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1 th in the context of mutant Apc (adenomatous polyposis coli).
2 -containing protein 2), and APC (adenomatous polyposis coli).
3 synthase kinase 3beta, axin, and adenomatous polyposis coli.
4 ism associated with mutations in Adenomatous Polyposis Coli.
5 urine tumor model of spontaneous adenomatous polyposis coli.
6 a recessive phenotype, multiple adenomas, or polyposis coli.
8 mline specific overexpression of Adenomatous Polyposis Coli 2 (APC2) rescued GSC loss in chic hypomor
9 cells for proper localization of Adenomatous polyposis coli 2 and E-cadherin at the hub-GSC interface
12 ignaling (RGS) domain that binds adenomatous polyposis coli and Galpha subunits, thereby providing a
13 nsulin-like growth factor 2, and adenomatous polyposis coli) and other solid tumors (e.g., NOTCH3) an
14 attributed to mutations in Axin, adenomatous polyposis coli, and beta-catenin that lead to constituti
15 grafted OPCs differentiated into adenomatus polyposis coli (APC(+)) OLs, and CNTF significantly incr
16 lly expressed a mutant allele of adenomatous polyposis coli (APC(cKO)) in murine uterine stroma cells
18 hypoxia-induced PH, we used the adenomatous polyposis coli (Apc(Min/+)) mouse, where reduced APC cau
19 t a cancer causing truncation in adenomatous polyposis coli (APC) (APC(1-1450)) dominantly interferes
20 partner of the tumor suppressor adenomatous polyposis coli (APC) [1]; however, the significance of E
21 titutive Wnt activation upon loss of Adenoma polyposis coli (APC) acts as main driver of colorectal c
25 n of the Wnt-regulating proteins adenomatous polyposis coli (APC) and APC2 in the pathogenesis of hum
26 pecific GSK3 substrates, such as adenomatous polyposis coli (APC) and collapsin response mediator pro
27 t two tumor suppressor proteins, adenomatous polyposis coli (APC) and Dlg1-SAP97, are required for th
28 le plus end-associated proteins, adenomatous polyposis coli (APC) and EB1, providing a potential link
29 nscriptional mechanisms and that adenomatous polyposis coli (APC) and GSK3beta, which are negative re
30 of the gut tumor suppressor gene adenomatous polyposis coli (Apc) and its role in the oligodendroglia
31 that mPar3 forms a complex with adenomatous polyposis coli (APC) and kinesin superfamily (KIF) 3A, p
32 lly, CBC stem cells deficient in adenomatous polyposis coli (Apc) and Math1 were able to promote inte
33 lorectal cancer tumor suppressor adenomatous polyposis coli (APC) and that KLF4 repressed the Wnt/bet
34 d that both the tumor suppressor adenomatous polyposis coli (APC) and the ADP-ribose polymerase Tanky
35 py to image the tumor suppressor adenomatous polyposis coli (APC) and the formin mDia1 during filamen
36 pected loss in the expression of adenomatous polyposis coli (APC) and the transcriptional repressor B
37 ients with germline mutations in adenomatous polyposis coli (APC) are susceptible to stomach polyps a
38 AP) but further study identified adenomatous polyposis coli (APC) as responsible for FAP and the phys
40 e find that the tumor suppressor adenomatous polyposis coli (APC) controls microtubule targeting to t
41 mice carrying the Min allele of Adenomatous polyposis coli (Apc) develop numerous adenomas along the
44 hat the tumor-suppressor protein adenomatous polyposis coli (APC) functions in localizing alpha3-nico
47 geted pigs with mutations in the adenomatous polyposis coli (APC) gene (APC) that are orthologous to
49 dels involve modification of the adenomatous polyposis coli (Apc) gene and are excellent models for f
50 n cells with deficiencies in the adenomatous polyposis coli (APC) gene and in cells stimulated with t
51 We show that a deficiency in the adenomatous polyposis coli (APC) gene and subsequent activation of b
53 Patients with mutations in the Adenomatous Polyposis Coli (APC) gene are at increased risk of devel
58 l lines bearing mutations on the adenomatous polyposis coli (APC) gene as a model of FAP-related mali
60 -LoxP strategy to inactivate the Adenomatous Polyposis Coli (Apc) gene in the murine renal epithelium
67 al cancers have mutations of the adenomatous polyposis coli (APC) gene or the beta-catenin gene that
70 ce with inactivating mutation of adenomatous polyposis coli (APC) gene reduces intestinal adenomatous
72 operate with inactivation of the adenomatous polyposis coli (Apc) gene to accelerate intestinal tumou
73 eta-catenin or defective for the adenomatous polyposis coli (APC) gene to reinvestigated the identity
75 r as conditional deletion of the adenomatous polyposis coli (Apc) gene within the adult bladder led r
77 arcinogenesis is mutation of the adenomatous polyposis coli (APC) gene, which leads to activation of
78 ar inactivating mutations of the adenomatous polyposis coli (APC) gene, whose product is an important
89 nd epigenetic changes induced by adenomatous polyposis coli (Apc) inactivation in intestinal crypts.
91 utations in the tumor suppressor adenomatous polyposis coli (APC) initiate most colon cancers and hav
93 brain, and the tumor suppressor adenomatous polyposis coli (APC) is a key negative regulator of Wnt/
102 Mutation of the tumor suppressor adenomatous polyposis coli (APC) is considered an initiating step in
105 The tumor suppressor protein adenomatous polyposis coli (APC) is multifunctional - it participate
108 ing loss of the tumor suppressor adenomatous polyposis coli (APC) is thought to initiate colon adenom
110 s of heterozygosity rates at the adenomatous polyposis coli (Apc) locus are unaffected by Atm loss.
111 Today, the tumor suppressor adenomatous polyposis coli (APC) may have the same complaint about a
112 stinal epithelial suppression of adenomatous polyposis coli (Apc) mitigates RIGS lethality in vivo af
114 IP-Tag2 transgenic mouse tumors, adenomatous polyposis coli (apc) mouse adenomas, and implanted MCa-I
115 y oral administration of HFCS in adenomatous polyposis coli (APC) mutant mice, which are predisposed
117 itiation of colorectal cancer by adenomatous polyposis coli (APC) mutation is mediated by dysregulati
121 In this study, we show that adenomatous polyposis coli (APC) mutations found in human colorectal
122 nin pathway activation caused by adenomatous polyposis coli (APC) mutations occurs in approximately 8
123 duals with heterozygous germline adenomatous polyposis coli (APC) mutations or familial adenomatous p
125 pletion of the tumor suppressors adenomatous polyposis coli (APC) or Axin dramatically increased macr
126 nitiating mutation occurs in the adenomatous polyposis coli (APC) or beta-catenin gene, activating th
127 been associated with loss of the adenomatous polyposis coli (APC) or constitutive activation of beta-
132 essing NeuN positive neurons and adenomatous polyposis coli (APC) positive mature oligodendrocytes in
135 SK-3beta and accumulation of the adenomatous polyposis coli (APC) protein at the plus ends of leading
136 rt that the expression status of adenomatous polyposis coli (APC) protein determines the relative sen
142 Fap1 also interacts with the adenomatous polyposis coli (Apc) protein, but the functional signifi
144 iciencies in mismatch repair and adenomatous polyposis coli (APC) proteins, diet, inflammatory proces
145 ut allele in the gatekeeper gene Adenomatous polyposis coli (Apc) recapitulates familial colon cancer
146 The tumor suppressor protein adenomatous polyposis coli (APC) regulates cell protrusion and cell
148 lly important for cell migration.Adenomatous polyposis coli (APC) regulates the localization of some
149 ing in mice, we demonstrate that adenomatous polyposis coli (APC) serves an essential function in the
150 The tumor suppressor protein adenomatous polyposis coli (APC) stabilizes microtubules both in vit
151 way the tumor-suppressor protein adenomatous polyposis coli (APC) targets RNAs to cell protrusions, f
152 ave defined a repeat sequence in adenomatous polyposis coli (APC) that binds to EB1's COOH-terminal d
153 responsive cells were defined by adenomatous polyposis coli (APC) time-of-flight mass cytometry (CyTO
155 KIF17 participates in localizing adenomatous polyposis coli (APC) to the plus ends of a subset of MTs
157 ed or inherited mutations in the adenomatous polyposis coli (APC) tumor suppressor gene are causally
162 with truncating mutations in the adenomatous polyposis coli (APC) tumor suppressor gene through inhib
169 specific allelic deletion of the adenomatous polyposis coli (Apc) tumor suppressor locus, Ikkbeta(EE)
173 tain truncating mutations in the adenomatous polyposis coli (APC) tumor suppressor, a negative regula
174 is negatively controlled by the adenomatous polyposis coli (APC) tumor suppressor, which induces pro
176 the in vivo mutation rate of the adenomatous polyposis coli (APC) tumor-suppressor gene is presented.
177 etic pathway whereby loss of the adenomatous polyposis coli (APC) tumour suppressor and activation of
178 the granules associate with the adenomatous polyposis coli (APC) tumour suppressor and the fragile X
182 dy, the tumor suppressor protein adenomatous polyposis coli (APC) was found to be important for the u
183 found that the tumor suppressor adenomatous polyposis coli (APC) was required for microtubule intera
184 h1 (Atoh1(Deltaintestine)), the adenomatosis polyposis coli (APC)(min) mutation, both mutations (Atoh
185 These mice were crossed with adenomatous polyposis coli (Apc)(min/+) mice, or given azoxymethane
186 ic relationship between MPC1 and Adenomatous polyposis coli (APC), a key tumor suppressor in colorect
187 Inactivating mutations within adenomatous polyposis coli (APC), a negative regulator of Wnt signal
189 uggest that the tumor suppressor adenomatous polyposis coli (APC), a regulator of Wnt signaling and t
193 Specific site of CpG islands of adenomatous polyposis coli (APC), a well studied tumor suppressor ge
195 uction complex components Axin1, adenomatous polyposis coli (APC), and GSK3beta were also proteolytic
196 containing the proteins axin and adenomatous polyposis coli (APC), both of which bind directly to bet
197 plex with axin (axis inhibitor), adenomatous polyposis coli (APC), casein kinase 1alpha (CK1alpha), a
198 ic exchange factor stimulated by adenomatous polyposis coli (APC), contributing to colorectal cancer
199 with its direct binding partner adenomatous polyposis coli (APC), EB1 can stabilize microtubules.
200 ons in known driver genes [e.g., adenomatous polyposis coli (APC), KRAS, or PIK3CA] found in the prim
202 y patients induced colon p53 and adenomatous polyposis coli (APC), reversing progrowth GH signals.
203 gainst beta-catenin (Ctnnb1) and adenomatous polyposis coli (Apc), two commonly mutated genes in hepa
204 naling by targeting the gene for Adenomatous Polyposis Coli (Apc), which controls Wnt signaling activ
205 hat the tumor suppressor protein adenomatous polyposis coli (APC), which is a known MT-associated pro
206 ion and activity using models of adenomatous polyposis coli (APC)- and chemotherapy-induced apoptosis
211 e cortical localizations of the adenomatosis polyposis coli (APC)-related protein APC2/E-APC and the
212 litis-associated and spontaneous adenomatous polyposis coli (APC)-related tumors of the intestinal ep
213 osed the discovery of truncating adenomatous polyposis coli (APC)-selective inhibitor 1 (TASIN-1), a
222 sses beta-catenin activity in an adenomatous polyposis coli (APC)/glycogen synthase kinase-3 (GSK3)-i
225 ve cell imaging, and a mutant of Adenomatous polyposis coli (APC-m4) defective in actin nucleation to
227 or suppressor candidate 33, N33; adenomatous polyposis coli, APC; mut-L homolog 1, MLH1; and O(6)-met
228 eted for proteolysis by the Axin/Adenomatous polyposis coli (Apc1 and Apc2)/Zeste-white 3 destruction
229 defect (POP-1)/TCF, APC related/adenomatosis polyposis coli (APR-1)/APC, and LIT-1/NLK (loss of intes
230 lloproteinases 1, 2, and 3, and adenomatosis polyposis coli) are known for their antiangiogenic funct
231 thway mutations, such as loss of adenomatous polyposis coli, are insensitive to this novel hypoxic ef
232 he destruction complex component adenomatous polyposis coli at a similar SLS motif to the effect that
233 lex, consisting of the proteins adenomatosis polyposis coli, Axin and glycogen synthase kinase 3beta
236 ted with colon cancer, including adenomatous polyposis coli, beta-catenin, p53, c-myc, cyclin D1, and
237 umors driven by mutations in the adenomatous polyposis coli/beta-catenin pathway and activates AP-1.
240 activated canonical signaling in adenomatous polyposis coli/beta-catenin wild-type colon cancer cells
241 n site family (WNT)/beta-catenin/adenomatous polyposis coli (CTNNB1/APC) pathway has been identified
245 neoplasia (Min) mutation of the adenomatous polyposis coli gene (Apc) and homozygous for the tumor r
246 e with germline mutations in the adenomatous polyposis coli gene (Apc) and/or DNA mismatch repair gen
248 rectal cancers, mutations in the adenomatous polyposis coli gene (APC) or CTNNB1 constitutively activ
250 n family 1 gene RASSF1A, and the adenomatous polyposis coli gene APC in tumors and in histologically
251 rrying and non-sense mutation in Adenomatous polyposis coli gene at site R850, which designated Apc (
252 ause of germline mutation of the adenomatous polyposis coli gene is characterized by development of c
254 gative regulators, such as axin, adenomatous polyposis coli gene product (APC), and glycogen synthase
255 by inhibiting its binding to the adenomatous polyposis coli gene product and subsequent glycogen synt
256 ly rare missense variants in the adenomatous polyposis coli gene, which is responsible for familial a
260 lineages by deletion of the Apc (adenomatous polyposis coli) gene causes spontaneous T cell activatio
261 through Disheveled (Dvl), Axin, adenomatous polyposis coli, glycogen synthase kinase 3beta, and case
262 hway regulatory genes, including adenomatous polyposis coli, GSK3beta, axin 1, beta-catenin, lymphoid
264 due to inactivating mutations of adenomatous polyposis coli (in colorectal cancer) or activating muta
265 e tumor suppressor protein, APC (adenomatous polyposis coli), in the regulation of base excision repa
266 the Wnt repressor APC (encoding adenomatous polyposis coli) leads to a state of aberrant and unrestr
267 ned mutations in either the APC (adenomatous polyposis coli) locus or in an allele of beta-catenin.
270 Crossing Tfam(+/-) mice to the adenomatous polyposis coli multiple intestinal neoplasia (APC(Min/+)
272 ted and somatic mutations in the adenomatous polyposis coli occur in most colon cancers, leading to a
274 by loss of the tumor suppressor adenomatous polyposis coli or casein kinase 1alpha uncovered new reg
275 xamination of one or more of the adenomatous polyposis coli, p14ARF, p16INK4a, or death associated pr
276 formation about the roles of the adenomatous polyposis coli protein (APC) and its binding partner EB1
277 ated depletion of two kMAPs, the adenomatous polyposis coli protein (APC) and its binding partner, EB
278 in Axin and the tumor suppressor adenomatous polyposis coli protein (APC) are critical components of
280 eport that the tumour suppressor adenomatous polyposis coli protein (APC) directs the localization an
284 f a region similar to one in the adenomatous polyposis coli protein involved in EB1 binding blocks Ml
285 actin-nucleating ability of the adenomatous polyposis coli protein is required for disassembly of fo
287 i of the beta-catenin antagonist adenomatous polyposis coli results in the regeneration of a tail at
288 However, little is known about adenomatous polyposis coli's (APC's) role in the mammalian brain.
289 tably transformed with wild-type adenomatous polyposis coli showed decreased beta-catenin protein and
290 -catenin, a component of the Wnt-adenomatous polyposis coli signaling pathway, contribute to the deve
291 ifferent autoantigen, except for adenomatous polyposis coli that was recognized by sera of two patien
292 s the tumor suppressor gene APC (adenomatous polyposis coli), thereby affecting Wnt (Wingless-related
294 le motor cytoplasmic dynein, the adenomatous polyposis coli tumor suppressor protein (APC), and glyco
297 enin activation or loss of APC - adenomatous polyposis coli) upon expression of CRE recombinase in th
298 All patients were tested for the adenomatous polyposis coli variants I1307K and E1317Q, and variants
299 tivation of the tumor suppressor adenomatous polyposis coli, with the resultant activation of beta-ca