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1 FAP expression is minimal or absent in most normal adult
2 FAP inhibition is investigated as a therapeutic option f
3 FAP is a hereditary disease predisposing to cancer in mu
4 FAP knockout A. thaliana plants show elevated alpha-lino
5 FAP(+) cells from three sites, skeletal muscle, adipose
6 FAP(+) cells of skeletal muscle are the major local sour
7 FAP-1 was demonstrated to be responsible for the reduced
8 FAP-mediated collagen processing leads to increased coll
9 FAPs expressed desmosome proteins, including desmoplakin
10 FAPs isolated from the Pdgfra-Cre:Eyfp:Dsp(W/F) mouse he
16 9.7%), indeterminate colitis (n = 63, 1.7%), FAP (n = 223, 6%), Crohn's disease (n = 150, 4%), cancer
18 acid, fatty acid, and mineral profiles (AAP, FAP, and MP, respectively), as well as protein degradati
20 s goal, a sample corresponding to 33% of all FAP patients who undergone a liver transplantation in th
27 than 50 years were more likely to receive an FAP liver [odds ratio (OR) 1.94, confidence interval (CI
31 oromethyl)sulfonyl]imide (NTf(2)(-)) anions, FAP-based ILs are significantly more hydrophobic and hyd
32 macrophage antibody), or (111)In-28H1 (anti-FAP antibody), respectively, with nonspecific controls i
38 dy was to assess whether a radiolabeled anti-FAP antibody could be used to monitor the efficacy of tr
40 noimaging of activated fibroblasts with anti-FAP antibodies might be an attractive noninvasive imagin
46 , 1-butyl-1-methylpyrrolidinium FAP ([BMPL] [FAP]), and 1-(6-amino-hexyl)-1-methylpyrrolidinium FAP (
48 xamine whether circulating CAF identified by FAP and alpha-SMA co-expression (cCAF) could be distingu
52 le structure of the ionic liquid [C18mim](+)[FAP](-) near its free surface was studied by complementa
53 al cells from patients with IBD, IBD-cancer, FAP-adenoma, and colorectal cancer, but not in patients
55 fluorescence intensity assay for circulating FAP activity based on a recently identified natural subs
57 ibition constants but does not inhibit close FAP homologues dipeptidyl peptidase IV, dipeptidyl pepti
63 ntly affected the formation of 3-dimensional FAP-positive cell matrix, as demonstrated by reducing th
65 nally, the assay was used to detect elevated FAP activity in human patients diagnosed with liver cirr
67 of yearly gastrointestinal follow-up, every FAP patient in our registry was offered thyroid ultrasou
69 drugs was screened against cells expressing FAP-tagged beta(2)ARs, all 33 known beta(2)AR-active lig
70 atment arms: best (ie, longest time to first FAP-related event [rectal/pouch polyposis]), intermediat
72 MMVTx is a valuable therapeutic option for FAP patients who are in need for visceral transplantatio
74 dentifying inhibitors that are selective for FAP over both the dipeptidyl peptidases (DPPs), with whi
75 unced stromal elements staining strongly for FAP, and hypothesized that targeting tumor stroma with F
77 results show the iBody is a useful tool for FAP targeting in vitro and potentially also for specific
82 his idea, we examined 16 desmoid tumors from FAP-associated and sporadic cases, finding that all 16 o
86 0.7 and 0.1 to 1.2 microg L(-1) for [HMIM] [FAP], [PH(3)T] [FAP], 1-butyl-1-methylpyrrolidinium FAP
91 conclusion, daily sulindac administration in FAP patients significantly altered colorectal stem cell
97 of intermediate-sized collagen fragments in FAP-deficient mouse lungs, consistent within vitrostudie
98 39 and rapamycin, decreased proliferation in FAP-COs, but also affected cell proliferation in wild-ty
103 ype 2 cytokine signaling is also required in FAPs, but not in myeloid cells, for rapid clearance of n
108 French Ile107Val, Ser77Tyr, and LateVal30Met FAP showed more rapid and severe disease progression; on
110 PH(3)T] [FAP], 1-butyl-1-methylpyrrolidinium FAP ([BMPL] [FAP]), and 1-(6-amino-hexyl)-1-methylpyrrol
113 The iBody inhibits both human and mouse FAP with low nanomolar inhibition constants but does not
118 body, named E3, which could attenuate 35% of FAP cleavage of the fluorescent substrate Ala-Pro-7-amid
119 tively distinguish endopeptidase activity of FAP from that of other related enzymes such as prolyl en
120 ovel single mutation (Phe33Ile) in a case of FAP with vitreous amyloidosis from India is reported.
121 Prior studies established that depletion of FAP(+) cells inhibits tumor growth by augmenting antitum
123 sensor allowed femtomolar (fM) detection of FAP, a detection limit well adapted and promising for qu
125 d provide support for further development of FAP(+) stromal cell-targeted therapies for the treatment
126 here could thus be utilized for diagnosis of FAP-related pathologies and for the therapeutic developm
128 peptidase DPPIV, the extracellular domain of FAP can be released into circulation as a functional enz
133 ine permitting the bioluminescent imaging of FAP(+) cells, we find that they reside in most tissues o
134 tic deletion and pharmacologic inhibition of FAP inhibited tumor growth in both an endogenous mouse m
135 icability of this iBody for the isolation of FAP from cell lysates and blood serum as well as for its
136 biopsies were performed on the distal leg of FAP patients with a follow-up duration of 3.8 +/- 1.6 ye
138 nesis-related genes, and increased levels of FAP-alpha, a crucial suppressor of antitumor immunity.
139 estoration of FAP expression in the lungs of FAP-deficient mice decreases lung hydroxyproline content
140 for HuR inhibition as an effective means of FAP chemoprevention, with caution advised in the setting
141 HuR inhibition in APC(Min) mice, a model of FAP and colon cancer, diminished the number of small int
146 umors, we set out to investigate the role of FAP in mouse models of epithelial-derived solid tumors.
152 tion of these cells, by adoptive transfer of FAP-targeted chimeric antigen receptor (CAR) T cells, re
153 l mimetic of TIMP3 blocked the conversion of FAPs into adipocytes, pointing to a strategy to combat f
154 Ps, IL-4 inhibited Dex-induced conversion of FAPs into adipocytes; this did not occur in FAPs express
155 -4/IL-13 signaling promotes proliferation of FAPs to support myogenesis while inhibiting their differ
164 ned with the trihexyl(tetradecyl)phosphonium FAP ([PH(3)T] [FAP]) IL for compounds with high molecula
165 -adapted, filamentous anoxygenic phototroph (FAP) that lacks chlorosomes, the dominant antenna found
167 omponent of familial amyloid polyneuropathy (FAP) due to mutated transthyretin, with sudomotor failur
169 most common familial amyloid polyneuropathy (FAP), transthyretin (TTR) displays this role primarily a
171 rs from familial amyloidotic polyneuropathy (FAP) patients is a well-described technique and useful f
172 ed with familial amyloidotic polyneuropathy (FAP), a neurodegenerative disease characterized by senso
173 n (TTR) familial amyloidotic polyneuropathy (FAP; n = 20), (2) TTR mutation carriers without peripher
175 atients with familial adenomatous polyposis (FAP) and the technical feasibility of performing spleen-
176 atients with familial adenomatous polyposis (FAP) are at markedly increased risk for duodenal polyps
177 atients with familial adenomatous polyposis (FAP) coli who have germ line mutations in the APC gene.
178 37 patients, familial adenomatous polyposis (FAP) in 12 patients, and colonic ischemia in 1 patient.
179 atients with Familial adenomatous polyposis (FAP) in a prospective study of thyroid neck US screening
183 PC) underlie familial adenomatous polyposis (FAP), an inherited cancer syndrome characterized by the
184 ate colitis, familial adenomatous polyposis (FAP), and a select group of patients with Crohn's diseas
185 efficacy in familial adenomatous polyposis (FAP), signal of benefit from imaging-based early detecti
191 atients with familial adenomatous polyposis (FAP-iPSCs) harboring germline mutations in the WNT-signa
194 rimers (MGP) and Forslund-Antonsson primers (FAP) and identified by Luminex (for types detected by MG
195 ise to fibroblast and adipocyte progenitors (FAPs) and to their differentiated progeny, fibroblasts a
197 lite cells and fibro/adipogenic progenitors (FAPs) from muscle; satellite cells did not differentiate
199 uscle-resident fibro/adipogenic progenitors (FAPs) that play a supportive role in muscle regeneration
203 form combining fluorogen-activating protein (FAP) technology with high-throughput flow cytometry to d
204 ically encoded fluorogen-activating protein (FAP) that binds a heavy atom-substituted fluorogenic dye
205 e we identify fibroblast activation protein (FAP) as the enzyme that cleaves and inactivates human FG
214 rine protease fibroblast activation protein (FAP) is selectively expressed on tumor-associated fibrob
215 Expression of fibroblast activation protein (FAP) is upregulated in stromal fibroblasts in more than
216 rane-inserted fibroblast activation protein (FAP) that is transiently expressed during epithelial-der
226 ry promoter 1B point mutations but only rare FAP-affected families carry similar mutations, the colon
228 nation) for preventing a clinically relevant FAP-related progression event in individuals with FAP.
230 In addition, administration of a selective FAP inhibitor acutely increased circulating intact FGF21
232 basis of our findings, we propose selective FAP inhibition as a potential therapeutic approach to in
233 ciated with the most debilitating and severe FAP ever described, with rapid onset of tetraparesis and
235 ancer have been previously described in some FAP-affected individuals with large deletions around pro
236 we concluded that glucocorticoids stimulate FAPs to differentiate into adipocytes in injured muscles
239 ihexyl(tetradecyl)phosphonium FAP ([PH(3)T] [FAP]) IL for compounds with high molecular weight and fu
240 1.2 microg L(-1) for [HMIM] [FAP], [PH(3)T] [FAP], 1-butyl-1-methylpyrrolidinium FAP ([BMPL] [FAP]),
241 ved after cell-based immunotherapy targeting FAP cautions against its use as a universal target.
247 consistent within vitrostudies showing that FAP mediates ordered proteolytic processing of matrix me
251 e coated with the chemokine, CXCL12, and the FAP(+) CAF was the principal source of CXCL12 in the tum
252 ined the overriding immunosuppression by the FAP(+) cell: T cells were absent from regions of the tum
258 CXCL12, from a single stromal cell type, the FAP(+) CAF, may direct tumor immune evasion in a model o
263 ear-infrared excitation and emission of this FAP-TAPs provides a new spectral range for photosensitiz
265 e expressed and characterized for binding to FAP by surface plasmon resonance and flow cytometry.
272 odissected in placebo- and sulindac- treated FAP patient tissue after which the methylation patterns
273 he tris(pentafluoroethyl)trifluorophosphate (FAP) anion are paired with imidazolium, phosphonium, and
276 PMNFD were all significantly reduced in TTR-FAP patients versus healthy controls, whereas TTR-noPN s
279 in Type Familial Amyloid Polyneuropathy (TTR-FAP) and demonstrated a slowing of disease progression i
284 ce group for APC mutations in the unselected FAP population, we used the UMD-APC database referenced
292 rolled trial, enrolling 92 participants with FAP, conducted from July 2010 through June 2014 at Hunts
295 at desmoid tumors may arise in patients with FAP after MSCs acquire somatic mutations during the prol
297 tic mutations that put certain patients with FAP at high risk for desmoid tumors and could be future
301 ypothesized that targeting tumor stroma with FAP-reactive T cells would inhibit tumor growth in cance
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