CD40) and T cell-independent (anti-IgM or LPS) signals.

149 goes growth arrest and apoptosis either upon anti-IgM or TGF-beta signaling.

150 al B cells before and after stimulation with anti-IgM plus anti-CD40 showed the same complex binding

151 ostimulated B cells activated by anti-IgM or anti-IgM plus anti-CD40.

152 ulation with anti-IgM and the combination of anti-IgM plus anti-CD95.

153 Treatment of early G1 cells with anti-IgM prevented this increase in cyclin A-associated

154 Anti-IgM rapidly elevated the levels of NFkappaB p50/c-R

155 igation of CD40 alone or in combination with anti-IgM, resulted in B cell-specific expression of this

156 on of lyn-/- B cells with intact and F(ab')2 anti-IgM revealed defects in at least two mechanisms tha

157 Anti-IgM significantly increased mRNA translation in pri

158 CHMFL-BTK-11 potently blocked the anti-IgM stimulated BCR signaling in the Ramos cell line

159 Inhibition of PI3K revealed anti-IgM-stimulated Ca(2+) flux has a PI3K-independent c

160 We suggest that inactivation of the NHE1 in anti-IgM-stimulated cells results in intracellular acidi

161 ith either IL-4 or anti-CD40 interferes with anti-IgM-stimulated ERK2 activation.

162 ype B29 but showed significant impairment in anti-IgM-stimulated signaling events including mitogen-a

163 In BTK-competent chicken B cells, anti-IgM-stimulated tyrosine phosphorylation of STAT5 pr

164 d protein kinase C agonists partially mimics anti-IgM stimulation and elicits a strong up-regulation

165 The prosurvival effects promoted by anti-IgM stimulation and nurselike cells were abrogated

166 alphaA and their proliferation and survival, anti-IgM stimulation of B cells induces NFATc1/alphaA an

167 Anti-IgM stimulation of these cells failed to induce mos

168 e presence of wild-type but not mutated BTK, anti-IgM stimulation reduced apoptotic cell death.

169 Similarly, anti-IgM stimulation resulted in enhanced tyrosine phosp

170 reconstituted several signaling events upon anti-IgM stimulation, including Syk phosphorylation and

171 eased expression of cyclin D2 and cdk4 after anti-IgM stimulation, unlike mature stage B cells they f

172 underwent Syk-dependent phosphorylation upon anti-IgM stimulation.

173 similar to that of wild-type controls after anti-IgM stimulation.

174 a normal STAT5A phosphorylation response to anti-IgM stimulation.

175 However, when challenged with anti-IgM the bcl-xL transfectants produced levels of cer

176 to inducing NF-kappaB factors, together with anti-IgM, these signals also support the generation of N

177 gy to stimulation through their Ag receptor (anti-IgM), TLR4 (LPS), and CD40 (anti-CD40).

178 B cells, is mobilized to co-cap with IgM on anti-IgM-treated B cells and to colocalize with GM1, a m

179 of the same molecular mass as those seen in anti-IgM-treated B cells, except for a 72-kDa protein.

180 Coprecipitation of CDK2 with p21 in anti-IgM-treated cells and the unchanged level of cyclin

181 We also found that anti-IgM-treated cells contained increased amounts of th

182 of apoptosis by suppressing its induction in anti-IgM-treated Daudi cells through a p21 antisense exp

183 the drop in NF-kappaB/Rel binding following anti-IgM treatment activates apoptosis of WEHI 231 cells

184 ociated kinase activity, were insensitive to anti-IgM treatment and were able to complete the cell cy

185 and B6gld mice underwent apoptosis following anti-IgM treatment at a level similar to that of the C57

186 bservations indicate that the outcome of the anti-IgM treatment depends on NHE1-controlled pH(i).

187 itive cell lines (Daudi, Raji, and Namalwa), anti-IgM treatment for 24 h results in growth inhibition

188 We found that anti-IgM treatment induces the appearance of an inhibito

189 levels of NF-kappaB/Rel activity induced by anti-IgM treatment led to cell death.

190 Anti-IgM treatment of Burkitt's lymphoma cells is follow

191 bcl-x mRNA was induced by anti-IgM treatment of otherwise sensitive (CD40 ligand-t

192 Anti-IgM treatment of WEHI 231 cells increased expressio

193 Cross-linking PS before anti-IgM treatment sequesters this lipid and alters sign

194 Anti-IgM treatment stabilized IkappaB-alpha and IkappaB-

195 perimental design with blinded exposures and anti-IgM treatment to induce Ins 1,4,5-P3 production as

196 In B cell lines, anti-IgM treatment up-regulates AND-34 transcript levels

197 f CpG DNA can be delayed for up to 3 h after anti-IgM treatment with no decrease in the protection.

198 levels of IkappaB beta were increased after anti-IgM treatment.

199 clin A levels sharply declined by 24 h after anti-IgM treatment.

200 ssion of EGR-1 protein was also inhibited by anti-IgM treatment.

201 from growth arrest and apoptosis induced by anti-IgM treatment.

202 th show growth inhibition and apoptosis upon anti-IgM treatment; CA46 cells shown only growth inhibit

203 In contrast, in normal B cells, anti-IgM triggered selective phosphorylation of BIM(EL)

204 Shorter exposure times to anti-IgM (up to 8 h) failed to elicit apoptosis and did

205 , because in vitro activation in response to anti-IgM was also observed in cells coexpressing autorea

206 onatal B cells to proliferate in response to anti-IgM, which was further enhanced by IL-6.

207 ound to provide considerable protection from anti-IgM, which was still significant to 20 days.

208 l heterodimers in the presence or absence of anti-IgM, while control non-CpG DNA failed to induce NFk

209 n receptor-mediated cell death, responded to anti-IgM with an early increase in intracellular pH (pH(