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 paralyzed the subsequent Ca(2+) response to anti-IgM.

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

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

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

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

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

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

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

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

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

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

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

24 Anti-IgM activated B cells expressing either CD22 mutant

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

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

27 Anti-IgM also increased mRNA translation in normal blood

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

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

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

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

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

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

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

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

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

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

38 10delta subunits of PI3K both participate in anti-IgM and mIg/CD19 coligation-induced Ca(2+) flux, al

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

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

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

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

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

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

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

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

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

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

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

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

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

52 Anti-IgM antibodies induced transient tyrosine phosphory

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

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

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

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

57 -4 showed a unique protective effect against anti-IgM apoptotic signals on transitional B cell checkp

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

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

60 ry FL cells to DC-SIGN, which does not block anti-IgM binding, reversibly paralyzed the subsequent Ca

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

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

63 ed that poseltinib had the highest impact on anti-IgM + CD40L stimulated B cells, however, lower impa

64 In anti-IgM + CD40L stimulated B cells, poseltinib inhibite

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

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

67 nal receptor cross-talk pathways since, like anti-IgM, DC-SIGN down-modulated cell surface expression

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

83 milar downstream transcriptional response to anti-IgM in primary FL cells, characterized by activatio

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

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

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

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

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

89 Anti-IgM induced IkappaB alpha degradation followed by i

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

123 2,4,6-trinitrophenyl-Ficoll response, anti-IgM-induced proliferation, B1 cell development, and

124 tection from exogenous antigen by paralyzing anti-IgM-induced signaling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

144 Anti-IgM modulation induced heterogeneous BCR signaling

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

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

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

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

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

150 In addition, whereas stimulation with anti-IgM or anti-Igkappa L chain Abs resulted in strong

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

166 Anti-IgM significantly increased mRNA translation in pri

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

201 Anti-IgM treatment of WEHI 231 cells increased expressio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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