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1 asein was then dephosphorylated using potato acid phosphatase.
2 oclasts was determined by tartrate-resistant acid phosphatase.
3 ase, NT5E, and to a lesser extent, prostatic acid phosphatase.
4 , TRAF6, cathepsin K, and tartrate-resistant acid phosphatase.
5 the nuclear entry of lipin 1, a phosphatidic acid phosphatase.
6 m of activated PMN by secreting at least one acid phosphatase.
7 Mlo like protein, protein kinases and purple acid phosphatase.
8 ng peptide fragment of the protein prostatic acid phosphatase.
9 alkaline phosphatase, or tartrate-resistant acid phosphatase.
10 hematoxylin and eosin or tartrate-resistant acid phosphatase.
11 ith hematoxylin-eosin and tartrate-resistant acid phosphatase.
12 stimulate T-cell immunity against prostatic acid phosphatase.
13 hese genes is PHO5, which encodes a secreted acid phosphatase.
14 strated by the underglycosylation of surface acid phosphatase.
15 cts, such as androgen receptor and prostatic acid phosphatase.
16 ologue, murine Kv3.1b, are both modulated by acid phosphatases.
17 uld successfully identify previously unknown acid phosphatases.
18 and Pfr-GAP, to describe the three groups of acid phosphatases.
19 identify a large number of formerly unknown acid phosphatases.
20 lso identified by these profiles as putative acid phosphatases.
21 as 10(-10)) to bacterial class A nonspecific acid phosphatases.
22 and is the prototype of class C nonspecific acid phosphatases.
23 hanistic similarity to iron-dependent purple acid phosphatases.
24 of the P substrate spectrum based on purple acid phosphatases.
25 ge disequilibrium block containing the ACP1 (acid phosphatase 1) gene, a gene whose expression is sig
27 e protein (VCIP), also known as phosphatidic acid phosphatase 2b (PAP2b), in a functional assay of an
29 ins in different tissues, led us to identify acid phosphatase 5 (ACP5) as a candidate for the enzyme
30 of target genes like cathepsin K (Ctsk) and acid phosphatase 5 (Acp5) during osteoclast differentiat
31 , cathepsin K (Cstk), and tartrate-resistant acid phosphatase 5 (TRAP) with receptor activator of NF-
32 d gene encoding calcitonin receptor (Calcr), acid phosphatase 5, tartrate resistant (Acp5), cathepsin
33 erine/threonine protein phosphatases, purple acid phosphatases, 5'-nucleotidase, and DNA repair enzym
35 e phosphatase (B-ALP) and tartrate-resistant acid phosphatase 5b (TRAP-5b), and calcium and alveolar
38 -terminal propeptide, and tartrate-resistant acid phosphatase 5b were associated with higher odds of
40 N-terminal propeptide, or tartrate-resistant acid phosphatase 5b; these values corresponded to the up
41 evels of human OPG-Fc and tartrate-resistant acid phosphatase-5b (TRAP-5b) were measured throughout t
42 The N-terminal portion of the M. catarrhalis acid phosphatase A (MapA) was most similar (the BLAST pr
46 hu S4 the pathogenic roles of three distinct acid phosphatases, AcpA, AcpB, and AcpC, that are most c
47 se-1-phosphate (G1P) adsorbed on goethite by acid phosphatase (AcPase) can be of the same order of ma
49 of this study was to delete the four primary acid phosphatases (Acps) from Francisella novicida and e
50 nd tartrate-sensitive and tartrate-resistant acid phosphatase activities and influences the appearanc
52 alcium release or uptake, tartrate-resistant acid phosphatase activity (marker for osteoclasts), alka
53 unrecognized link between tartrate-resistant acid phosphatase activity and interferon metabolism and
54 ucture, but resulted in complete loss of its acid phosphatase activity as well as its anti-insect act
56 ne in M. catarrhalis strain O35E reduced the acid phosphatase activity expressed by this organism, an
59 e acid phosphatase domain in MapA eliminated acid phosphatase activity in the recombinant MapA protei
60 es (PBL) and enhanced the respiratory burst, acid phosphatase activity, chemotactic activity, and gen
61 which contributes most of the F. tularensis acid phosphatase activity, is secreted into the culture
67 cuolar H(+)-ATPase; TRAP, tartrate-resistant acid phosphatase; alphaMEM D10, minimal essential media,
68 tions and increased serum tartrate-resistant acid phosphatase and 25-hydroxyvitamin D concentrations
70 (248-286) is a peptide fragment of prostatic acid phosphatase and has been reported to form amyloid f
71 L-specific genes, such as tartrate-resistant acid phosphatase and immunoreceptor OCL-associated recep
75 HAD1 is a functional HAD protein having both acid phosphatase and phytase activities, it showed littl
76 arley, we found that the dynamics with which acid phosphatase and protease activities changed were di
77 involved in phosphate acquisition (the Pho1 acid phosphatase and the phosphate transporter SPBC8E4.0
79 ntly related to the other types, (2) class C acid phosphatases and (3) generic acid phosphatases (GAP
81 , 2, and 3 are Mg(2+)-dependent phosphatidic acid phosphatases and catalyze the penultimate step of t
82 Finally, the structures suggest that class B acid phosphatases and CCAPs share a common strategy for
83 lies, which include known pathogens, class C acid phosphatases and GAP proteins are found in a variet
86 roteinase 9, cathepsin K, tartrate-resistant acid phosphatase, and carbonic anhydrase II in bone marr
87 of the HCL markers CD25, tartrate-resistant acid phosphatase, and cyclin D1, smoothening of leukemic
88 resorption, detection of tartrate-resistant acid phosphatase, and determination of gene expression.
89 eceptors for AGEs (RAGE), tartrate-resistant acid phosphatase, and proliferating cell nuclear antigen
90 receptor for AGEs (RAGE), tartrate-resistant acid phosphatase, and proliferating cell nuclear antigen
93 hate is removed from NMN in the periplasm by acid phosphatase (AphA), and the produced nicotinamide r
94 ogether, this body of evidence suggests that acid phosphatases are general regulatory partners of Sha
96 d expression of tartrate-sensitive prostatic acid phosphatase as a broadly acting ectonucleotidase.
98 n this study, we identified ACPT (testicular acid phosphatase) biallelic mutations causing non-syndro
100 proteolytic peptide fragments from prostatic acid phosphatase can form amyloid fibrils termed SEVI (s
102 eceptor, but they express tartrate-resistant acid phosphatase, cathepsin K, and beta(3) integrin, sug
105 rophosphorylation was decreased in prostatic acid phosphatase cDNA-transfected stable subclones of C-
106 spho-monoesterase, i.e. a tartrate-resistant acid phosphatase (Cl MAcP) was also found to be up-expre
107 main fold similar to that of human prostatic acid phosphatase, consisting of an alpha/beta core domai
109 -growing cells by cellular form of prostatic acid phosphatase (cPAcP) expression, a negative growth r
112 o measure and characterise the activities of acid phosphatase, cysteine protease and nitrate reductas
113 orters upon proteolytic cleavage, as well as acid phosphatase cytochemistry to identify which endocyt
114 ein tyrosine phosphatase, cellular prostatic acid phosphatase, decreased correspondingly in those cel
115 dAMP, and BPQ-dCMP adducts were confirmed by acid phosphatase dephosphorylation of the BPQ-nucleotide
117 phosphatase was consistent with phosphatidic acid phosphatase domain containing 2 (PPAPDC2), an uncha
118 (H233A) in the predicted active site of the acid phosphatase domain in MapA eliminated acid phosphat
120 nsgenic construct using a tartrate-resistant acid phosphatase exon 1C promoter to drive expression of
122 the rhizosphere (as a result of citrate and acid phosphatase exudation) compared with maize roots.
124 ologous dendritic cells expressing prostatic acid phosphatase (for prostate cancer) or with autologou
125 fs in known alkaline phosphatases and purple acid phosphatase from red kidney bean shows that most of
128 results, we cloned genes encoding candidate acid phosphatases from genomic DNA or recovered from met
130 infection (SEVI) originating from prostatic acid phosphatase greatly increase XMRV infections of pri
131 e four Acps (AcpA, AcpB, AcpC, and histidine acid phosphatase [Hap]) in an F. novicida strain (DeltaA
132 ssed by histomorphometry, tartrate-resistant acid phosphatase histoenzymology, and cathepsin B (CATB)
133 ssed by histomorphometry, tartrate-resistant acid phosphatase histoenzymology, beta-galactosidase, sc
134 uencing of ACP5, encoding tartrate-resistant acid phosphatase, identified biallelic mutations in each
136 volution of a phosphate starvation-inducible acid phosphatase in C. glabrata relative to most yeast s
137 o-terminal propeptide and tartrate-resistant acid phosphatase in KO mice confirmed reduced bone remod
138 the unexpected mitotic induction of the PHO5 acid phosphatase in rich medium requires the transcripti
140 Lipin-1 is a Mg(2+)-dependent phosphatidic acid phosphatase involved in the de novo synthesis of ph
141 des a class of Mg(2+)-dependent phosphatidic acid phosphatases involved in the de novo synthesis of p
143 se (TMPase, also known as fluoride-resistant acid phosphatase) is a classic histochemical marker of s
144 n phosphate transporter (LaPT1) and secreted acid phosphatase (LaSAP1) promoter-reporter genes when t
145 body mass index, race, Gleason score, stage, acid phosphatase level, prostatectomy history, and nodal
146 Mutants lacking either the known secreted acid phosphatases, lipases, phospholipase C, lysophospho
147 activator of the ER-associated phosphatidic acid phosphatase lipin that promotes synthesis of major
149 d reactive substances, acetylcholinesterase, acid phosphatase), no significant effects were detected.
150 that inactivation of Ned1, the phosphatidic acid phosphatase of the lipin family, by CDK phosphoryla
152 orphology was analyzed in tartrate-resistant acid phosphatase or F-actin-stained samples, and bone re
155 regulated by the cellular form of prostatic acid phosphatase (PAcP), a prostate-unique protein tyros
156 absent on vacuoles lacking the phosphatidic acid phosphatase Pah1, which also lack Ypt7, the phospha
157 ined much less Mg(2+)-dependent phosphatidic acid phosphatase (PAP) activity than tissues from wild t
158 unized with a DNA vaccine encoding prostatic acid phosphatase (PAP) and a trans-vivo delayed-type hyp
160 nts of the abundant semen proteins prostatic acid phosphatase (PAP) and semenogelins form amyloid fib
161 and Ingenuity Systems) identified prostatic acid phosphatase (PAP) as an enzyme overexpressed in pro
162 LPIN1, which encodes lipin-1, a phosphatidic acid phosphatase (PAP) controlling the rate-limiting ste
164 pins (lipin 1, 2, and 3) act as phosphatidic acid phosphatase (PAP) enzymes, which are required for t
165 enotype was caused by activation of a purple acid phosphatase (PAP) gene, AtPAP15, which contains a d
166 e X-ray crystal structure of human prostatic acid phosphatase (PAP) in complex with a phosphate ion h
167 ccine (pTVG-HP [MVI-816]) encoding prostatic acid phosphatase (PAP) in patients with recurrent, nonme
171 odology is able to report on human prostatic acid phosphatase (PAP), a tumor marker, with a limit of
172 al to the transmembrane isoform of prostatic acid phosphatase (PAP), an enzyme with unknown molecular
173 ostate-specific antigen (PSA), and prostatic acid phosphatase (PAP), and is derived from the highly a
174 pain may be mediated by decreased prostatic acid phosphatase (PAP), as PAP levels are markedly reduc
175 tion and, as a Mg(2+)-dependent phosphatidic acid phosphatase (PAP), is a key enzyme in the biosynthe
176 using Sipuleucel-T, an autologous prostatic acid phosphatase (PAP)-loaded dendritic cell immunothera
178 HT-1, while its mammalian homolog, prostatic acid phosphatase (PAP; also known as ACPP-201) stably as
182 gy to members of the phosphoglycerate mutase/acid phosphatase (PGM/AcP) family of enzymes, with resid
183 st the gene encoding a phosphate-repressible acid phosphatase (PHO5) present in many yeasts including
184 port studies on a native E. coli periplasmic acid phosphatase, phytase (AppA), which contains three c
187 tein, along with elevated tartrate-resistant acid phosphatase-positive (TRAP+) OCs and alveolar bone
188 in (IL)-1beta levels, and tartrate-resistant acid phosphatase-positive (TRAP+) osteoclast numbers wer
190 pletion of PDGF-BB in the tartrate-resistant acid phosphatase-positive cell lineage show significantl
191 number of multinucleated tartrate-resistant acid phosphatase-positive cells along the alveolar bone
192 osteoclasts with reduced tartrate-resistant acid phosphatase-positive cells and dentine resorption c
194 ly enhanced the number of tartrate-resistant acid phosphatase-positive multinuclear osteoclast-like c
195 by counting the number of tartrate-resistant acid phosphatase-positive multinucleated cells and measu
196 from pannus invasion, and tartrate-resistant acid phosphatase-positive multinucleated cells at sites
197 9, and the generation of tartrate-resistant acid phosphatase-positive multinucleated cells in both c
200 ctivity was analyzed with tartrate-resistant acid phosphatase-positive osteoclasts and preosteoclasts
201 zed by reduced numbers of tartrate-resistant acid phosphatase-positive osteoclasts at the tumor-bone
202 teoblasts and diminished tartrate resistance acid phosphatase-positive osteoclasts in the defects.
204 ssed for the abundance of Tartrate Resistant Acid Phosphatase-positive osteoclasts, which revealed th
206 e marrow macrophages into tartrate-resistant acid phosphatase-positive preosteoclasts in culture but
207 nished formation of TRAP (tartrate-resistant acid phosphatase-positive) multinucleated osteoclasts, a
208 ibited reduced numbers of tartrate-resistant acid-phosphatase-positive cells and more proliferating c
209 bitory compounds for three of the four major acid phosphatases produced by F. tularensis SCHU4: AcpA,
210 d vaccines such as those targeting prostatic acid phosphatase, prostate-specific antigen, and cellula
211 hosphatase enzymes that also includes purple acid phosphatases, protein phosphatases, and nucleotide
215 3.1.3.2), a periplasmic class B nonspecific acid phosphatase, significantly increased activity in pa
216 own to deposphorylate the yeast phosphatidic acid phosphatase Smp2p, and we show that Dullard dephosp
217 A parallel series of tartrate resistant acid phosphatase-stained sections were evaluated for ost
221 assessed via quantitative tartrate-resistant acid phosphatase staining and degradation of human bone
223 ere expressed widely, and tartrate-resistant acid phosphatase staining notably was absent in the suba
225 tomography analysis, and tartrate-resistant acid phosphatase staining revealed reduced trabecular bo
230 tic cells was assessed by tartrate-resistant acid phosphatase staining, whereas the secretion of matr
234 n to OCs was confirmed by tartrate-resistant acid phosphatase staining; bone resorbing activity was a
235 n maize but greater exudation of citrate and acid phosphatase, suggesting a greater capacity to mobil
236 sella spp. is a respiratory-burst-inhibiting acid phosphatase that also exhibits phospholipase C acti
237 rancisella tularensis contains four putative acid phosphatases that are conserved in Francisella novi
239 hematoxylin and eosin and tartrate-resistant acid phosphatase to confirm the presence of osteolytic b
241 However, the absence of tartrate-resistant acid phosphatase (TRAP) activity and the lack of F4/80-p
242 inuclear cells expressing tartrate-resistant acid phosphatase (TRAP) activity produced by RANK-L-stim
243 of osteoclastogenesis and tartrate-resistant acid phosphatase (TRAP) activity was evaluated in RANKL-
244 e larger, fail to express tartrate-resistant acid phosphatase (TRAP) activity, and display a propensi
245 gnificantly reduced femur tartrate resistant acid phosphatase (TRAP) activity, suggesting potential r
247 mber of cells stained for tartrate-resistant acid phosphatase (TRAP) and immunohistochemical staining
248 dia and cell lysates, and tartrate-resistant acid phosphatase (TRAP) and mRNA detection for the osteo
249 ase (AP) for osteoblasts; tartrate-resistant acid phosphatase (TRAP) for osteoclasts; and the mineral
252 ously to the proximal region of the tartrate acid phosphatase (TRAP) gene promoter and suppresses nuc
253 ), osteocalcin (OCN), and tartrate-resistant acid phosphatase (TRAP) immunohistochemical staining wer
258 membranes as indicated by tartrate-resistant acid phosphatase (TRAP) staining and pit formation.
259 munohistochemistry, using tartrate-resistant acid phosphatase (TRAP) staining to identify osteoclasts
264 formation of multinuclear tartrate-resistant acid phosphatase (TRAP)(+) osteoclasts, associated with
265 ), osteoprotegerin (OPG), tartrate-resistant acid phosphatase (TRAP), and activated caspase-3 were pe
266 NK-kappaB ligand (RANKL), tartrate-resistant acid phosphatase (TRAP), and osteoclast-associated recep
267 opeptidase 13 (MMP13) and tartrate-resistant acid phosphatase (TRAP), leading to an acceleration in p
268 ere fixed and stained for tartrate-resistant acid phosphatase (TRAP), Oregon Green 488-phalloidin, a
269 A, the positive cells for tartrate-resistant acid phosphatase (TRAP), receptor activator of nuclear f
271 etected the appearance of tartrate-resistant acid phosphatase (TRAP)-negative multinucleated giant (M
272 vel of bone loss and less tartrate-resistant acid phosphatase (TRAP)-positive cell induction than M0
273 ased bone mass, increased tartrate-resistant acid phosphatase (TRAP)-positive cell number, and enhanc
274 rmation of multinucleated tartrate-resistant acid phosphatase (TRAP)-positive cells from primary muri
275 e loss in mice with fewer tartrate-resistant acid phosphatase (TRAP)-positive cells in alveolar bone.
276 ment cells displayed more tartrate-resistant acid phosphatase (TRAP)-positive cells than the co-cultu
282 numbers of multinucleated tartrate-resistant acid phosphatase (TRAP)/cathepsin K(+) OCs expressing ph
285 etry and immunohistology (Tartrate-Resistant Acid Phosphatase-TRAP, Osteocalcin and human specific an
288 d, cathepsin K, and serum tartrate-resistant acid phosphatase type 5b, but ankle loading reduced oste
289 ed the LPA-degrading enzyme lysophosphatidic acid phosphatase type 6 (ACP6), leading to upregulation
290 based on rhamnulose-1-phosphate aldolase and acid phosphatase using racemic glyceraldehyde and dihydr
291 with ECM fungal richness and abundance, and acid phosphatase was correlated with nonECM fungal abund
293 kappaB ligand (RANKL) and tartrate resistant acid phosphatase were significantly diminished in CIA-ch
294 lthough levels of type 5b tartrate-resistant acid phosphatase were significantly lower than those obs
295 broad range, phosphate starvation-regulated acid phosphatase, which functionally replaces PHO5 in th
296 F. tularensis subspecies encode a series of acid phosphatases, which have been reported to play impo
297 into the following three types: (1) class B acid phosphatases, which were distantly related to the o