ライフサイエンスコーパス: APC

1 APC activation may explain many of the clinical manifest

2 APC and Axin are core components of a destruction comple

3 APC is an essential component of a cytoplasmic protein c

4 APC-ms are composed of individual high-aspect-ratio sili

5 APC/C(CDC20) is regulated by CDK1-cyclin B and counterac

6 APC/C-mediated proteolysis of cyclin B and securin promo

7 APCs were incubated with PN and other stimulants, and ge

8 tman plots depicted varying agreement across APC platforms.

9 ted vaccine and injected Ag-pulsed activated APC at the predicted effector checkpoint to provide Ag p

10 0.29% [0.01%-0.59%]) but decreased for ALD (APC = -0.44% [-0.78% to -0.40%]), HCV (APC = -0.50% [-0.

11 made of alkyl carbon, alkylphosphocholines (APCs) and quaternary ammonium compounds (QACs) had signi

12 Type I blocks all APC activities, whereas type II preserves APC's cytoprot

13 This allows APC/C to decorate histones with ubiquitin chains branche

14 ulatory signals and effector functions among APC and autologous TILs.

15 ule end-tracking proteins (+TIPs) [2-5], and APC binding to EB1 promotes EB1 association with microtu

16 eep crosstalk between E2F, SCF-Cyclin F, and APC/C in regulating the oscillator underlying human cell

17 ors such as Ras, Myc, beta-catenin, p53, and APC.

18 These studies define distinct thrombin and APC dynamic signaling profiles and a rich array of prote

19 obal phosphoproteome induced by thrombin and APC signaling in endothelial cells with the quantificati

20 mic phosphoproteome profiles of thrombin and APC signaling, an enrichment of associated biological fu

21 The C-terminal basic domain of APC (APC-B) directly nucleates actin assembly, and this activ

22 logical synapse, with cellular or artificial APC, in a pattern we refer to as a 'CD2 corolla'.

23 rance of tumor-initiating mutations, such as APC mutations that stabilize beta-catenin and cause inte

24 antigen for which it is specific, as well as APC-to-T-cell adhesion.

25 Given the emerging role of B cells as APCs in these diseases, in this study, we addressed whet

26 vered that HR(+)-ETP-derived DCs function as APCs in the thymus and promote deletion of myelin-reacti

27 mory CD8(+) T cells responding to autologous APCs, equivalent thresholds were also observed for diffe

28 among PLWH decreased significantly (average APC = -3.2% per year, P < .001) from 136/100 000 to 97/1

29 Notably, CD81 is not only a beige APC marker but also required for de novo beige fat bioge

30 sensor of external inputs and controls beige APC proliferation and whole-body energy homeostasis.

31 This beige APC population is proliferative and marked by cell-surfa

32 model that multivalent interactions between APC and Axin drives the beta-catenin destruction complex

33 entally that several chromatin proteins bind APC/C, oscillate during the cell cycle, and are degraded

34 Here, we show that EB1 binds APC-B and inhibits its actin nucleation function by bloc

35 However, loss of adducin-1 blocked APC-induced Akt signaling.

36 ed by inhibitory Cdk1 phosphorylation but by APC-Cdh1-mediated proteolysis of the Cdk1 activator, cyc

37 Whether mitotic slippage is caused by APC/C(CDC20) activity that is able to escape spindle-ass

38 C20), and ends upon mitotic exit mediated by APC/C bound to CDC20 homolog 1 (CDH1).

39 pes presented directly or cross-presented by APC and demonstrate the unusual ability of dendritic cel

40 omal degradation following ubiquitination by APC/C-CDH1 or SCF(FBXW7).

41 ading to predominant uptake of immuno-NPs by APCs.

42 uppressed generation of activated protein C (APC) by TM-thrombin complex and in upregulation of inter

43 n anticoagulant through activated protein C (APC) generation, the observed limited systemic anticoagu

44 Activated protein C (APC) is a plasma serine protease with antithrombotic and

45 In contrast, activated protein C (APC), an anticoagulant protease, activates PAR1 through

46 ion, otaplimastat, 3K3A-activated protein C (APC), intra-arterial verapamil and intra-arterial hypoth

47 Genetic deletion of LRP5/6 in CD11c(+) APCs in mice (LRP5/6(DeltaCD11c)) resulted in enhanced s

48 ion of beta-catenin specifically in CD11c(+) APCs or in vivo administration of IL-10 protected LRP5/6

49 r-promoting inflammatory factors in CD11c(+) APCs via the beta-catenin-IL-10 axis.

50 -IL-10 signaling axis in intestinal CD11c(+) APCs protects mice from CAC by regulating the expression

51 ide VP2(121-130) Loss of H-2D(b) on CD11c(+) APCs mitigates the CD8 T cell response, preventing early

52 We observed that CD11c(+) APCs are critical for early priming of CD8 T cells again

53 complex/cyclosome and its coactivator CDC20 (APC/C(CDC20)) form the main ubiquitin E3 ligase for thes

54 to depend on their antigen-presenting cell (APC) activity.

55 ression by specific antigen-presenting cell (APC) types are required for clonal deletion and for regu

56 ins the symmetry and stability of the T cell-APC synaptic contact.

57 Antigen (Ag)-presenting cells (APC) instruct CD4+ helper T (Th) cell responses, but it

58 orelbine activates antigen-presenting cells (APC), and abrogates local and metastatic tumor growth by

59 unction in primary antigen-presenting cells (APCs) and fibroblasts were performed.

60 Synthetic antigen-presenting cells (APCs) are used to mediate scalable ex vivo T-cell expans

61 scriminate between antigen-presenting cells (APCs) displaying either self ligands or a mixture of sel

62 y elicited by host antigen-presenting cells (APCs) expressing MHC-encoded major HLA disparities or ex

63 resent them to the antigen-presenting cells (APCs) in the spleen.

64 ceptible CD14(pos) antigen-presenting cells (APCs) in the thymus and throughout the body.

65 tion to phagocytic antigen-presenting cells (APCs) in the tumor and activates complementary innate im

66 y, the majority of antigen-presenting cells (APCs) in tissue in acute GVHD were donor derived, and do

67 Antigen-presenting cells (APCs) including dendritic cells and monocytes instruct n

68 f naive T cells by antigen-presenting cells (APCs) is an essential step in mounting an adaptive immun

69 ll phagocytosis by antigen presenting cells (APCs) is critical to the generation of antitumour immuni

70 r signals activate antigen-presenting cells (APCs) to efficiently present alloantigen to donor T cell

71 sing" of recipient antigen presenting cells (APCs) with intact donor major histocompatibility complex

72 of immunocompetent antigen presenting cells (APCs) within the skin makes this organ an attractive tar

73 ells together with antigen-presenting cells (APCs) within the spinal cord leptomeninges in experiment

74 t cancer cells and antigen presenting cells (APCs), CTLA-4 expressed on the breast cancer cells bind

75 tent activators of antigen-presenting cells (APCs), however, they also induce severe side effects due

76 T cells encounter antigen-presenting cells (APCs), they arrest and form radially symmetric, stable i

77 ) become competent antigen-presenting cells (APCs).

78 d immunosuppressed antigen-presenting cells (APCs).

79 unique subset of adipocyte progenitor cells (APCs) that possessed the cell-intrinsic plasticity to gi

80 the two different adipose progenitor cells (APCs).

81 2014 to 2016), and annual percentage change (APC) in persons aged 20 to 29, 30 to 39, 40 to 49, and 5

82 ed in Eastern Europe (annual percent change [APC] = 2.18% [0.89%-3.49%]), whereas the largest decreas

83 ardized KS rates and annual percent changes (APCs) in rates were estimated by age, sex, race/ethnicit

84 Automated patch clamp (APC) instruments enable efficient evaluation of electrop

85 origenesis in an adenomatous polyposis coli (APC(Delta14/+)) mouse model.

86 mammals, loss of adenomatous polyposis coli (APC) causes Drosophila intestinal stem cells to form ade

87 mutations in the adenomatous polyposis coli (APC) gene.

88 tumor suppressor adenomatous polyposis coli (APC) is frequently mutated in colorectal cancers.

89 The adenomatous polyposis coli (APC) tumor suppressor protein is associated with the reg

90 Adenomatous polyposis coli (APC), a protein with both tumor suppressor and cytoskele

91 proliferation in Adenomatous polyposis coli (APC)-mutated intestine.

92 tumor suppressor Adenomatous Polyposis Coli (APC).

93 vates the alternative pathway of complement (APC).

94 nsitions through Anaphase-promoting complex (APC/C) bound to Cell division cycle protein 20 (CDC20),

95 activator of the anaphase promoting complex (APC/C) E3 ubiquitin ligase, Ama1.

96 ,7), recruit the anaphase-promoting complex (APC/C) to specific transcription start sites during mito

97 epetitive-scanning motility while contacting APCs.

98 Meanwhile, continued APC/C activity promotes proteolysis of other mitotic reg

99 Corresponding APCs were 1.6% (P < 0.050), 2.2% (P < 0.050), and 1.2% (

100 s that modify the functions of these crucial APCs.

101 ell migration (e.g., Ccl3, Ccl5, or Cxcl10), APC activation (e.g., Cd86), and IFN-inducible genes (e.

102 The anaphase promoting complex/cyclosome (APC/C) controls unidirectional progression through the c

103 of the anaphase promoting complex/cyclosome (APC/C) during mitosis.

104 The anaphase-promoting complex/cyclosome (APC/C) is an E3 ubiquitin ligase and critical regulator

105 Anaphase promoting complex/cyclosome (APC/C) is reported to play an important role in metaphas

106 ng the anaphase promoting complex/cyclosome (APC/C) until all chromosomes are properly attached to mi

107 ligase anaphase-promoting complex/cyclosome (APC/C), which also controls E2F7 and E2F8.

108 of the anaphase-promoting complex/cyclosome (APC/C).

109 he anaphase-promoting complex, or cyclosome (APC/C), is a large E3 ubiquitin ligase composed of 14 su

110 B1, secondary to increased Cdc14B-dependent APC-Cdh1 activation and reduced Emi1-dependent inhibitio

111 ing evidence for a role for monocyte-derived APC (MoAPC) in tissue-resident memory T cell (Trm) forma

112 e GVHD were donor derived, and donor-derived APCs were observed directly adjacent to host T cells.

113 meobox 1 (PROX1) was reduced in desmoplastic APC-mutant human CRCs.

114 Recently, we developed APC-mimetic scaffolds (APC-ms), which present signals to

115 sponses, but it is unclear whether different APC subsets contribute uniquely in determining Th differ

116 C/C activation, consistent with being direct APC/C substrates.

117 cells, and this can be rescued by disrupting APC-mediated actin nucleation.

118 skin and gut being stimulated against donor APCs in the form of monocyte-derived macrophages.

119 Conversely, encounters of dynamic APC-positive microtubule tips with the cell edge induce

120 2S feeds back and directly stimulates the E3 APC/C to promote substrate priming and subsequent multiu

121 icrotubule dynamics [7], we propose that EB1-APC interactions govern bidirectional cytoskeletal cross

122 akening of SAC during mitotic arrest enables APC/C(CDC20) to degrade cyclin B1, cumulating in the cel

123 oparticle (immuno-NP) to activate and expand APCs in the tumor and induce local secretion of interfer

124 (B6 x PWD) F1 APC (Min) offspring mice were largely free of intestinal

125 Finally, APC mutations in colorectal cancer, KRAS in gastric canc

126 protocols (to minimize variance) using five APC platforms across 17 sites.

127 he effects of full-length, wild-type APC (fl-APC) on cell-cell adhesion genes and p120-catenin isofor

128 rm switching in SW480 colon cancer cells: fl-APC increased the expression of genes implicated in cell

129 g the cell cycle, and are degraded following APC/C activation, consistent with being direct APC/C sub

130 colorectal cancers (CRCs) initiate following APC mutations, resulting in Wnt ligand-independent stabi

131 on in the presence of Apc (Min) or following APC loss remained moderate in intestines carrying PWD ch

132 Here we provide a detailed protocol for APC-ms synthesis and use for human T-cell activation, an

133 However, a role for APC in this inhibition has not been shown.

134 Suppression of the APC/C or forced APC/C activation by targeting its repressor EMI1 are bot

135 (APC = -0.50% [-0.81% to -0.18%]), and HBV (APC = -1.43% [-1.71% to -0.40%]).

136 ALD (APC = -0.44% [-0.78% to -0.40%]), HCV (APC = -0.50% [-0.81% to -0.18%]), and HBV (APC = -1.43%

137 th the regulation of Wnt signaling; however, APC also controls other cellular processes including the

138 ral genes, including TP53, RB1, SMAD4, HRAS, APC, PIK3CA and GNAQ were recurrently somatically altere

139 ed the regulatory dynamics of UBE2S, a human APC/C-associated E2 that ensures the faithful ubiquitina

140 PN induces RALDH2 in human APCs by signaling through the TLR1/TLR2 heterodimer.

141 tumor models and robust activation of human APCs.

142 a suppressor mutagenesis screen to identify APC/C(CCS52A2) substrates or regulators, resulting in th

143 n CRC cells with full-length APC, but not if APC was truncated or depleted.

144 atenin and SRY-box transcription factor 9 in APC(+/+) c-Cbl(+/-) mice.

145 of adenoma and CRC, and somatic mutations in APC and CTNNB1 in colorectal tumors.

146 of adenoma and CRC and somatic mutations in APC and CTNNB1 in tumors in an international cohort of p

147 e colorectal crypt, we see that mutations in APC can lead directly to mutant cell invasion.

148 Mutations in APC promote colorectal cancer (CRC) progression through

149 Somatic mutations in APC were found in 75% of tumors from patients with patho

150 ng multiple models we find that mutations in APC, a key component in the Wnt signalling pathway, can

151 ectal cancer (CRC) is driven by mutations in APC, KRAS, SMAD4, and TP53, known as the adenoma-carcino

152 mutation in CTNNB1, but all had mutations in APC.

153 ammatory cytokine that plays a major role in APC recruitment.

154 esterol biosynthetic pathway, as a target in APC mutant colorectal cancer and also have implications

155 or for betacatenin-mediated transcription in APC mutant CRC cells.

156 RALDH2 induction by PN in APCs and RA-promoted T(H)2 differentiation could be an i

157 we investigated TLR3 signaling responses in APCs and fibroblasts from the patient.

158 imulator of interferon genes (cGAS-STING) in APCs, resulting in more efficient T cell priming.

159 receptor 3 responses that were unaffected in APCs but diminished in fibroblasts are in line with prev

160 Hours later, cells inactivate APC/C(CDH1) and cross the final commitment point.

161 ASDR for cirrhosis-NAFLD increased (APC = 0.29% [0.01%-0.59%]) but decreased for ALD (APC =

162 Finally, Treg cell depletion increases APC numbers in the spinal cord and exaggerates ongoing n

163 interacting T cells assemble the individual APC-ms microrods into a biodegradable 3D matrix.

164 hat the type II mAb can specifically inhibit APC's anticoagulant function without compromising its cy

165 atenin-IL-10 signaling pathway in intestinal APCs in resolving chronic intestinal inflammation and pr

166 novel mechanism of cell navigation involving APC-dependent assembly of branched actin networks on mic

167 refully separated from inf-cDC2s, MCs lacked APC function.

168 lasma membrane, and (3) requires full-length APC for this relocalization.

169 The expression of full-length APC in SW480 colorectal cancer cells (SW480+APC) not onl

170 local Wnt cue in CRC cells with full-length APC, but not if APC was truncated or depleted.

171 degradation depends on the ubiquitin ligase APC(Ama1) and is mediated by the proteasome.

172 we identify Isc10 as an inhibitor that links APC/C(Ama1) to Smk1 activation.

173 rast, animals with H-2D(b)-deficient LysM(+) APCs retained early priming of D(b):VP2(121-130) epitope

174 it has remained challenging to globally map APC/C substrates.

175 Compared to conventional methods, APC-ms facilitates several-fold greater polyclonal T-cel

176 Haploinsufficient c-Cbl mice (APC(Delta14/+) c-Cbl(+/-)) displayed a significant (thre

177 trast to the APC(Delta14/+) c-Cbl(+/+) mice, APC(Delta14/+) c-Cbl(+/-) crypts showed nuclear beta-cat

178 CD8+ DCs in a manner independent of monocyte APC activity.

179 markedly enhanced the capacity of monocytic APC to stimulate MAIT cells.

180 During later growth and multilayering, APC(-/-) tumors induce rho in tumor cells by autonomous

181 nts showed that CD137L deficiency on myeloid APCs was associated with T1D suppression.

182 Recruitment requires Axin and not APC, and Axin's RGS domain plays an important role.

183 significant role in GC progression, but not APC, AXIN, and GSK3beta.

184 tion with mitotic exit and the activation of APC/C(Cdh1).

185 o replicate independently of the activity of APC/C and in various cell cycle conditions.

186 Moreover, interfering with the activity of APC/C did not lead to major changes in the production of

187 Here, we investigated the activity of APC/C during the lytic replication cycle of KSHV and fou

188 rpesvirus (KSHV) deregulates the activity of APC/C during the lytic replication cycle.

189 Barr virus (EBV) both impair the activity of APC/C during their lytic replication cycle through virus

190 The activity of APC/C oscillates during the cell cycle to ensure a timel

191 C/C(CDC20), indicating a feedback control of APC/C to SAC during prolonged mitotic arrest.

192 -catenin isoform 3A; similarly, depletion of APC altered the p120-catenin protein isoform profile.

193 Disruption of APC results in pathologic stabilization of beta-catenin

194 ypothesize that virus-mediated disruption of APC/C is necessary to establish a unique mitotic collaps

195 The C-terminal basic domain of APC (APC-B) directly nucleates actin assembly, and this

196 We conclude that re-expression of APC restores the cell-cell adhesion gene and posttranscr

197 Whether EB1 interactions govern functions of APC beyond microtubule regulation has not been explored.

198 the intrinsically disordered region (IDR) of APC, which contains multiple beta-catenin and Axin inter

199 ed partial loss of c-Cbl and inactivation of APC significantly contribute to CRC tumorigenesis.

200 n the hypothesis that specific inhibition of APC's anticoagulant but not its cytoprotective activity

201 its expression correlates with the level of APC.

202 ogression to adenocarcinoma in the milieu of APC(Delta14/+), a phenomenon not found with wild-type AP

203 atectomy in patients with double mutation of APC and PIK3CA and others was analyzed.

204 Double mutation of APC and PIK3CA predicts inferior response to preoperativ

205 Forty-five patients had double mutation of APC and PIK3CA; 351 did not.

206 ngly, with low CDK4/6 activity, the order of APC/C(CDH1) and Rb inactivation is reversed in both cell

207 T cells but was dependent on the presence of APC and T cells.

208 sms underlying the differential responses of APC-mutant CRCs to chemotherapy are not well understood.

209 While emphasizing the role of APC as a gatekeeper in CRC, this study also demonstrates

210 This impacts the utility of APC platforms for assessing a drug's cardiac safety marg

211 We determined variability of APC data from multiple sites that measured blocking pote

212 t trans-endocytosis of CD80, the capacity of APCs to activate T cells was significantly attenuated.

213 d increase the T cell activating capacity of APCs.

214 This led to a significant expansion of APCs, resulting in an 11.5-fold increase of dendritic ce

215 strong to displace CD80 from the surface of APCs to be internalized by breast cancer cells.

216 calization which appeared to be dependent on APC and less so on Axin.

217 he loss of kinetochore MAD2 was dependent on APC/C(CDC20), indicating a feedback control of APC/C to

218 b and a type II mAb binding to an exosite on APC (required for anticoagulant activity) as shown by X-

219 not through their action on CD8+ T cells or APC.

220 roteins not previously linked to thrombin or APC signaling, a function for afadin and adducin-1 actin

221 Unlike other APC substrates, however, CYP24A1 acted as a pseudo-subst

222 crease occurred in high-income Asia Pacific (APC = -2.88% [-3.58 to -2.18%]).

223 In peripheral APCs, gamma-IFN-inducible lysosomal thiol reductase (GIL

224 the activation of mouse, human, and porcine APC, with increased expression of costimulatory molecule

225 l features of known substrates, we predicted APC/C substrates in silico.

226 ll APC activities, whereas type II preserves APC's cytoprotective function.

227 We demonstrate that AB002 produces APC on platelet aggregates and competitively inhibits th

228 et cells and cross-presented by professional APC, specifically dendritic cells.

229 Dendritic cells (DCs) are professional APCs, which sample Ags in the periphery and migrate to t

230 etaphase-to-anaphase transition by promoting APC/C(CDC20)-dependent destruction of cyclin B in human

231 re regulated by the tumor-suppressor protein APC.

232 , even when enhanced by additional Ag-pulsed APC, presented Ag for 3 d or less and generated few CD4

233 a2-1 mutant plants, marking it as a putative APC/C(CCS52A2) substrate.

234 We report for the first time that recipient APC cross-dressing can be transiently detected in the ci

235 ew function for EB1 in negatively regulating APC-mediated actin assembly.

236 n are thus controlled by a single regulator (APC/C), which provides a robust mechanism for maintainin

237 ignaling inversion, Rb inactivation replaces APC/C(CDH1) inactivation as the point of no return.

238 for experiments; activation of TCC required APC, with clozapine interacting directly at therapeutic

239 Dephosphorylation requires APC/C-dependent destruction of cyclin B and was resolved

240 -epitope proinsulin antigen to skin-resident APCs, in vivo, in a form that enables antigen presentati

241 ecently, we developed APC-mimetic scaffolds (APC-ms), which present signals to T cells in a physiolog

242 differentiation does not require specialized APC subsets, but is driven by inducible and pathogen-spe

243 ed the expression of RALDH2 in PN-stimulated APCs by 70%.

244 uppressed KLF2, TM, and eNOS levels, subdued APC generation, declined KLF2 binding ability to TM and

245 tal cancer through loss of tumor suppressors APC and TP53 and gain of the KRAS oncogene.

246 venting the inactivation of the cell-surface APC convertase.

247 APC in SW480 colorectal cancer cells (SW480+APC) not only reduces Wnt signaling, but increases membr

248 cell-cell adhesion-related proteins in SW480+APC cells revealed an increase in p120-catenin isoform 3

249 regulatory protein 1) is increased in SW480+APC cells, and its depletion results in reversion to the

250 Several of them target APC/C, a key cellular machinery that controls the timely

251 ass I-restricted Ag presentation in targeted APC subpopulations.

252 QACs were more effective than APCs and had activity against cysts.

253 We conclude that APC/C coordinates crosstalk between cell cycle and chrom

254 dings with other recent studies showing that APC interactions regulate EB1-dependent effects on micro

255 ween the cytoskeletons of the T cell and the APC, where the actin cytoskeleton serves as a mechanical

256 Concurrent costimulatory signals at the APC-T-cell interface (eg, CD80/CD86-CD28, CD40-CD40L, OX

257 ngal pathogens to track and characterize the APC populations that drive Th responses in vivo.

258 Mutations in the APC gene and other genes in the Wnt signaling pathway co

259 ed diameter of model proteins, including the APC-superfamily lysine transporter Lyp1.

260 Expression of the APC IDR in colorectal cells promotes Axin puncta formati

261 ule H-2D(b) The identity and function of the APC(s) involved in the priming of this T cell response i

262 Despite the importance of the APC/C during cell proliferation, the number of identifie

263 oss of DNA-PKcs prevents inactivation of the APC/C in nocodazole-treated cells.

264 Suppression of the APC/C or forced APC/C activation by targeting its repres

265 scovered that E2F8 is a direct target of the APC/C ubiquitin ligase.

266 induced by the unscheduled activation of the APC/C-CDH1 complex affects the number and integrity of K

267 e increased the density of peptide Ag on the APC to high levels.

268 ion of intestinal stem cells that retain the APC protein; these effects are reversed by TGFB inhibito

269 In contrast to the APC(Delta14/+) c-Cbl(+/+) mice, APC(Delta14/+) c-Cbl(+/-

270 quired for the recruitment of this E2 to the APC/C and is autoubiquitinated as substrate abundance be

271 itination-induced turnover of UBE2S when the APC/C is not fully active.

272 HCMV, the KSHV lytic cycle occurs while the APC/C is active.

273 CMV, KSHV lytic replication occurs while the APC/C is active.

274 gions of the tumor, which coincided with the APC-rich tumor areas leading to predominant uptake of im

275 The APCs responded efficiently to stimulation with TLR3 liga

276 al responses depended on the identity of the APCs.

277 t cancer cells bind to CD80 expressed on the APCs, and underwent trans-endocytosis to deplete CD80.

278 cles from the surface of erythrocytes to the APCs in the spleen.

279 GILT expression was enriched in thymic APCs capable of mediating deletion, namely medullary thy

280 Thus, GILT expression in thymic APCs, and mTECs in particular, preferentially facilitate

281 entation of endogenous TRP1 by pooled thymic APCs.

282 (MHCII) expression is usually restricted to APC but can be expressed by cancer cells.

283 to enhance processing of vaccine epitopes to APCs.

284 TASIN (Truncated APC-Selective Inhibitors) compounds are selectively toxi

285 x (D-box) motif that allows binding with two APC adaptors, CDC20-homologue 1 (CDH1) and cell division

286 cribes the effects of full-length, wild-type APC (fl-APC) on cell-cell adhesion genes and p120-cateni

287 14/+), a phenomenon not found with wild-type APC.

288 of best practices would ensure less variable APC datasets and improved safety margins and proarrhythm

289 through cleavage of PAR1 by thrombin versus APC result in unique active receptor conformations that

290 ins and pathways utilized by thrombin versus APC signaling to induce opposing cellular functions are

291 The most frequently altered genes were APC (81%), TP53 (77%), and KRAS (37%).

292 rotubule-branched network interface, whereas APC knockdown nearly eliminates branched actin in growth

293 However, the molecular mechanism by which APC promotes beta-catenin degradation is unclear.

294 unting for its accumulation in late G1 while APC/C(Cdh1) is still active.

295 ved cells, their existence could explain why APC functions have been attributed to MCs.

296 tively toxic to colorectal cancer cells with APC mutations, although their mechanism of action remain

297 that loss-of-function of ZAP synergizes with APC-deficiency to drive malignant colorectal cancer in v

298 te or inhibition of MC-derived tryptase with APC 366 prevented all of GA-like phenotypes following MC

299 Th17 cells meander widely, interact with APCs, and exhibit cytosolic Ca(2+) transients and elevat

300 hway studies revealed an increase in the WNT/APC/MYC signaling pathway gene signature, as well as tha

301 , which is strictly dependent on CD11c+XCR1+ APCs, numerous antigen-presenting partners, both hematop