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1 adenoma growth in the context of mutant Apc (adenomatous polyposis coli).
2 ducin repeat-containing protein 2), and APC (adenomatous polyposis coli).
3 ng glycogen synthase kinase 3beta, axin, and adenomatous polyposis coli.
4 genic mechanism associated with mutations in Adenomatous Polyposis Coli.
5 urden in a murine tumor model of spontaneous adenomatous polyposis coli.
8 sly in germ cells for proper localization of Adenomatous polyposis coli 2 and E-cadherin at the hub-G
10 tive regulators of beta-catenin, such as the adenomatous polyposis coli and Axin tumor suppressor pro
11 G-protein signaling (RGS) domain that binds adenomatous polyposis coli and Galpha subunits, thereby
12 member 1, insulin-like growth factor 2, and adenomatous polyposis coli) and other solid tumors (e.g.
13 of the postsynaptic density, among them the adenomatous polyposis coli, and 2) proteins with express
14 aditionally attributed to mutations in Axin, adenomatous polyposis coli, and beta-catenin that lead t
16 e conditionally expressed a mutant allele of adenomatous polyposis coli (APC(cKO)) in murine uterine
17 al crypt, augmenting CRC tumorigenesis in an adenomatous polyposis coli (APC(Delta14/+)) mouse model.
18 n on chronic hypoxia-induced PH, we used the adenomatous polyposis coli (Apc(Min/+)) mouse, where red
19 ve shown that a cancer causing truncation in adenomatous polyposis coli (APC) (APC(1-1450)) dominantl
20 as a binding partner of the tumor suppressor adenomatous polyposis coli (APC) [1]; however, the signi
24 contribution of the Wnt-regulating proteins adenomatous polyposis coli (APC) and APC2 in the pathoge
25 ested that specific GSK3 substrates, such as adenomatous polyposis coli (APC) and collapsin response
26 we show that two tumor suppressor proteins, adenomatous polyposis coli (APC) and Dlg1-SAP97, are req
27 wo microtubule plus end-associated proteins, adenomatous polyposis coli (APC) and EB1, providing a po
28 onal and transcriptional mechanisms and that adenomatous polyposis coli (APC) and GSK3beta, which are
29 expression of the gut tumor suppressor gene adenomatous polyposis coli (Apc) and its role in the oli
30 e, we report that mPar3 forms a complex with adenomatous polyposis coli (APC) and kinesin superfamily
32 associate with the tumor suppressor protein adenomatous polyposis coli (APC) and p150glued, a compon
33 ed by the colorectal cancer tumor suppressor adenomatous polyposis coli (APC) and that KLF4 repressed
34 ther, we find that both the tumor suppressor adenomatous polyposis coli (APC) and the ADP-ribose poly
35 nce microscopy to image the tumor suppressor adenomatous polyposis coli (APC) and the formin mDia1 du
36 firmed an expected loss in the expression of adenomatous polyposis coli (APC) and the transcriptional
37 First, patients with germline mutations in adenomatous polyposis coli (APC) are susceptible to stom
38 polyposis (FAP) but further study identified adenomatous polyposis coli (APC) as responsible for FAP
41 C57BL/6J mice carrying the Min allele of Adenomatous polyposis coli (Apc) develop numerous adenom
43 rectal cancers consistently contained mutant adenomatous polyposis coli (APC) DNA molecules in their
44 show here that the tumor-suppressor protein adenomatous polyposis coli (APC) functions in localizing
46 mice bearing a heterozygote mutation in the adenomatous polyposis coli (APC) gene (Apc(Min/+) mice).
47 ted gene-targeted pigs with mutations in the adenomatous polyposis coli (APC) gene (APC) that are ort
49 of these models involve modification of the adenomatous polyposis coli (Apc) gene and are excellent
50 ased in human cells with deficiencies in the adenomatous polyposis coli (APC) gene and in cells stimu
58 l cancer cell lines bearing mutations on the adenomatous polyposis coli (APC) gene as a model of FAP-
60 using a Cre-LoxP strategy to inactivate the Adenomatous Polyposis Coli (Apc) gene in the murine rena
67 ost colorectal cancers have mutations of the adenomatous polyposis coli (APC) gene or the beta-cateni
70 letion in mice with inactivating mutation of adenomatous polyposis coli (APC) gene reduces intestinal
72 ssf1a can cooperate with inactivation of the adenomatous polyposis coli (Apc) gene to accelerate inte
73 ization of beta-catenin or defective for the adenomatous polyposis coli (APC) gene to reinvestigated
75 n the bladder as conditional deletion of the adenomatous polyposis coli (Apc) gene within the adult b
77 intestinal carcinogenesis is mutation of the adenomatous polyposis coli (APC) gene, which leads to ac
78 requently bear inactivating mutations of the adenomatous polyposis coli (APC) gene, whose product is
87 e generated mice lacking the beta-catenin or adenomatous polyposis coli (Apc) genes in osteoblasts.
88 here that the mouse tumor suppressor protein adenomatous polyposis coli (APC) has a role in AChR clus
90 criptional and epigenetic changes induced by adenomatous polyposis coli (Apc) inactivation in intesti
94 ncluding the brain, and the tumor suppressor adenomatous polyposis coli (APC) is a key negative regul
111 aling following loss of the tumor suppressor adenomatous polyposis coli (APC) is thought to initiate
112 ore, the loss of heterozygosity rates at the adenomatous polyposis coli (Apc) locus are unaffected by
114 te that intestinal epithelial suppression of adenomatous polyposis coli (Apc) mitigates RIGS lethalit
116 vessels in RIP-Tag2 transgenic mouse tumors, adenomatous polyposis coli (apc) mouse adenomas, and imp
117 ects of daily oral administration of HFCS in adenomatous polyposis coli (APC) mutant mice, which are
119 esis that initiation of colorectal cancer by adenomatous polyposis coli (APC) mutation is mediated by
124 nt/beta-catenin pathway activation caused by adenomatous polyposis coli (APC) mutations occurs in app
128 (CRCs), an initiating mutation occurs in the adenomatous polyposis coli (APC) or beta-catenin gene, a
129 n that have been associated with loss of the adenomatous polyposis coli (APC) or constitutive activat
134 nestin expressing NeuN positive neurons and adenomatous polyposis coli (APC) positive mature oligode
137 ibition of GSK-3beta and accumulation of the adenomatous polyposis coli (APC) protein at the plus end
138 ere, we report that the expression status of adenomatous polyposis coli (APC) protein determines the
144 rating cells, and induces the interaction of adenomatous polyposis coli (Apc) protein with the plus e
148 inked to deficiencies in mismatch repair and adenomatous polyposis coli (APC) proteins, diet, inflamm
149 ing a knockout allele in the gatekeeper gene Adenomatous polyposis coli (Apc) recapitulates familial
152 is functionally important for cell migration.Adenomatous polyposis coli (APC) regulates the localizat
153 gene targeting in mice, we demonstrate that adenomatous polyposis coli (APC) serves an essential fun
155 ne such pathway the tumor-suppressor protein adenomatous polyposis coli (APC) targets RNAs to cell pr
156 Here, we have defined a repeat sequence in adenomatous polyposis coli (APC) that binds to EB1's COO
157 ting factor-responsive cells were defined by adenomatous polyposis coli (APC) time-of-flight mass cyt
159 In turn, KIF17 participates in localizing adenomatous polyposis coli (APC) to the plus ends of a s
166 cells lines with truncating mutations in the adenomatous polyposis coli (APC) tumor suppressor gene t
167 found in patients harboring mutations in the adenomatous polyposis coli (APC) tumor suppressor gene.
173 ce with IEC-specific allelic deletion of the adenomatous polyposis coli (Apc) tumor suppressor locus,
175 atase 2A (PP2A) and must be protected by the adenomatous polyposis coli (APC) tumor suppressor protei
177 rcinomas contain truncating mutations in the adenomatous polyposis coli (APC) tumor suppressor, a neg
178 in signaling is negatively controlled by the adenomatous polyposis coli (APC) tumor suppressor, which
180 calculating the in vivo mutation rate of the adenomatous polyposis coli (APC) tumor-suppressor gene i
181 ollows a genetic pathway whereby loss of the adenomatous polyposis coli (APC) tumour suppressor and a
182 RNAs in the granules associate with the adenomatous polyposis coli (APC) tumour suppressor and t
186 In this study, the tumor suppressor protein adenomatous polyposis coli (APC) was found to be importa
189 ne the genetic relationship between MPC1 and Adenomatous polyposis coli (APC), a key tumor suppressor
192 approaches suggest that the tumor suppressor adenomatous polyposis coli (APC), a regulator of Wnt sig
198 atenin destruction complex components Axin1, adenomatous polyposis coli (APC), and GSK3beta were also
199 ein complex containing the proteins axin and adenomatous polyposis coli (APC), both of which bind dir
200 forms a complex with axin (axis inhibitor), adenomatous polyposis coli (APC), casein kinase 1alpha (
201 Rac1-specific exchange factor stimulated by adenomatous polyposis coli (APC), contributing to colore
202 Together with its direct binding partner adenomatous polyposis coli (APC), EB1 can stabilize micr
205 in acromegaly patients induced colon p53 and adenomatous polyposis coli (APC), reversing progrowth GH
206 e designed against beta-catenin (Ctnnb1) and adenomatous polyposis coli (Apc), two commonly mutated g
207 ical Wnt signaling by targeting the gene for Adenomatous Polyposis Coli (Apc), which controls Wnt sig
208 e, we show that the tumor suppressor protein adenomatous polyposis coli (APC), which is a known MT-as
209 its expression and activity using models of adenomatous polyposis coli (APC)- and chemotherapy-induc
213 ulation and epithelial over-proliferation in Adenomatous polyposis coli (APC)-mutated intestine.
214 o develop colitis-associated and spontaneous adenomatous polyposis coli (APC)-related tumors of the i
215 iously disclosed the discovery of truncating adenomatous polyposis coli (APC)-selective inhibitor 1 (
223 ation suppresses beta-catenin activity in an adenomatous polyposis coli (APC)/glycogen synthase kinas
226 py, FRAP, live cell imaging, and a mutant of Adenomatous polyposis coli (APC-m4) defective in actin n
228 I, IGF2; tumor suppressor candidate 33, N33; adenomatous polyposis coli, APC; mut-L homolog 1, MLH1;
229 Arm is targeted for proteolysis by the Axin/Adenomatous polyposis coli (Apc1 and Apc2)/Zeste-white 3
230 a-catenin pathway mutations, such as loss of adenomatous polyposis coli, are insensitive to this nove
231 atenin and the destruction complex component adenomatous polyposis coli at a similar SLS motif to the
232 e glycogen synthase kinase 3beta (GSK3beta)- adenomatous polyposis coli-axin-mediated degradation pat
234 kers associated with colon cancer, including adenomatous polyposis coli, beta-catenin, p53, c-myc, cy
235 intestinal tumors driven by mutations in the adenomatous polyposis coli/beta-catenin pathway and acti
238 erived WNT2 activated canonical signaling in adenomatous polyposis coli/beta-catenin wild-type colon
239 V integration site family (WNT)/beta-catenin/adenomatous polyposis coli (CTNNB1/APC) pathway has been
241 otubule organization and capture dynamics in adenomatous polyposis coli-deficient radial progenitors.
242 e intestinal neoplasia (Min) mutation of the adenomatous polyposis coli gene (Apc) and homozygous for
243 By using mice with germline mutations in the adenomatous polyposis coli gene (Apc) and/or DNA mismatc
245 t human colorectal cancers, mutations in the adenomatous polyposis coli gene (APC) or CTNNB1 constitu
247 iation domain family 1 gene RASSF1A, and the adenomatous polyposis coli gene APC in tumors and in his
248 Mice carrying and non-sense mutation in Adenomatous polyposis coli gene at site R850, which desi
249 olyposis because of germline mutation of the adenomatous polyposis coli gene is characterized by deve
251 its other negative regulators, such as axin, adenomatous polyposis coli gene product (APC), and glyco
252 eta-catenin by inhibiting its binding to the adenomatous polyposis coli gene product and subsequent g
253 in, where carrier proteins like axin and the adenomatous polyposis coli gene product APC interact wit
254 comparatively rare missense variants in the adenomatous polyposis coli gene, which is responsible fo
258 g in T cell lineages by deletion of the Apc (adenomatous polyposis coli) gene causes spontaneous T ce
259 and function through Disheveled (Dvl), Axin, adenomatous polyposis coli, glycogen synthase kinase 3be
260 -catenin pathway regulatory genes, including adenomatous polyposis coli, GSK3beta, axin 1, beta-caten
261 olocalizes with the tumor suppressor protein adenomatous polyposis coli in the TJs of epithelial cell
262 alignancies due to inactivating mutations of adenomatous polyposis coli (in colorectal cancer) or act
263 nction of the tumor suppressor protein, APC (adenomatous polyposis coli), in the regulation of base e
264 mutation of the Wnt repressor APC (encoding adenomatous polyposis coli) leads to a state of aberrant
265 that contained mutations in either the APC (adenomatous polyposis coli) locus or in an allele of bet
266 ted signaling and glycogen synthase kinase-3/adenomatous polyposis coli-mediated beta-catenin activat
272 ling induced by loss of the tumor suppressor adenomatous polyposis coli or casein kinase 1alpha uncov
273 Additional examination of one or more of the adenomatous polyposis coli, p14ARF, p16INK4a, or death a
274 Most information about the roles of the adenomatous polyposis coli protein (APC) and its binding
275 at RNAi-mediated depletion of two kMAPs, the adenomatous polyposis coli protein (APC) and its binding
276 olding protein Axin and the tumor suppressor adenomatous polyposis coli protein (APC) are critical co
278 Here we report that the tumour suppressor adenomatous polyposis coli protein (APC) directs the loc
282 n from Mlp of a region similar to one in the adenomatous polyposis coli protein involved in EB1 bindi
283 ows that the actin-nucleating ability of the adenomatous polyposis coli protein is required for disas
285 versely, RNAi of the beta-catenin antagonist adenomatous polyposis coli results in the regeneration o
287 W480 cells stably transformed with wild-type adenomatous polyposis coli showed decreased beta-catenin
288 on, and beta-catenin, a component of the Wnt-adenomatous polyposis coli signaling pathway, contribute
289 cognized a different autoantigen, except for adenomatous polyposis coli that was recognized by sera o
290 ectly targets the tumor suppressor gene APC (adenomatous polyposis coli), thereby affecting Wnt (Wing
293 he microtubule motor cytoplasmic dynein, the adenomatous polyposis coli tumor suppressor protein (APC
294 centrosome function and cortically localized Adenomatous Polyposis Coli tumor suppressor protein to o
297 her beta-catenin activation or loss of APC - adenomatous polyposis coli) upon expression of CRE recom