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1                                              ALP activity in AVICs induced by TLR2 and TLR4 agonists
2                                              ALP activity in osteoblasts and TRAP activity in RAW264.
3                                              ALP activity was released from larval BBMVs prepared by
4                                              ALP analysis, on the contrary, detected similar amounts
5                                              ALP deserves routine monitoring, and the cause for an el
6                                              ALP is not a good proxy to assess Vtg levels in marine m
7                                              ALP response was defined as a >40% decrease from baselin
8                                              ALP was chosen as the biomarker due to its age-dependent
9                                              ALP-catalyzed hydrolysis of p-nitrophenyl phosphate (pNP
10                                              ALP/OXP-specific T cells reacted immediately to the addi
11 th CAD/MI (ALT OR 0.74, 95% CI 0.54 to 1.01, ALP OR 0.86, 95% CI 0.64 to 1.16 and GGT OR 1.08, 95% CI
12 omains in an ATN-1(alpha-actinin)- and ALP-1(ALP/Enigma)-dependent manner, where it contributes to th
13 ormal serum alkaline phosphatases (ALP) 74%; ALP above 1.5 times the upper limit of normal 13%; and c
14 h this novel sorting signal targets A(F-->A)-ALP into clathrin/AP-1 vesicles at the EE for retrieval
15                                     A(F-->A)-ALP was found to reach the PVC via early endosomes (EEs)
16 line phosphatase gene into the striatum (AAV.ALP).
17 were reached by week 12, no patient achieved ALP response or remission.
18 ease of both the substrate and/or the active ALP, in a biodegradable and low-cost material such as ze
19  (PTH), total alkaline phosphatase activity (ALP), calcium, and phosphorus, in minority infants and c
20                                 Allopurinol (ALP) hypersensitivity is a major cause of severe cutaneo
21                   Genetically predicted ALT, ALP and GGT were not clearly associated with CAD/MI (ALT
22                                     AlfA, an ALP that pushes plasmids apart in Bacillus, relies on a
23 scein diphosphate as a signal reporter in an ALP-linked immunosorbent assay, the proposed system prov
24 s in groups 1 and 2, respectively, showed an ALP decline of more than 30% (P = 0.04).
25 s in groups 1 and 2, respectively, showed an ALP decline.
26 osorbent assays, the probe was coupled to an ALP-linked immunosorbent assay for the sensitive and sel
27 gnificantly and positively related with ANC, ALP, and ferritin, suggesting phthalates may be associat
28  SH3 domains in an ATN-1(alpha-actinin)- and ALP-1(ALP/Enigma)-dependent manner, where it contributes
29       The mean levels of plasma Hcy, ALT and ALP were significantly reduced in responders within 10 w
30 drolysis adenosine-5'-triphosphate (ATP) and ALP can hydrolysis pyrophosphate, both reactions produce
31 defined as a >40% decrease from baseline and ALP remission as ALP normalization (if baseline ALP 1.67
32 d TLR4 in AVICs reduced BMP-2 expression and ALP activity to PVIC levels.
33 and GGT levels and between the ABO locus and ALP levels.
34            One common feature of the PKA and ALP catalyzing process is that PKA can hydrolysis adenos
35 s tool has the potential to simplify PKA and ALP clinical measurement, thereby improving diagnostics
36              The detection limit for PKA and ALP were much lower than existing assays.
37 le of detecting the activity of both PKA and ALP.
38  the activity and inhibition of both PKA and ALP.
39                                      PSA and ALP were measured before each treatment cycle and 4 wk a
40               Combined elevations of PTH and ALP occurred in only 2.5% of children.
41 % of subjects had elevations of both PTH and ALP.
42  stanniocalcin 1 (STC1) but not of RUNX2 and ALP in DFCs.
43 dition, we provide evidence that the UPS and ALP might be functionally connected such that impairment
44                              Considering any ALP decline as a response, no patient with increasing AL
45  decrease from baseline and ALP remission as ALP normalization (if baseline ALP 1.67x-2.8x ULN) or <1
46 ygotic twin males) were established to assay ALP activity, in vitro mineralization, and gene expressi
47  Mutations that affect the Z-disk-associated ALP-Enigma proteins have been linked to human muscular a
48 0.57, 0.83) for abnormal levels of ALT, AST, ALP, and GGT, respectively.
49  liver enzymes and continuous levels of AST, ALP, and GGT.
50 elopment by upregulating the levels of ATF4, ALP and RUNX2, and it stimulated angiogenesis of endothe
51  detection was performed after adding avidin-ALP to perform avidin-biotin reaction; the signal was ge
52 t decreased serum CTX levels and increased b-ALP levels.
53 Levels of serum bone alkaline phosphatase (B-ALP) and myeloperoxidase (MPO) activity in gingival tiss
54 nd IL-10, serum bone alkaline phosphatase (B-ALP) and tartrate-resistant acid phosphatase 5b (TRAP-5b
55 um, phosphorus, bone alkaline phosphatase (b-ALP), and terminal C telopeptide of collagen Type I (CTX
56  affect gingival IL-1beta and IL-10, serum B-ALP and TRAP-5b levels, or alveolar bone compared with c
57 ound in gingival IL-1beta and IL-10, serum B-ALP and TRAP-5b, and calcium and alveolar bone levels be
58 day 18, the animals were sacrificed, serum B-ALP, TRAP-5b, and calcium levels were measured, gingiva
59 oups treated with antioxidant according to B-ALP, MPO, RANKL, and BDI values (P <0.05).
60 ical characterization of the nanoceria-based ALP activity assay was established using a 1-naphthyl ph
61 mol/L); 13 of 20 (65%) patients had baseline ALP >3x ULN.
62 P 1.67x-2.8x ULN) or <1.67x ULN (if baseline ALP >2.8x ULN).
63  remission as ALP normalization (if baseline ALP 1.67x-2.8x ULN) or <1.67x ULN (if baseline ALP >2.8x
64                                      Because ALP is widely used in enzyme-linked immunosorbent assays
65 quacy of the procedure should be done before ALP is further assumed as a proxy of Vtg in other bivalv
66  is much data supporting differences between ALP families, there is little data regarding conservatio
67  retinopathy and in the former group between ALP treated and nontreated patients.
68  EILPs as an intermediate progenitor between ALPs and ILCps.
69 % confidence interval (CI) 1.62 to 5.52) but ALP OR 0.92 (95% CI 0.71 to 1.19) and GGT OR 0.88 (95% C
70 o form nanofibrils upon dephosphorylation by ALP, but CES-catalyzed cleavage of the ester bond on the
71     The ensuing T cell responses elicited by ALP or OXP were not limited to particular TCR Vbeta repe
72  cells from patients with MM, as measured by ALP activity at d 14 and Alizarin Red staining at d 21 (
73 herapy, did not otherwise appreciably change ALP and overt proof-of-concept was not established as pe
74 tinct from actin and the other characterized ALPs.
75 attachment or function, although circulating ALP activity was correlated significantly with incisor c
76 t differentiation markers, including COL1A1, ALP, and OC, in osteoblasts and PDL cells cultured on EM
77  while the two cell lines exhibit comparable ALP activities.
78 substrates and enzyme labels of conventional ALP assays.
79  UDCA administration significantly decreased ALP and sMet levels, and reduced relative liver weight.
80   For the first time, we were able to detect ALP at a concentration of approximately 4 x 10(-15) M or
81                                     Elevated ALP at 1 year, affecting 30% of patients, predicted both
82 ne monitoring, and the cause for an elevated ALP should be sought.
83 t with developmental delay, ID, and elevated ALP, we identified compound-heterozygous variants c.439d
84 steogenic transcription factors and enhanced ALP activity.
85                                     Finally, ALP maturation kinetics in vac8Delta and vac17Delta cell
86           The detection limits were 15fM for ALP and 0.75mM for pNPP.
87 on limit at a signal-to-noise ratio of 3 for ALP was estimated to be 0.02 units/L (~6 pM; 1 ng/mL).
88 tform and has demonstrated functionality for ALP detection in human serum.
89 n to design a turn-on fluorescence probe for ALP sensing.
90 doplasmic reticulum (ER) export receptor for ALP; and AP-3 subunit genes.
91 sion level of early osteogenic marker genes, ALP, Runx2, and type I collagen, which play a critical r
92 ccurrence of biliary sludge and lowered GGT, ALP, and ALT.
93                       Maximum levels of GGT, ALP, and ALT were lower in the late PN group (P < 0.01).
94             Thirty-seven patients had a high ALP level (19 from group 1 and 18 from group 2).
95 P and BMP2 demonstrated significantly higher ALP and mineralization activity (P <0.05).
96                         Of these, histology, ALP, and TE came out as the most promising.
97  though associated with a modest decrease in ALP after 28 weeks of therapy, did not otherwise appreci
98 ssue formation with significant increases in ALP and DMP1 staining in vivo, whereas DPSC/E106Q cells
99 nd decreases in cell number and increases in ALP and local factors typical of MG63 cells grown on SLA
100 ts given OCA had at least a 20% reduction in ALP compared with 8% (3 of 37) of patients given placebo
101           Silencing MGP by siRNA resulted in ALP activity that was increased by 197% +/- 8.4% (P </=
102 sphate) that could previously not be used in ALP assays can be conveniently colorimetrically detected
103 protein expression of bone markers including ALP, Cbfa-1, and periostin.
104 ne as a response, no patient with increasing ALP showed a PSA response (P = 0.036).
105 the Id2-mediated inhibition of Cbfa1-induced ALP activity and OCL production.
106 he fact that mutant alpha-synucleins inhibit ALP functioning by tightly binding to the receptor on th
107 milarly, SSRIs (except citalopram) inhibited ALP and bone mineralization by OB but only at 30 mumol/L
108           At higher doses of the inhibitors, ALP levels were attenuated, but dexamethasone-induced bi
109 ad applications in sensing schemes involving ALP.
110 oid progenitors and, unexpectedly, Irf8(-/-) ALPs produced more neutrophils in vivo than their wild-t
111 enching of BODIPY-ATP can be paired with its ALP-mediated dephosphorylation to design a turn-on fluor
112                A detection limit of 0.04 U/L ALP with a linear range up to 2U/L was obtained with asc
113  and osteocalcin (OCL) gene, leading to less ALP activity and osteocalcin (OCL) production.
114 that express approximately 15-20 times lower ALP activity compared to SaOs2) not being affected at co
115 reased activity of the calcification marker, ALP, in glaucomatous trabecular meshworks might be indic
116 ally significant relative reductions in mean ALP from baseline to the end of the study (P < .0001 all
117              BPS804 treatment increased mean ALP and bone-specific ALP enzymatic activity between day
118   However, at BMP2 concentrations >10 ng/mL, ALP, in vitro mineralization, and osteonectin were downr
119   Trabecular meshwork tissue showed moderate ALP activity at 13 days postinjection.
120  of the control specimens was 7.3 +/- 1.6 ng ALP/microg DNA (n = 4), whereas that of the glaucomatous
121 the glaucomatous tissue was 37.0 +/- 10.7 ng ALP/microg genomic DNA (n = 5; P </= 0.04).
122    Only 1 in 6 patients with AMAs and normal ALP will develop PBC after 5 years.
123               Among the patients with normal ALP and no evidence of cirrhosis, the 5-year incidence r
124                               The normalized ALP of the control specimens was 7.3 +/- 1.6 ng ALP/micr
125 ds, adaptive L(infinity)-norm penalized NSC (ALP-NSC) and adaptive hierarchically penalized NSC (AHP-
126 for human health, the mechanism of action of ALP-Enigma proteins is largely unknown.
127 cles as redox active catalytic amplifiers of ALP signals.
128  present a molecular and genetic analysis of ALP-Enigma function in C. elegans.
129 elastography (TE); histology; combination of ALP+histology; and bilirubin.
130 ancement was related to the concentration of ALP.
131                      Area under the curve of ALP in predicting graft loss from rejection was 0.81 (95
132 ers a straightforward and rapid detection of ALP activity with the enzyme present in the nanomolar co
133 hold a potential application in diagnosis of ALP-related diseases or evaluation of ALP functions in b
134 L required by legislation, (2) estimation of ALP in saliva and (3) chlorpyrifos control in commercial
135 sis of ALP-related diseases or evaluation of ALP functions in biological systems.
136 and resistant (58%) to butyrate induction of ALP activity.
137   The primary outcome was change in level of ALP from baseline (day 0) until the end of the study (da
138 gradable Dex-peptides had elevated levels of ALP activity and calcium deposition, whereas no elevated
139 ors exhibited significantly higher levels of ALP activity than their matched counterparts with normal
140            In the extension study, levels of ALP continued to decrease to a mean level of 202 +/- 11
141                                    Levels of ALP decreased 21%-25% on average from baseline in the OC
142 r evaluation and the physiological levels of ALP in healthy people, the applicability of this assay i
143 10 to 50 mg, significantly reduced levels of ALP, gamma-glutamyl transpeptidase, and alanine aminotra
144 eased relative liver weight, serum levels of ALP, sMet, and loss of intracellular glycogen.
145 anchored and that the proper localization of ALP-1 at dense bodies is dependent on alpha-actinin.
146                      The immune mechanism of ALP-induced severe cutaneous adverse reactions is poorly
147 susceptible to pharmacological modulation of ALP function.
148 t that aggregation-dependent perturbation of ALP function is a relevant pathogenic mechanism for AD-A
149  upon exposure to the hydrolytic products of ALP.
150 st has been shown in identifying the role of ALP in neurodegeneration.
151     This probe was used for the screening of ALP inhibitors, including Na3VO4, imidazole, and arginin
152                             The stability of ALP in serum allows for the differentiation between old
153 a2 significantly induced the upregulation of ALP activity in two trabecular meshwork primary cell lin
154            Using uncompetitive inhibitors of ALPs and fluorescent D-tetrapeptides, we delineate that
155 he cancer cell lines express higher level of ALPs are more susceptible to inhibition by the phosphory
156 i strains use their different repertoires of ALPs to create diversity in their metabolic niches, by a
157 inkage between the dysfunction of the UPS or ALP and the occurrence of this disorder.
158 pulation sampled in the American Life Panel (ALP).
159             The autophagy-lysosomal pathway (ALP) is involved in the degradation of long-lived protei
160 em (UPS) or the autophagy-lysosomal pathway (ALP).
161 system (UPS) and autophagy-lysosome pathway (ALP) are the two most important mechanisms that normally
162 s to explain the autophagy-lysosome pathway (ALP) dysfunction in cells from AD-ANCL patients.
163 ctivation of the autophagy-lysosome pathway (ALP) in a mammalian target of rapamycin (mTOR)-independe
164                               Median percent ALP reduction from baseline to week 28 was 12.1%.
165 ALP) elevations were also common, persistent ALP elevations lasting up to 17.6 years were seen in 25%
166 , P = 0.007-0.03), and alkaline phosphatase (ALP) (HR 1.05, P < 0.001).
167 % women) and levels of alkaline phosphatase (ALP) 1.5- to 10-fold the upper limit of normal.
168               Elevated alkaline phosphatase (ALP) activities and calcium deposition levels were obser
169 ls exhibited increased alkaline phosphatase (ALP) activity and expression of osteogenic genes in vitr
170  observations of lower alkaline phosphatase (ALP) activity and higher expression of CD105, a stem cel
171  analogs for detecting alkaline phosphatase (ALP) activity and inhibition.
172 dependent reduction in alkaline phosphatase (ALP) activity and osteocalcin mRNA expression was observ
173 tedly, Wnt-1 inhibited alkaline phosphatase (ALP) activity and the formation of mineralized nodules i
174 5-fold decrease in the alkaline phosphatase (ALP) activity in comparison to cells treated with osteog
175 shwork (HTM) cells and alkaline phosphatase (ALP) activity in the angle tissue.
176 RP gradually increased alkaline phosphatase (ALP) activity in the cells in a dose-dependent manner.
177 y for the detection of alkaline phosphatase (ALP) activity is reported based on the surface reactivit
178 erentiation of DFCs by alkaline phosphatase (ALP) activity measurement, alizarin red staining, and el
179 s analyzed in terms of alkaline phosphatase (ALP) activity of KS483-4C3 mouse progenitor cells, and t
180                        Alkaline phosphatase (ALP) activity was used as a marker of osteogenic differe
181 elated genes, elevated alkaline phosphatase (ALP) activity, and enhanced mineralization.
182 evidenced by increased alkaline phosphatase (ALP) activity, compared to the direct infusion of Dex in
183 nd biosensors based on alkaline phosphatase (ALP) activity/inhibition in the presence of phosphatase
184 ion as demonstrated by alkaline phosphatase (ALP) activity/staining as well as alizarin red S stainin
185 s had higher levels of alkaline phosphatase (ALP) and alpha-fetoprotein (AFP) and lower level of alan
186 days were assessed for alkaline phosphatase (ALP) and bone mineralization.
187 minotransferase (ALT), alkaline phosphatase (ALP) and gamma glutamyltransferase (GGT), on diabetes an
188 minotransferase (AST), alkaline phosphatase (ALP) and gamma-glutamytransferase (gamma-GT).
189 arious enzymes such as alkaline phosphatase (ALP) and horseradish peroxidise (HRP).
190 d transcription of the alkaline phosphatase (ALP) and osteocalcin (OCL) gene, leading to less ALP act
191 ' fragments of an anti-alkaline phosphatase (ALP) antibody to orient all the antigenic binding sites
192 otein kinase (PKA) and alkaline phosphatase (ALP) are clinically relevant enzymes for a number of dis
193 gonist Sclerostin, and alkaline phosphatase (ALP) are two additional targets of mir-204/211.
194 nylphosphate (pNPP) by alkaline phosphatase (ALP) bound on paramagnetic-beads was performed into a sm
195                        Alkaline phosphatase (ALP) catalyzes the hydrolisis of sodium thiophosphate (T
196     Although transient alkaline phosphatase (ALP) elevations were also common, persistent ALP elevati
197   Calcification marker alkaline phosphatase (ALP) enzyme activity was assayed by fluorescence produce
198 the tissue-nonspecific alkaline phosphatase (ALP) enzyme.
199 nt export of secretory alkaline phosphatase (ALP) from the endoplasmic reticulum depends on the conse
200 tection sensitivity of alkaline phosphatase (ALP) in electrochemical assays by using nanoceria partic
201 ly can be triggered by alkaline phosphatase (ALP) in solution or in situ by the ALP produced by osteo
202 2), and three loci for alkaline phosphatase (ALP) levels (ALPL on chromosome 1, GPLD1 on chromosome 6
203 ent strategy to detect alkaline phosphatase (ALP) under physiological conditions has been developed.
204 f assay for the enzyme alkaline phosphatase (ALP) using PPi as the substrate is developed.
205                        Alkaline phosphatase (ALP) was visualized in the vossicles to assess osteoblas
206 vacuolar maturation of alkaline phosphatase (ALP), a cargo of the AP-3 pathway.
207  showed elevated serum alkaline phosphatase (ALP), a GPI-anchored enzyme, in all three affected child
208 ntified, the levels of alkaline phosphatase (ALP), a marker commonly used in clinical diagnostics cor
209                        Alkaline phosphatase (ALP), alpha2 and beta1 mRNA, but not alpha5, alpha v, be
210 des tissue nonspecific alkaline phosphatase (ALP), an enzyme that promotes mineralization by reducing
211 minotransferase (AST), alkaline phosphatase (ALP), and gamma-glutamyl transaminase (GGT) were measure
212 ly osteogenic markers, alkaline phosphatase (ALP), and osteoprotegerin (OPG) by hMSCs and transcripto
213 ence of high levels of alkaline phosphatase (ALP), and presence of the efflux transporter, P-glycopro
214 ific antigen (PSA) and alkaline phosphatase (ALP), as well as the correlation of PSA changes with the
215 minotransferase (ALT), alkaline phosphatase (ALP), gamma-glutamyl transpeptidase (GGT), or total bili
216          Expression of alkaline phosphatase (ALP), in vitro mineralization along with osteonectin exp
217  of homocysteine, ALT, alkaline phosphatase (ALP), lipid profile and liver ultrasonographic examinati
218 ranscription factor 2, alkaline phosphatase (ALP), osteocalcin (OC), and collagen1alpha1 (COL1A1), an
219 y was quantified using alkaline phosphatase (ALP), relative liver weight, and confirmed by histologic
220 of tissue non-specific alkaline phosphatase (ALP), resulting in increased pyrophosphate (PP(i)) and a
221     We discovered that alkaline phosphatase (ALP), the enzyme broadly used in enzyme-linked immuno-so
222  phosphate (1-NP), for alkaline phosphatase (ALP).
223 g disease progression: alkaline phosphatase (ALP); transient elastography (TE); histology; combinatio
224 ic acid therapy (i.e., alkaline phosphatase [ALP] >1.67x upper limit of normal [ULN] after >/=6 month
225 ic phenotypic changes (alkaline phosphatase [ALP] activity, calcified nodule formation) than PVICs.
226 bin) and inflammation (alkaline phosphatase [ALP], absolute neutrophil count [ANC], ferritin [adjuste
227  transpeptidase [GGT], alkaline phosphatase [ALP], twice weekly; n = 3,216) were quantified.
228 ers of liver function (alkaline phosphatase, ALP, and aspartate aminotransferase, AST) and total seru
229 ers 46%; normal serum alkaline phosphatases (ALP) 74%; ALP above 1.5 times the upper limit of normal
230 lesterases (CESs) and alkaline phosphatases (ALPs).
231 ells that overexpress alkaline phosphatases (ALPs).
232                       Alkaline phosphatases (ALPs, EC 3.1.3.1) isolated from lepidopteran and diptera
233 indirect technique, alkali labile phosphate (ALP), that assumes that vitellogenin is the most abundan
234  indicated by increased alkaline phosphates (ALP) activity and calcium deposition.
235 A116T) mice featured 50% reduction in plasma ALP activity compared with wild-type controls.
236 s were identified that accumulated precursor ALP, many with established defects in vacuolar protein t
237 ed the mechanism by which Erv26p couples pro-ALP to the coat protein complex II (COPII) export machin
238 ee assays that monitor interactions with pro-ALP cargo and packaging into COPII vesicles.
239 ins of Erv26p inhibited interaction with pro-ALP, whereas mutations in the C-terminal tail sequence i
240 ips between EILPs, all-lymphoid progenitors (ALPs), and ILC precursors (ILCps).
241 differentiate into all lymphoid progenitors (ALPs).
242               The 101 adhesin-like proteins (ALPs) in the pan-genome (45 +/- 6 per strain) exhibit st
243 ea contain a variety of actin-like proteins (ALPs) that form filaments with surprisingly diverse arch
244 er cells by assembly of actin-like proteins (ALPs).
245 y (mouse-anti BoNT/E) followed by RalphaMIgG-ALP/AuNPs.
246 onalized with gold nanoparticles (RalphaMIgG-ALP/AuNPs).
247 i-mouse IgG-alkaline phosphatase (RalphaMIgG-ALP) functionalized with gold nanoparticles (RalphaMIgG-
248 e HLA-B*58:01 molecule for drug recognition, ALP-specific T cells also were restricted to other MHC c
249   Overexpression of MGP in HTM cells reduced ALP activity in a model of BMP2-induced osteogenesis.
250 PP-PDL cells exhibited significantly reduced ALP and mineralizing capacity, which were rescued by add
251 eolar development and function under reduced ALP, bringing attention to direct effects of HPP on alve
252 onation and fluorescence microscopy revealed ALP transport defects in yck3Delta cells.
253 of osteoblast marker genes, including Runx2, ALP, OC, BSP, OPG, and DMP-1, with concurrent upregulati
254            In real time (i.e. in about 1 s), ALP (Ascending Ladder Program) calculates the E-values f
255  to coordinately modulate Runx2, Sclerostin, ALP and Dlx5 proteins at levels appropriate for optimal
256  and suggests that divergent DNA-segregating ALPs with different assembly properties operate via diff
257 eatment increased mean ALP and bone-specific ALP enzymatic activity between days 2 and 29.
258 elegans provides an excellent model to study ALP-Enigma function.
259    Taken together, our data demonstrate that ALP-1 and alpha-actinin function together to stabilize a
260  analysis of alp-1 mutants demonstrates that ALP-1 functions to maintain actin filament organization
261                                 We show that ALP-1 and alpha-actinin colocalize at dense bodies where
262 notype of the alp-1 mutants, suggesting that ALP-1 and alpha-actinin function in the same cellular pr
263                                          The ALP-catalyzed hydrolysis of BODIPY-ATP resulted in the f
264                                          The ALP-catalyzed PPi hydrolysis would disable the complexat
265 le with increased alpha-synuclein burden the ALP is recruited.
266 gregated CSPalpha are degraded mainly by the ALP but this disease-causing mutation exhibits a faster
267 sphatase (ALP) in solution or in situ by the ALP produced by osteosarcoma cell line, SaOs2.
268               In Caenorhabditis elegans, the ALP-Enigma protein family is encoded by a single gene, a
269 arch have therefore focused on enhancing the ALP in neurodegenerative diseases.
270 -on mode provides a high selectivity for the ALP assay.
271                               R code for the ALP-NSC and the AHP-NSC algorithms are available from au
272 nse to ALP is demonstrated to arise from the ALP catalyzed hydrolysis of PPi to phosphate (Pi).
273  did not show a significant reduction in the ALP activity.
274                              Deficits in the ALP result in protein aggregation, the generation of tox
275 ents demonstrate signal amplification of the ALP activity assay by nanoceria for all three products,
276              We review the regulation of the ALP and TFEB and their impact on neurodegenerative disea
277 anges after interaction with products of the ALP catalyzed reaction, resulting in charge transfer com
278 his topic and discuss the unique role of the ALP in this neurogenerative disorder and the putative th
279 pports the assumption that impairment of the ALP may be related to the development of Parkinson's dis
280                                  None of the ALP-associated SNPs were associated with other liver tes
281 ity enabled oxidation of the products of the ALP-catalyzed reaction.
282 y, the inhibition effect of phosphate on the ALP activity was also studied.
283         These results show evidence that the ALP method is not providing reliable information about V
284 ts provide a novel link between the UPS, the ALP, and alpha-synuclein pathology and may have importan
285 red the results with those obtained with the ALP method.
286 terize the interaction of nanoceria with the ALP-generated products.
287 d the putative therapeutic potential through ALP enhancement.
288 d requirement is bypassed by fusing Atg18 to ALP, a vacuolar transmembrane protein, vac14Delta vacuol
289 TCR, we generated T cell lines that react to ALP or its metabolite oxypurinol (OXP) from HLA-B*58:01(
290 ay solution; however, the signal response to ALP is demonstrated to arise from the ALP catalyzed hydr
291                          The best understood ALP, ParM, has a core set of biochemical properties that
292      In agreement with this, ALN upregulated ALP activity considerably in vossicles.
293        PDL cells and osteoblasts upregulated ALP and in vitro mineralization in a dose-dependent mann
294 atically generated products of commonly used ALP substrates were detected at a screen printing electr
295 with a subsample of highly educated, wealthy ALP subjects as well as elite law school students and un
296  10(-15) M or at single-molecule levels when ALP was incubated with BCIP for 1 h in the Tris-HCl buff
297 cific interaction of analyte (antibody) with ALP-labeled antibody can be detected through formation o
298               The specific associations with ALP levels may point to genes for bone or intestinal dis
299 ate (FDP) and immuno-complex conjugated with ALP.
300                   The PDR group treated with ALP had significantly lower subbasal nerves number compa

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