ライフサイエンスコーパス: Id

1 Id acts by inhibiting the sequence-specific binding of C

2 Id degradation promotes the differentiation of neuroblas

3 Id proteins (Id1 to Id4) are helix-loop-helix transcript

4 Id proteins are a class of dominant-negative antagonists

5 Id proteins are helix-loop-helix transcription factors t

6 Id proteins play important roles in osteogenic different

7 Id-1 expression levels positively correlate with glioma

8 Id-1 knockdown dramatically reduces glioblastoma cell in

9 Id-based immunotherapy has been explored in patients wit

10 Id-FTR (prevalence 12%) was associated with aging and at

11 Id-FTR is frequent, linked to aging and atrial fibrillat

12 Id-FTR valvular alterations (versus controls) were large

13 Id-specific CTLs specifically lysed myeloma cells via MH

14 ional regulator, inhibitor of DNA binding-1 (Id-1), previously shown to function as an oncogene in se

15 The 44.1-Id elicited in response to intact Pn14 was expressed in

16 ge of the 44.1-Id, although significant 44.1-Id expression is elicited in response to conjugate attac

17 er genetic control and suggest that the 44.1-Id is derived from marginal zone B cells.

18 The 44.1-Id usage was linked to the Igh(a), but not Igh(b), allot

19 In this study, we identify an idiotype (44.1-Id) that dominates the PPS14-specific IgG, but not IgM,

20 conjugate exhibit minimal usage of the 44.1-Id, although significant 44.1-Id expression is elicited

21 The 44.1-Id, however, is not expressed in the repertoire of natur

22 in conjugate, avidity maturation of the 44.1-Id-dominant PPS14-specific IgG responses was limited, ev

23 Ubiquitinated Id-1/Id-2 can then bind to p62 and be transported to autolyso

24 and right ventricular (RV) remodeling in 141 Id-FTR matched to 140 PHTN-FTR and to 99 controls with t

25 ination of inhibitor of differentiation 1/2 (Id-1/2) by catalyzing phosphorylation of Id proteins and

26 The interrelationship between COX-2, PGE(2), Id-1, and cell invasiveness was also compared in nontumo

27 Deletion of 3 Id genes induced rapid release of GICs from the perivasc

28 ally delete Id1 against global Id3 ablation (Id cDKOs), which develops adult-onset dilated cardiomyop

29 diotypically related family of nephritic Abs Id(LN)F(1), when compared with untreated SNF(1) mice.

30 The ability of PGE(2) to activate Id-1 transcription was mediated by enhanced binding of E

31 X-2-derived prostaglandin (PGE(2)) activated Id-1 transcription, leading in turn to increased invasiv

32 NKL-induced osteoclastogenesis by activating Id genes and their associated pathways.

33 Injection of LSKL into adult Id cDKO mice led to downregulation of fibrotic molecules

34 ADX40-Id vaccination resulted in significantly retarded tumor

35 were detected at elevated levels after ADX40-Id immunization; however, in vivo depletion of CD4 and/o

36 ival was obtained with 2 injections of ADX40-Id as with 8 injections using the standard therapy of ke

37 Co-administration of ADX40-Id with 3-O-deacyl-4'-monophosphoryl lipid A further sig

38 lts of the present study show that the ADX40-Id conjugate vaccine is a potential candidate as a stand

39 This molecule (alphaCD19-Id) was designed to penetrate lymph nodes and bind to no

40 Indeed, the alphaCD19-Id molecule accumulated on B cells in vivo after s.c. ad

41 Consequently, the alphaCD19-Id molecule induced a robust Id-specific antibody respon

42 To streamline the production of an Id vaccine, we engineered a small diabody (Db) molecule

43 ghts into the relationship between COX-2 and Id-1 and their potential role in metastasis.

44 Cyclooxygenase-2 (COX-2) and Id-1 are overexpressed in a variety of human malignancie

45 eptors significantly reduced the Smad1/5 and Id responses.

46 oxyestradiol decreased phospho-Smad1/5/8 and Id expression in female hPASMCs while increasing these i

47 Induction of phospho-Smad1/5/8 and Id protein by BMP4 was also reduced in female hPASMCs.

48 Understanding the mechanisms of BMP and Id function elucidates a key step during pancreas embryo

49 We hypothesized that BMP4 and Id proteins play a role in the expansion and differentia

50 Since opsonized whole tumor cell-DC and Id vaccines appear to target distinct tumor antigens, op

51 It is now well established that the E and Id protein axis regulates multiple steps in lymphocyte d

52 Thus, we provide insight into E and Id protein regulation of iNKT cell proliferation and dif

53 nisms that control the balance between E and Id proteins during DC subset specification remain unknow

54 insight into the dynamic regulation of E and Id proteins during this process.

55 However, it remains unknown how E and Id proteins mechanistically enforce and maintain the nai

56 PHTN-FTR and Id-FTR were also matched for TR effective-regurgitant-or

57 I and Id were separated by preparative RP-HPLC.

58 The expression levels of Ib and Id were very low.

59 ation (ODD) domain, the isoforms Ib, Ic, and Id had 1 or 2 deletions in the ODD domain.

60 oCl2 treatment, whereas HIFalpha Ib, Ic, and Id showed reduced or no hypoxia regulation.

61 icantly higher levels of anti-nucleosome and Id(LN)F(1) Abs but did not develop lupus nephritis.

62 Together, Cbfa1, p204, and Id proteins form a regulatory circuit and act in concert

63 ectively induced Smad1/5 phosphorylation and Id gene expression in HPAECs.

64 d the deficit in Smad1/5 phosphorylation and Id gene expression in PASMCs harboring mutations in BMPR

65 Transcription factors of the E-protein and Id families are important arbiters of T cell development

66 E proteins and Id proteins also function to inhibit or promote cell pro

67 The E proteins and Id proteins are, respectively, the positive and negative

68 pendent, dominated by the IgG1 subclass, and Id specific.

69 8 phosphorylation, nuclear translocation and Id-1 expression, cell spreading, and tubulogenesis of en

70 ne protected animals from both wild-type and Id-negative variant tumor cells, indicating that Id is n

71 ctivities of E proteins and their antagonist Id proteins, but how these factors regulate early T cell

72 Anti-Id antibody responses (humoral immune responses [IRs]) w

73 Anti-Id B cells from BCR knock-in mice, together with Id-spec

74 Anti-Id-specific Abs were detected at elevated levels after A

75 In the MyVax group (n=195), anti-Id IRs were observed in 41% of patients, with a median P

76 s present GAD65Ab that are inhibited by anti-Id, masking them in conventional detection methods.

77 aldehyde Id-KLH vaccines fail to elicit anti-Id immune and clinical responses in many patients, possi

78 h mouse anti-hMR Ab clone 19.2 elicited anti-Id-specific humoral immunity while non-Tg mice were unre

79 e mechanism by which Id(+) Ig generates anti-Id Abs is essentially unknown.

80 Anti-idiotope (anti-Id) Abs have a role in therapy against B cell lymphomas,

81 ished a correlation between the induced anti-Id antibody responses and favorable clinical outcomes.

82 sses V regions of a somatically mutated anti-Id mAb with intermediate affinity (affinity constant [Ka

83 lls and elicit spontaneous formation of anti-Id Abs in vivo.

84 The results underscore the potency of anti-Id B cells in MHC class II-restricted presentation of Id

85 f vaccinated patients mounting specific anti-Id responses had superior outcomes.

86 own in serum-free medium mounted strong anti-Id responses.

87 ment, and secretion of isotype-switched anti-Id Abs.

88 The anti-Id mice have normal peripheral B cell populations, and a

89 pitopes of Ab V regions and can trigger anti-Id immune responses, but immunization with several nonad

90 perculum (OPf) and dysgranular insular area (Id).

91 tion is controlled by HLH inhibitors such as Id and SCL/TAL1 proteins, which recently have been sugge

92 a support the evaluation of sulfhydryl-based Id-KLH vaccines in lymphoma clinical trials and possibly

93 ct, ET2, suggesting that the balance between Id and E proteins plays a role in regulating lipid metab

94 or other reasons (n = 5), median DFS between Id-vaccine and control arms was 23.0 versus 20.6 months,

95 highlight IGFbp3 as a potential link between Id and its vascular effectors.

96 lix (HLH) proteins inhibitor of DNA binding (Id) 2 and Id3, both of which are coordinately expressed

97 Inhibitors of DNA binding (Id) family members are key regulators of cellular differ

98 n, are enhanced by inhibitor of DNA binding (Id) gene family members, Id1, Id2 and Id3, which can be

99 we identified the inhibitors of DNA binding (Id) Id1-3 and the Wilm's Tumor 1 as potential downstream

100 by members of the inhibitor of DNA binding (Id) protein family.

101 hibitors of differentiation and DNA binding (Id) proteins are known to negatively regulate many bHLH

102 Inhibitor of DNA binding (Id) proteins bind to and inhibit the function of basic h

103 Inhibitor of differentiation/DNA binding (Id) proteins comprise a class of helix-loop-helix transc

104 Inhibitor of DNA binding (Id) proteins play important roles in regulating cardiac

105 y expressed E2A or inhibitor of DNA binding (Id) proteins to activate or inhibit transcription, respe

106 Inhibitor of DNA binding (Id) proteins, including Id1-4, are transcriptional regul

107 odel, we show that inhibitor of DNA binding (Id)2 is essential for the development of experimental au

108 anscription factor inhibitor of DNA binding (Id)2 modulates T cell fate decisions, but the molecular

109 otein-1 (Blimp-1), inhibitor of DNA binding (Id)2, and T-box expressed in T cells (T-bet), transcript

110 expression in general, and the CD44 and BMP4-Id signaling pathway in particular, is important in rest

111 s expressed in T-BET(+) NKT1 cells, and both Id proteins were required for the formation of this subl

112 p204 overcame this inhibition by Id proteins in consequence of (i) binding and sequesteri

113 curs by the sequestration of E2A proteins by Id.

114 s respond so rapidly to bacterial challenge, Id-positive and -negative MZ B cells were sort purified

115 cromolecular structure of Class Ia and Class Id resinite is presented.

116 e of succinic acid within Class Ia and Class Id resinite is to cross-link the macromolecular structur

117 Ia resinite and ozol pyrolysates from Class Id resinite to elute with unbroken succinyl ester cross-

118 lly to the macromolecular structure of Class Id resinite.

119 odology, communol (Class Ia) and ozol (Class Id) moieties within the polylabdane matrix are shown to

120 In the Class Id resinite, the methodology also allowed the detection

121 aring a specific vaccine (MyVax), comprising Id chemically coupled to keyhole limpet hemocyanin (KLH)

122 ng results between this and other controlled Id-vaccine trials.

123 led to reduced PGE(2) production, decreased Id-1 expression, and reduced migration of cells through

124 These findings indicate that deregulated Id activity might be useful to reprogramme quiescent neu

125 tion with patient-specific hybridoma-derived Id vaccine after chemotherapy-induced CR/CRu may prolong

126 B cells can present V region-derived Id peptides on their MHC class II molecules to Id-specif

127 Inhibitor of differentiation (Id) family helix-loop-helix proteins regulate the prolif

128 member of the inhibitor of differentiation (Id) family, was markedly increased upon knockdown of mut

129 ression of the inhibitor of differentiation (Id) gene family.

130 ous or ectopic inhibitor of differentiation (Id) proteins inhibited the differentiation of P19 cells

131 tablished that inhibitor of differentiation (Id) proteins, including Id1, Id2, and Id3, associate wit

132 -regulation of inhibitor of differentiation (Id-1).

133 deficient for inhibitor of differentiation (Id-1).

134 es from a simulated gastrointestinal digest (Id) from Amaranthus mantegazzianus proteins (I), which h

135 nd, cannabidiol, significantly downregulates Id-1 gene expression and associated glioma cell invasive

136 ells support the proliferation of anti-dsDNA Id(+) B cells in mice suffering from systemic autoimmune

137 en receptor and/or cytokine signaling, the E-Id protein axis modulates the activities of the PI3K-AKT

138 previous observations, we propose that the E-Id protein axis specifies innate and adaptive lymphoid c

139 CRISPR/Cas9-mediated ablation of the entire Id (Id1-4) family in mouse embryos leads to failure of a

140 with C. canis, C. felis, and subtype family Id of C. hominis were associated with diarrhea, and infe

141 DFS after randomization was 44.2 months for Id-vaccine arm versus 30.6 months for control arm (HR, 0

142 R confirmed increased expression of all four Id genes in Mecp2-deficient mouse brain.

143 circadian pattern of expression of all four Id genes in multiple tissues including the suprachiasmat

144 which we transferred bone marrow cells from Id cDKO mice into lethally irradiated WT mice.

145 ence and clinical context of idiopathic FTR (Id-FTR) (without overt TR cause) are unknown.

146 keyhole limpet hemocyanin (KLH) to generate Id/KLH.

147 However, glutaraldehyde Id-KLH vaccines fail to elicit anti-Id immune and clinic

148 Importantly, standard glutaraldehyde Id-KLH conjugation procedures could result in "overconju

149 t tumor-bearing mice, whereas glutaraldehyde Id-KLH had little efficacy.

150 tandard therapy of keyhole limpet hemocyanin Id + GM-CSF.

151 Hence, Id-driven T cell-B cell collaboration supported the prod

152 This study identifies Id proteins as negative regulators of T cell specificati

153 Idiotype (Id) protein, secreted by myeloma cells, is a tumor-speci

154 tologous tumor immunoglobulin (Ig) idiotype (Id) conjugated to keyhole limpet hemocyanin (KLH) and ad

155 and the dominant DEX-specific J558 idiotype (Id) is not detected in TdT(-/-) mice when compared with

156 ection than a traditional lymphoma idiotype (Id) protein vaccine, and in combination with chemotherap

157 Clinical studies of idiotype (Id) vaccination in patients with lymphoma have establish

158 therapy of lymphoma based on tumor idiotype (Id) has shown anti-idiotype humoral immune responses in

159 d (52.9 v 28.7 months; P = .001) but not IgG-Id vaccine (35.1 v 32.4 months; P = .807) compared with

160 icantly prolonged for patients receiving IgM-Id (52.9 v 28.7 months; P = .001) but not IgG-Id vaccine

161 In Id-FTR, excess annular and RV-basal enlargement exhausts

162 nd normal length (RV conical deformation) in Id-FTR versus longest RV with elliptical/spherical defor

163 m upregulation of thrombospondin-1 (TSP1) in Id cDKO hearts.

164 ed with human Igs analogous to those used in Id-KLH clinical trials.

165 K1/2 --> Egr-1 pathway, leading to increased Id-1 transcription and cell invasion.

166 -MB-231 cells, treatment with PGE(2) induced Id-1, an effect that was mimicked by an EP(4) agonist.

167 A-MB-231 cells, COX-2-derived PGE(2) induced Id-1, leading in turn to increased cell invasiveness.

168 iption factors and their natural inhibitors, Id proteins, play critical and complex roles during lymp

169 transcription factors and their inhibitors, Id proteins, is important for the myeloid-versus-lymphoi

170 responses, suggesting a mechanism involving Id protein- and E protein-mediated survival and differen

171 J558 Id V(D)J rearrangements are detected as early as 7 d aft

172 riant of TdT-restored WT proportions of J558 Id+ clones and also abrogated the development of the min

173 body response to the highly polymorphic loop Id, previously identified as a major target of strain-sp

174 -targeting moiety (anti-CD19) and a lymphoma Id.

175 abrogated the development of the minor M104E Id+ clones.

176 Maleimide Id-KLH conjugates eradicated A20 lymphoma from most tumo

177 Maleimide Id-KLH elicited tumor-specific IgG Abs and T cells, with

178 Maleimide Id-KLH vaccines also demonstrated superior efficacy in 3

179 Mechanistically, Id proteins specify cardiac cell fate by repressing two

180 We show that previously unstimulated (naive) Id-specific B and T cells collaborate efficiently in viv

181 Our results demonstrate a new, Id protein-dependent, molecular mechanism of Notch1 repr

182 Other Shh targets (Nmyc, Id factors) were induced under both conditions of pathwa

183 ese activities are related to the ability of Id proteins to antagonize E proteins and other transcrip

184 Thus, ablation of Id genes in the vasculature leads to distinct postnatal

185 inactivation in HGG by selective ablation of Id in tumor cells and after tumor initiation in a new mo

186 training factor of the oncogenic activity of Id proteins in neural tumors.

187 encies and in the presence of low amounts of Id(+) Ig, resulting in germinal center formation, plasma

188 the regulation of autophagic degradation of Id may be an effective therapeutic strategy to induce ce

189 mechanism by which autophagic degradation of Id proteins can regulate cell differentiation.

190 which bind to the helix-loop-helix domain of Id proteins in vitro and in vivo.

191 ele, leading to an overall reduced dosage of Id proteins.

192 gned patients receiving at least one dose of Id vaccine or control.

193 rentiation, but a specific downregulation of Id expression was observed in individual cells that diff

194 hemistry was used to enhance the efficacy of Id-KLH vaccines.

195 ese studies show that the entire ensemble of Id proteins has the ability to interact with E47, identi

196 at E47 interacts with the entire ensemble of Id proteins, namely, Id1, Id2, Id3, and Id4.

197 s through the induction of the expression of Id genes.

198 ased messenger RNA and protein expression of Id genes.

199 hypoxic, but it is unknown if expression of Id proteins is regulated in hypoxic cells.

200 s and suggest that deregulated expression of Id proteins may be an epigenetic mechanism to silence ex

201 Studies involving ectopic expression of Id proteins, which inhibit E2A as well as other basic he

202 cell signaling regulating the expression of Id-1 and ATF-3, thus contributing to melanoma metastasis

203 The immunogenicity of Id-3F7.A10 raises the possibility that diverse Ids of nu

204 phosphorylation of Smad1/5 and induction of Id genes, suggesting that BMP signaling is necessary for

205 patients received at least one injection of Id/KLH, and 31 were assessed for efficacy.

206 Importantly, genetic knockdown of Id-1 leads to a significant increase in survival in an o

207 oteasomes, and (iii) decreasing the level of Id proteins in the nucleus by increasing their transloca

208 The overexpression of Id, a dominant-negative repressor of MyoD, prevents mate

209 invasion through Id-1, as overexpression of Id-1 in MUC18-silenced cells resulted in increased MMP-2

210 8, which reversed the expression patterns of Id-1 and ATF-3.

211 /2 (Id-1/2) by catalyzing phosphorylation of Id proteins and recruiting TRAF-6.

212 s in MHC class II-restricted presentation of Id(+) Ig and suggest that Id-specific T cell-B cell coll

213 The majority of WT recipients of Id cDKO bone marrow cells phenocopied Id cDKO cardiac fi

214 which is mediated through its regulation of Id family members.

215 The divergent regulation of Id proteins in distinct hypoxic cells may explain some o

216 cient for this hypoxia-induced repression of Id-1.

217 Consistent with the role of Id proteins, Id2 prevents activation of p57Kip2 expressi

218 To elucidate postnatal roles of Id genes, we ablated the Id3 gene and conditionally abla

219 hality precluded the studies of the roles of Id in the postnatal heart.

220 proliferation and enhanced the secretion of Id protein and cytokines by myeloma cells.

221 Further study of Id/KLH is recommended in other settings where efficacy m

222 Treatment of Id cDKO cardiac explants with LSKL, a peptide antagonist

223 cells, it is unclear whether other types of Id-specific T cells, such as type-1 T-helper (Th1) and t

224 Although upregulation of Id proteins is associated with a broad spectrum of tumor

225 in the healing of excisional skin wounds of Id cKO mice.

226 absence of adjuvant and is not dependent on Id-presentation by dendritic cells.

227 atients with tumor-specific Ig (idiotype, or Id) chemically coupled to the immunogenic foreign carrie

228 Reducing the levels of other Id family members (Id1 and Id3) in Gfi-1(-/-) mice did n

229 static potential and expression of the other Id family members was observed.

230 nts of Id cDKO bone marrow cells phenocopied Id cDKO cardiac fibrosis 4 months post-transplantation.

231 As negative regulators of E proteins, Id proteins have been implicated in lymphocyte developme

232 diabody, could then stimulate the more rare Id-specific B cells.

233 Patients received Id/KLH 1 mg on day 1 subcutaneously, with granulocyte-ma

234 For 117 patients who received Id vaccine (n = 76) or control (n = 41), median DFS afte

235 Recombinant Id protein was manufactured and covalently linked with k

236 Additionally, we found that MUC18 regulated Id-1 expression at the transcriptional level via ATF-3,

237 uced transcription factor HIF-1 up-regulates Id-1 in hypoxic neuroblastoma cells.

238 show here that the transcriptional regulator Id-1 plays a critical role in modulating the invasivenes

239 F-3 in hypoxic neuroblastoma cells represses Id-1 and prevents the loss of these markers.

240 , the alphaCD19-Id molecule induced a robust Id-specific antibody response and protected animals from

241 consequence of (i) binding and sequestering Id proteins, (ii) accelerating their ubiquitination and

242 Single Id knockout studies have not reported cardiomyopathies.

243 Depletion of Cdh1 stabilizes Id proteins in neurons, whereas Id2 D-box mutants are im

244 hed TCR-transgenic mice, enabled us to study Id-specific T cell-B cell collaboration by dilution of t

245 median PFS observed in patients without such Id-induced IRs and in those receiving control immunother

246 Surviving Id cKO mice exhibited fibrotic vasculature, cardiac enla

247 produced PC-reactive Abs largely of the T15 Id.

248 ays in glioblastoma and that drugs targeting Id-1 represent a novel and promising strategy for improv

249 The results support the concept that Id-specific Th cells may trigger the development of SLE

250 In human cells, we demonstrate that Id genes are expressed in human acute myelogenous leukem

251 We further demonstrate that Id-specific T cell-B cell collaboration occurs readily i

252 This trial demonstrates that Id/KLH alone can induce tumor regression and durable obj

253 egative variant tumor cells, indicating that Id is not a major target of the induced tumor immunity.

254 We further show that Id-1 expression is negatively regulated by 2ME(2), which

255 Here we show that Id-1 is down-regulated in multiple primary, immortalized

256 These results show that Id-specific CTL and Th1 are promising effector cells, wh

257 We show that Id-specific Th cells support the proliferation of anti-d

258 Although previous studies have shown that Id-specific CTLs are able to lyse myeloma cells, it is u

259 Our results suggest that Id-1 regulates multiple tumor-promoting pathways in glio

260 ed presentation of Id(+) Ig and suggest that Id-specific T cell-B cell collaboration is of physiologi

261 The Id family of genes encodes negative regulators of basic

262 The Id proteins play an important role in proliferation, dif

263 The Id-2 transcriptional inhibitor was essential for product

264 , including modulation of DNA binding by the Id proteins, association with the transcriptional modula

265 ergistic activity of Gata4 and Nkx2.5 by the Id proteins.

266 Under lysosomal processing conditions, the Id-carrier protein linkage was cleavable only after male

267 the depletion of CD4+ T cells converted the Id protein-FrC conjugate vaccine into an inhibitor.

268 defining a role for Id2 and implicating the Id targets, E protein transcription factors, in the regu

269 iduals potentially carrying mutations in the Id axis are applied in clinical settings.

270 and hypertrophic markers were altered in the Id cKO hearts, but addition of Insulin-Like Growth Facto

271 gulated at 1 h following immunization in the Id-positive MZ B cells.

272 E proteins and their natural inhibitors, the Id proteins, control the timing of differentiation and t

273 the cognate BCR efficiently internalizes the Id in an IC with nucleosomes.

274 Half of the Id cKO mice died at birth.

275 Id2 and other members of the Id family are very unstable proteins that are eliminated

276 specific expression for Id2, a member of the Id gene family of transcriptional repressors, was identi

277 so demonstrated significant induction of the Id genes, which are known direct targets of BMP signalin

278 sphorylation of Smad1/5 and induction of the Id genes.

279 ins to activate them, with expression of the Id protein Extramacrochaetae (Emc), which antagonizes bH

280 of SLE and suggest that manipulation of the Id-specific T cell repertoire could play a role in treat

281 n factors and their negative regulators, the Id proteins, control the development of iNKT sublineages

282 screening approaches, we discovered that the Id family of helix-loop-helix proteins is both necessary

283 These data suggest that the Id genes may be important for entrainment and operation

284 ifier screen in Drosophila, we show that the Id protein Extramacrochaetae enables growth by suppressi

285 sis showed increased binding of ATF-3 to the Id-1 promoter after MUC18 silencing.

286 mediated by enhanced binding of Egr-1 to the Id-1 promoter.

287 onstrated an antibody response against their Id.

288 Therefore, Id proteins are good candidates for regulating Math1 in

289 hat MUC18 promotes melanoma invasion through Id-1, as overexpression of Id-1 in MUC18-silenced cells

290 Thus, Id proteins play a central and evolutionarily conserved

291 peptides on their MHC class II molecules to Id-specific Th cells.

292 by expressing a variant of E47 resistant to Id-mediated inhibition prevents the myeloid cell fate wh

293 cient mice responded significantly weaker to Id-3F7.A10 than did TLR9-sufficient mice, suggesting tha

294 ntext, and mechanisms specific to FTR types, Id-FTR versus pulmonary hypertension-related (PHTN-FTR,

295 Ubiquitinated Id-1/Id-2 can then bind to p62 and be transported to aut

296 ar decrease in cell migration was found when Id-1 was silenced.

297 e these observations, the mechanism by which Id(+) Ig generates anti-Id Abs is essentially unknown.

298 However, which Id protein plays a physiologic role during lymphocyte de

299 cells from BCR knock-in mice, together with Id-specific CD4(+) T cells from previously established T

300 somatic nuclei to the same extent as without Id.