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1                                              APN also provides an exposed outer surface for coronavir
2                                              APN antagonists specifically inhibited angiogenesis in c
3                                              APN binds to, but does not degrade, NGR motifs in ECM pr
4                                              APN deficiency is associated with protection from chemic
5                                              APN exerts proinflammatory activities in the colon by in
6                                              APN expression produced sustained and significant elevat
7                                              APN induced AdipoR mRNA and protein expression by up-reg
8                                              APN inhibited the angiotensin type-1 receptor (AT1R), in
9                                              APN is a cell surface-anchored and seahorse-shaped zinc-
10                                              APN is expressed in the colon, luminal APN associates wi
11                                              APN knockout (KO) mice and their wild-type (WT) litterma
12                                              APN KO mice are protected from chemically induced coliti
13                                              APN receptors localize in the retina, particularly to pa
14                                              APN-KO mice also exhibited increased leukocyte adhesion
15                                              APN-KO mice exhibited enlarged brain infarction and incr
16                                              APN-KO mice showed decreased cerebral blood flow during
17                                 Adiponectin (APN) is an adipokine that regulates insulin sensitivity
18                                 Adiponectin (APN) is an adipose tissue-derived factor with anti-infla
19                                 Adiponectin (APN), a pleiotropic adipokine that exerts anti-inflammat
20 lectrochemical immunosensor for adiponectin (APN) using screen printed carbon electrodes (SPCEs) modi
21 ing, adipocyte-secreted hormone adiponectin (APN) exerts protective effects on the heart under stress
22 her increasing plasma levels of adiponectin (APN), a pleiotropic adipokine, provides therapeutic bene
23                           Serum adiponectin (APN) concentrations positively correlate with postnatal
24  studies have demonstrated that adiponectin (APN) attenuates cerebral ischemic/reperfusion via globul
25                           Antibodies against APN inhibited in vivo tumor homing by the NGR phage.
26 herapeutic both in vitro and in vivo against APN-expressing prostate cancer models.
27 hat have significantly reduced lung airspace APN but high serum APN levels had pulmonary inflammatory
28 ng loss of domain III binding eliminates all APN binding.
29 NA profiles to distinguish between allograft APN and AR.
30 derived from co-drugs combining a NEP and an APN inhibitor through a disulfide bond with side chains
31 s are evidence that the 106-kDa GPI-anchored APN is a specific binding protein, and a putative midgut
32 ical difference in expression between AR and APN.
33           The inconsistency between BBMV and APN binding data with Cry1Ab to M. sexta suggests the po
34 d extensive colocalization of T-cadherin and APN on cardiomyocytes in vivo.
35                                Cytokines and APN levels were measured.
36 phenotype controls the AdipoR expression and APN-mediated inflammatory response.
37 doplasmic reticulum stress is increased, and APN production is suppressed.
38                          For both ASGP-R and APN and for both treatments, the block in trafficking wa
39             Participants in the standard and APN counseling groups were not statistically different b
40      Direct correlation between toxicity and APN binding was observed for the mutant toxins using thi
41 regions are involved in in vivo toxicity and APN binding.
42 ites during cerebral ischemia in both WT and APN-KO mice.
43 uring ischemia did not differ between WT and APN-KO mice.
44 ntly reduced cerebral infarct size in WT and APN-KO mice.
45  compared with apoE single-deficient (apoE-/-APN+/+) mice.
46 otein E/adiponectin double-deficient (apoE-/-APN-/-) mice had increased plasma IP-10 levels, accelera
47 tility, we examined the interactions between APN and extracellular matrix (ECM) proteins.
48 the specific and stable interactions between APN and the NGR motifs in ECM proteins and tumor-homing
49 d pathological cardiac remodeling by binding APN and activating its cardioprotective functions.
50                        The receptors binding APN to cardiac tissue, however, have remained elusive.
51 ce of apoptotic cells by macrophages in both APN-KO and wild-type mice.
52 , apoptosis and TNF-alpha production in both APN-KO and wild-type mice.
53 uteum, blood vessels also expressed APN, but APN was not detected in blood vessels of various other n
54 cts on lung endothelium were demonstrated by APN's ability to inhibit LPS-induced IL-6 production in
55                                         CD13/APN is also found in nonhematopoietic tissues, and its n
56                                         CD13/APN is transactivated by a cooperative interaction betwe
57 use mutation of this sequence abrogates CD13/APN transcription.
58 and synergizes with c-Myb in activating CD13/APN expression.
59 yb regulated targets, such as Bcl-2 and CD13/APN, coupled with the activation of as yet undefined dif
60 ription of reporter plasmids containing CD13/APN proximal promoter sequences is significantly increas
61 to influence Ets-1- and c-Myb-dependent CD13/APN transcription.
62 his report, it is shown that endogenous CD13/APN levels in primary cells and cell lines are up-regula
63 tively rescued by addition of exogenous CD13/APN protein.
64 Ets-2 by RAS/MAPK is a prerequisite for CD13/APN endothelial induction and Ets-2 and its targets play
65 f this pathway that are responsible for CD13/APN induction.
66 Ets-2 phosphorylation is obligatory for CD13/APN induction.
67  confirm a role for endogenous Ets-2 in CD13/APN expression, we specifically abrogated Ets-2 mRNA and
68  knockdown that significantly inhibited CD13/APN transcription.
69 n immature myeloblastic cells inhibited CD13/APN-driven reporter gene activity (85 to 95% reduction)
70                  CD13/aminopeptidase N (CD13/APN) is a potent regulator of angiogenesis both in vitro
71              The CD13/aminopeptidase N (CD13/APN) metalloprotease is an important regulator of angiog
72 - and c-Myb-dependent aminopeptidase N (CD13/APN) promoter and an Ets-1-dependent artificial promoter
73 in tumor vasculature, the regulation of CD13/APN by factors contributing to angiogenic progression wa
74                   c-Maf's inhibition of CD13/APN expression correlates with its ability to physically
75 sential for the angiogenic induction of CD13/APN expression.
76  vitro and in vivo and transcription of CD13/APN in endothelial cells is induced by angiogenic growth
77 ere, we show that cytokine induction of CD13/APN in endothelial cells is regulated by distinct Ras ef
78 duced endogenous cell surface levels of CD13/APN in U937 cells.
79        To investigate the mechanisms of CD13/APN induction in tumor vasculature, the regulation of CD
80      Finally, functional antagonists of CD13/APN interfere with tube formation but not proliferation
81 d the possibility that the induction of CD13/APN is mediated by phosphorylation of Ets-2 via RAS/MAPK
82                           Assessment of CD13/APN promoter responsiveness demonstrated that hDMP1alpha
83            This pattern matched that of CD13/APN reporter gene expression, indicating that Maf modula
84                           Activation of CD13/APN required both the intact DNA binding and transactiva
85 mical inhibitors prevented induction of CD13/APN transcription in response to basic fibroblast growth
86                       Reintroduction of CD13/APN, a shared downstream target of these pathways, overr
87 ular endothelial cells, suggesting that CD13/APN functions in the control of endothelial cell morphog
88 se studies provide strong evidence that CD13/APN is an important target of Ras signaling in angiogene
89 xenograft tumor growth, indicating that CD13/APN plays an important functional role in vasculogenesis
90     These studies clearly establish the CD13/APN metalloprotease as an important regulator of endothe
91   In the hematopoietic compartment, the CD13/APN metalloprotease is one of the earliest markers of ce
92 factors mapped to a 38-bp region of the CD13/APN promoter containing an Ets-core motif that specifica
93 ore, hDMP1beta was found to inhibit the CD13/APN promoter transactivation ability of hDMP1alpha.
94  (MEK) stimulate transcription from the CD13/APN proximal promoter.
95 to a lesser extent Ets-1, transactivate CD13/APN promoter activity via the Ets-core motif, whereas Fl
96 2 mutant, T72A, failed to transactivate CD13/APN, suggesting that Ets-2 phosphorylation is obligatory
97               Treatment of animals with CD13/APN inhibitors significantly impaired retinal neovascula
98                                  Circulating APN binds to bFGF and HB-EGF, likely inhibiting their pr
99 N in ROP development and whether circulating APN concentrations are increased by dietary omega-3 LCPU
100                            Thus, in colitis, APN exerts an opposite role compared with atherosclerosi
101                        Expression of colonic APN overlaps with that of bFGF and HB-EGF, which play a
102  amount of APN care in minutes or contacts); APN (education, expertise, and experience); and host and
103                                  Conversely, APN uncovers a high-affinity epitope that is subsequentl
104 nce were used to confirm and characterize CP-APN interaction.
105 vity in sda mutants is caused by a defective APN gene that somehow increases seizure susceptibility.
106  Bm12 allografts into adiponectin-deficient (APN-/-, C57BL/6 background) or wild-type (APN+/+) mice.
107  injury, we subjected adiponectin-deficient (APN-KO) and wild-type (WT) mice to 1 hour of middle cere
108 chemia-reperfusion in adiponectin-deficient (APN-KO) mice resulted in increased myocardial infarct si
109                       Adiponectin-deficient (APN-KO) mice were impaired in their ability to clear apo
110 emic inflammatory response in APN-deficient (APN(-/-)) mice compared with wild-type (wt) littermates.
111 egulating AdipoR expression and differential APN-mediated macrophage inflammatory responses, which ca
112 an N-acetylgalactosamine moiety on L. dispar APN.
113  expression may prove helpful to distinguish APN from AR in renal allograft biopsies.
114 e used as a diagnostic marker to distinguish APN from lower UTI and function as a diagnostic marker i
115  essential in developing studies to document APN effects on outcomes important to the country and reg
116 le N displayed growth retardation in Vero E6-APN cells compared to the wild-type virus.
117             These structural features enable APN to function ubiquitously in peptide metabolism, inte
118 igh-molecular weight APN levels and enhanced APN localization in the artery wall.
119 s essential in developing studies to examine APN effectiveness internationally.
120 , in oxygen-induced retinopathy experiments, APN-deficient mice had a marked and dose-dependent defic
121                                   To explore APN-based tumor cell motility, we examined the interacti
122 tured APN and to cells engineered to express APN on their surface.
123 -null mice, recombinant adenovirus-expressed APN reduced exaggerated hypertrophy and infarct size and
124  corpus luteum, blood vessels also expressed APN, but APN was not detected in blood vessels of variou
125 ase N (APN) of their natural host and feline APN (fAPN) as receptors.
126 ycosylation differences between hAPN, feline APN (fAPN), and pAPN account for receptor specificity of
127                           Using mouse-feline APN chimeras, we identified three small, discontinuous r
128 rfusion models, T-cadherin was necessary for APN-dependent AMPK phosphorylation.
129  selected conditions, a calibration plot for APN was constructed showing a range of linearity extendi
130  dysfunction may be a sign more specific for APN and prognostic of potential recovery.
131 ely, and its sensitivity and specificity for APN were compared with those of dimercaptosuccinic acid
132 742 in fAPN and the homologous R741 in human APN (hAPN) were key determinants of host range for FCoV,
133 example, the human coronavirus can use human APN (hAPN) but not porcine APN (pAPN) as its cellular re
134 bitors of N. meningitides, porcine and human APNs, and the reference leucine aminopeptidase (LAP).
135 R phage specifically bound to immunocaptured APN and to cells engineered to express APN on their surf
136                This study further implicates APN as an integrin-like molecule that functions broadly
137                                           In APN-null mice, recombinant adenovirus-expressed APN redu
138 ation by 35% in wild-type mice and by 40% in APN-KO mice and leukostasis by 64% in wild-type mice and
139 tasis by 64% in wild-type mice and by 75% in APN-KO mice, which were associated with reduced TNF-alph
140 depicting focal parenchymal abnormalities in APN as was the 3- to 4-h DMSA routine procedure.
141       Adiponectin provision by adenovirus in APN-/- mice reversed these exacerbated responses to allo
142                   The rejected allografts in APN-/- mice contained significantly higher levels of tum
143 ide metabolites in plasma were attenuated in APN-KO mice compared with WT mice.
144                         Thus, cooperation in APN expression by both cancer cells and nonmalignant str
145  induce functional blood vessel formation in APN-null mice.
146         WBC, CRP, ESR and DNI were higher in APN than in lower UTI (p < 0.01).
147 activity of HB-EGF, restores inflammation in APN KO mice.
148 ost) cells on tumor growth and metastasis in APN-null mice.
149  enhanced pathological neovascularization in APN-KO mice by 34%, and the inhibitory effects of adipon
150 ung injury and inflammation were observed in APN(-/-) mice as early as 4 h after delivery of LPS.
151 xaggerated systemic inflammatory response in APN-deficient (APN(-/-)) mice compared with wild-type (w
152 in increased infarct size similar to that in APN-null mice.
153 e acute rejection relative to transplants in APN+/+ hosts accompanied by increased accumulation of CD
154        omega-3 LCPUFA feed in mice increases APN production by reducing adipose endoplasmic reticulum
155         Our findings suggest that increasing APN by omega-3 LCPUFA supplementation in total parental
156                               To investigate APN-based tumor-homing therapy, we determined the crysta
157  strains, derived from 129S6/SvEvTAC, AKR/J, APN, BALB/cJ, BTBR-T+ tf/tf, C3H/HeJ, C57BL/6J, DBA/2J,
158             A 70-kDa fragment of the 106-kDa APN was expressed in Escherichia coli.
159                      In our study, a 106-kDa APN, called AgAPN2, released by phosphatidylinositol-spe
160 nvolved in toxicity, we truncated the 70-kDa APN fragment into peptides of 28- and 30-kDa ta and tb,
161 mia was exacerbated in adiponectin-knockout (APN-KO) mice compared with wild-type mice (neovascular a
162 lleled corresponding defects in mice lacking APN.
163 s-derived, inbred strains: ALR/LtJ, ALS/LtJ, APN, APS, ICR/HaRos, NOD/LtJ, NON/LtJ, SJL/J, and SWR/J.
164       APN is expressed in the colon, luminal APN associates with colonic epithelial cells.
165                           In M1 macrophages, APN induced proinflammatory cytokines, TNF-alpha, IL-6,
166              In contrast, in M2 macrophages, APN induced the anti-inflammatory cytokine IL-10 without
167                In T-cadherin-deficient mice, APN failed to associate with cardiac tissue, and its lev
168       In two independent tumor graft models, APN activity in both the tumors and the host cells coope
169 alogs exhibited a high affinity for monozinc APNs associated with a reasonable selectivity versus diz
170 ng a recombinant adenovirus expressing mouse APN (AdAPN) and as control, adenovirus expressing green
171 quon present between aa 288 to 290 in murine APN.
172         Tumor cell surface aminopeptidase N (APN or CD13) has two puzzling functions unrelated to its
173 ic neuropeptidases, namely aminopeptidase N (APN) and neutral endopeptidase 24.11 (NEP 24.11).
174 een shown to activate CD13/aminopeptidase N (APN) and p19ARF gene expression via binding to canonical
175 e identify membrane alanyl aminopeptidase N (APN) as a receptor for pea enation mosaic virus (PEMV) c
176 sy moth (Lymantria dispar) aminopeptidase N (APN) biphasically.
177 phila homolog of the human aminopeptidase N (APN) gene.
178 e group 1 coronavirus, use aminopeptidase N (APN) of their natural host and feline APN (fAPN) as rece
179                  Mammalian aminopeptidase N (APN) plays multifunctional roles in many physiological p
180 assays were performed with aminopeptidase N (APN) purified from L. dispar and M. sexta BBMVs using su
181 inhibition of cell surface aminopeptidase N (APN) using actinonin, bestatin, or inhibitory peptides s
182        Recently, a 100-kDa aminopeptidase N (APN) was isolated from brush border membrane vesicles (B
183                            Aminopeptidase N (APN), a 150-kDa metalloprotease also called CD13, serves
184 t has been well studied is aminopeptidase N (APN), a multifunctional protease known to cleave biologi
185                  A 106-kDa aminopeptidase N (APN), called AgAPN2, was previously identified as a Cry1
186  nonspecific exopeptidase, aminopeptidase N (APN), is inhibited sequence-specifically by a synthetic
187 e-spanning apical resident aminopeptidase N (APN).
188                            Aminopeptidase N (APN, CD13; EC 3.4.11.2) is a transmembrane metalloprotea
189 in (NEP, EC 3.4.24.11) and aminopeptidase N (APN, EC 3.4.11.2).
190 es in tumor vasculature is aminopeptidase N (APN; also called CD13).
191        The metalloprotease aminopeptidase N (APN; CD13) is often overexpressed in tumor cells and has
192 ers revealed that the CD13/aminopeptidase N (APN; EC 3.4.11.2) promoter could bind and be activated b
193       Lepidopteran midgut aminopeptidases N (APNs) are phylogenetically divided into eight clusters,
194 assification by using associative Petri net (APN) for personalized ECG-arrhythmia-pattern identificat
195 elation is shown to exist between neutrophil APN activity and the sensitivity of donor cells to TNFal
196  with 46 (22.3%) of 206 survivors in the non-APN group (P < .001).
197  Documentation of advanced practice nurses' (APNs) effectiveness globally is essential in developing
198                  The proteolytic activity of APN promotes cancer angiogenesis and metastasis making i
199 est significant variation in the activity of APN/CD13 on the cell surface of neutrophils in normal in
200 hemically induced colitis; administration of APN restores inflammation.
201 ssification model and reasoning algorithm of APN are created for ECG arrhythmias classification.
202 actice site, region or country and amount of APN care in minutes or contacts); APN (education, expert
203 on (e.g., IL-6) only in endothelial cells of APN(-/-) mice when compared with wt mice.
204 e active site and peptide-binding channel of APN reside in cavities with wide openings, allowing easy
205 al findings compatible with the diagnosis of APN were, for MAG3-F(0), regional parenchymal dysfunctio
206 esults demonstrated a dynamic dysfunction of APN/AdipoR1 accompanying T1DM progression.
207  this hypothesis by comparing the effects of APN deficiency in allografted malignant (tumor) and nonm
208                                Expression of APN and heparin binding epidermal growth factor (HB-EGF)
209                                Expression of APN and its receptors, HB-EGF, and basic fibroblast grow
210       Among the 11 biopsies with features of APN, 4 biopsies showed good clustering with a pattern di
211 idney, n=4; unequivocal AR, n=5; features of APN, n=11).
212 entified 49 patients with biopsy features of APN, within the first 2 years posttransplant.
213 vo experiments support the identification of APN as the first receptor in a plant virus vector.
214 e to design a selective peptide inhibitor of APN that was an effective therapeutic both in vitro and
215 s of dopaminergic drugs on the mRNA level of APN and NEP 24.11 were determined by RNase protection as
216                                      Loss of APN expression by the host and/or the malignant cells al
217 ildren and adults with a clinical picture of APN, diuretic MAG3 scintigraphy with zero time injection
218 of this study was to investigate the role of APN in intestinal inflammation.
219                      We examined the role of APN in ROP development and whether circulating APN conce
220 is study elucidates multifunctional roles of APN and can guide therapeutic efforts to treat APN-relat
221   To understand the substrate specificity of APN for the development of targeted inhibitors, we used
222 rapy, we determined the crystal structure of APN complexed with a tumor-homing peptide containing a r
223 alytically active state, these structures of APN illustrate a detailed catalytic mechanism for its am
224                      Our previous studies of APN-null mice revealed impaired neoangiogenesis in model
225 inical and laboratory findings suggestive of APN, the 2 radiopharmaceuticals were used for imaging se
226 or downstream protective signaling target of APN.
227 cts consist of 3 components: dose (number of APNs at the clinical practice site, region or country an
228             Based on the body of research on APN effectiveness to date, two major factors have emerge
229  will provide for technologies based on PEMV-APN interaction designed to block plant virus transmissi
230              Moreover, the ischemic penumbra APN levels increased and peaked in T1DM-2W mice, and red
231 ting AngII-induced AAA and increasing plasma APN levels as a strategy to prevent advanced AAA.
232 t mouse (LDLR(-/-)) model, we induced plasma APN levels using a recombinant adenovirus expressing mou
233 rus can use human APN (hAPN) but not porcine APN (pAPN) as its cellular receptor, and porcine coronav
234  we determined crystal structures of porcine APN at 1.85 A resolution and its complexes with a peptid
235 e of DNI in predicting acute pyelonephritis (APN) or vesicoureteral reflux (VUR) using the data of 28
236                        Acute pyelonephritis (APN) versus acute rejection (AR) is a frequently encount
237 investigation of focal acute pyelonephritis (APN), especially in children with urinary tract infectio
238 onstrated that in the presence of excess Q7, APN quantitatively converts the pentapeptides Thr-Gly-Al
239                                  Recombinant APN expressed in Sf9 cells resulted in internalization o
240  in five patients with medication-refractory APN.
241 yb family proteins collaborate in regulating APN gene expression and point to a role for DMP1 in norm
242                                  Remarkably, APN inhibited the AAA development in AdAPN mice by suppr
243 y, in addition to vascular biology research, APN-null mice may be useful reagents in other medical fi
244 he APN enzymatic active site, but it resists APN degradation due to a distorted scissile peptide bond
245 .1 and PEMV bind to and compete for the same APN receptor.
246                                        Serum APN concentrations were correlated with ROP development
247 ons positively correlate with ROP, and serum APN concentrations positively correlate with serum omega
248 tly reduced lung airspace APN but high serum APN levels had pulmonary inflammatory responses after in
249 ega-3 LCPUFA supplementation increases serum APN concentrations, which then suppress retinopathy.
250  We found that in preterm infants, low serum APN concentrations positively correlate with ROP, and se
251 se findings indicate the importance of serum APN in modulating LPS-induced ALI and suggest that condi
252                         Association of serum APN with HB-EGF and bFGF was studied by coimmunoprecipit
253 smic reticulum, is the major source of serum APN.
254 on MAG3-F(0) may indicate either more severe APN or preexistent scars and that regional dysfunction m
255                                         Some APN-/- mice received adiponectin reconstitution by adeno
256                               In this study, APN's role in the early development of ALI to LPS was in
257               These studies strongly support APN therapeutic actions through multiple mechanisms inhi
258                   Inhibition of cell surface APN appears to interfere with the shedding of TNFRI, and
259                                Surprisingly, APN-null mice developed with no gross or histological ab
260                These findings establish that APN-null mice develop normally without physiological alt
261 ncer cells and suggested the hypothesis that APN expressed by nonmalignant cells might promote tumor
262     Immunohistochemical staining showed that APN expression is up-regulated in endothelial cells with
263 ion in controlling AdipoR expression and the APN-mediated inflammatory response has not been investig
264 sor exhibited a good reproducibility for the APN measurements, excellent storage stability and select
265 llow-up, 107 (52.2%) of 205 survivors in the APN group completed screening compared with 46 (22.3%) o
266 nual, 2 years, or 5 years), survivors in the APN group were > 2x more likely than those in the contro
267 ecies-specific amino acid differences in the APN proteins of different species.
268 ilar conformations with the NGR motif in the APN-bound tumor-homing peptide.
269 en no reports of in vivo inactivation of the APN gene to validate these findings.
270  we evaluated, by targeted disruption of the APN gene, whether APN participates in blood vessel forma
271 f syntheses of this and other members of the APN ligand family is assessed, and their applications in
272           The key structural features of the APN pharmacophore required for substrate recognition wer
273        The tumor-homing peptide binds to the APN enzymatic active site, but it resists APN degradatio
274 reduced to normal in T1DM-8W mice, while the APN receptor 1 (AdipoR1) expression change was the oppos
275  consider the concept of dose effects of the APNs.
276                                   Therefore, APN-based tumor cell motility and tumor-homing therapy r
277                                        These APN (atropos P,N) ligands require a specific type of bia
278                                        Thus, APN is involved in angiogenesis and can serve as a targe
279 ve in mice lacking T-cadherin in addition to APN.
280 t and/or family receptiveness to APNs and to APN practice).
281 a peptide previously demonstrated to bind to APN in the aphid gut and to impede PEMV uptake into the
282 ent protein (CP-P-GFP) specifically bound to APN.
283  within domain III affected binding rates to APN site 1, whereas mutations in domain II affected bind
284 tions in domain II affected binding rates to APN site 2.
285 oduced contrasting inflammatory responses to APN (EC50 5 microg/ml).
286                   Allografts transplanted to APN-/- mice showed severe acute rejection relative to tr
287 al or patient and/or family receptiveness to APNs and to APN practice).
288                    In mouse OIR, serum total APN and bioactive high-molecular-weight APN concentratio
289 N and can guide therapeutic efforts to treat APN-related diseases.
290 dations (n = 234), or standard care plus two APN telephone counseling sessions (n = 238).
291 t (APN-/-, C57BL/6 background) or wild-type (APN+/+) mice.
292                        In tumor vasculature, APN is overexpressed in the endothelium and promotes ang
293                                    In vitro, APN increases production of proinflammatory cytokines fr
294 elevation of total and high-molecular weight APN levels and enhanced APN localization in the artery w
295 otal APN and bioactive high-molecular-weight APN concentrations are increased by omega-3 LCPUFA feed.
296                  White adipose tissue, where APN is produced and assembled in the endoplasmic reticul
297 viduals and reveal a novel mechanism whereby APN/CD13 regulates TNFalpha-induced apoptosis via inhibi
298 targeted disruption of the APN gene, whether APN participates in blood vessel formation and function
299 cularization is reduced from 70% to 10% with APN deficiency.
300  cardiac stress through its association with APN in mice.

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