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

 
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