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1 s cellular receptor, dipeptidyl peptidase 4 (DPP4).
2 at incretins are only one of many targets of DPP4.
3 e that globally expresses human CD26 (hCD26)/DPP4.
4 cell lines were not, despite the presence of DPP4.
5 understanding of the potential importance of DPP4.
6 ulation of inflammation in adipose tissue by DPP4.
7 hibited by the addition of exogenous soluble DPP4.
8  in infected astrocytes, including CD147 and DPP4.
9 alysis showed these can inhibit both ACE and DPP4.
10 pressing large amounts of the viral receptor DPP4.
11 issivity for ferret, hamster, and guinea pig DPP4.
12                                         In a dpp4-7-11-disrupted P. gingivalis ATCC 33277, a DPP7-lik
13               One highly induced protein was DPP4, a measurable serum protein that has well-described
14             Moreover, glucocorticoid-induced DPP4 activation was also observed in proinflammatory M1-
15 cal model that interlinks aminopeptidase and DPP4 activities.
16 lated with HCV-RNA (r = 0.40, P < 0.001) and DPP4 activity (r = 0.53, P < 0.001).
17         Here we examine whether reduction of DPP4 activity alters inflammation.
18                  The regulation and roles of DPP4 activity are not well understood; therefore, the pu
19  activity of these CSFs can be enhanced when DPP4 activity is inhibited.
20                                              DPP4 activity was measured in the urine and serum of 426
21              Intact and truncated CXCL10 and DPP4 activity were quantified in all longitudinal sample
22    Sitagliptin therapy for 12 months reduces DPP4 activity yet does not increase markers of inflammat
23 es, without any difference in suppression of DPP4 activity.
24    Importantly, the differential presence of DPP4 allowed flow cytometry-mediated isolation of senesc
25  tetraspanin CD9 and dipeptidyl peptidase 4 (DPP4) along with multiple endosomal sorting complex requ
26 on of human DPP4 containing the five hamster DPP4 amino acids did not.
27 on of hamster DPP4 containing the five human DPP4 amino acids rendered BHK cells susceptible to MERS-
28 180 spike does not require MERS-CoV receptor DPP4 and antibodies developed against the MERS spike rec
29      Recent studies showed a linkage between DPP4 and down-regulation of certain chemokines and mitog
30  in preadipocyte 3T3-L1 and 3T3-F422A, while DPP4 and FAP inhibitors have no effect.
31  have a significant reduction in circulating DPP4 and increase in Glucagon-like peptide (GLP)-1 level
32 e novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH.
33                              Modeling of the DPP4 and MERS-CoV RBD interaction predicted the ability
34 ce of a novel protease complex consisting of DPP4 and seprase in human endothelial cells that were ac
35                                              DPP4 and seprase were coexpressed with the three major p
36 review will critically review the science of DPP4 and the effects of DPP4 inhibitors on the cardiovas
37  the virus receptor, dipeptidyl peptidase 4 (DPP4) and higher basal levels of interferon in these cel
38 ell surface receptor dipeptidyl peptidase 4 (DPP4), and evolutionary mechanisms that may facilitate h
39 entity and inhibits adipogenic commitment of DPP4+ and CD142+ cells.
40 pressing high amounts of the viral receptor, DPP4, and did not modulate MERS-CoV infectivity.
41 creased expression of intestinal genes (MGA, DPP4, and GLUT2).
42  including increased expression of IL6, TNF, DPP4, and IL8, as well as elevated SA-beta-gal activity.
43 terocytes among coronavirus receptors (ACE2, DPP4, ANPEP).
44 ated isolation of senescent cells using anti-DPP4 antibodies.
45 atory mucosal epithelium; ACE2, TMPRSS2, and DPP4 are highly expressed in the intestinal mucosal epit
46 expression across tissues; TMPRSS2, APN, and DPP4 are highly expressed in the respiratory mucosal epi
47 these analyses, LIF, CREG2, CST3, CCBE1, and DPP4 are likely osteoclast-derived coupling factors in h
48 ors in humans and uncover osteoclast-derived DPP4 as a potential link between bone remodeling and ene
49  neutralizing mAb for group 2c CoVs that use DPP4 as a receptor.
50                     However, employing mouse DPP4 as a scaffold, we identified two critical amino aci
51       Using flow cytometry, we identify CD26/DPP4 as a surface marker that allows isolation of this l
52  analysis identified TESC, ACVR1, MSRB3, and DPP4 as significantly associated with hippocampal volume
53 ied the exopeptidase dipeptidyl peptidase-4 (DPP4) as a critical glucocorticoid-responsive gene in TH
54  (MERS-CoV) utilizes dipeptidyl peptidase 4 (DPP4) as an entry receptor.
55 omedary camels using dipeptidyl peptidase-4 (DPP4) as its receptor.
56 er, NPY conversion by dipeptidylpeptidase 4 (DPP4) augmented Y5R activation and function in liver can
57      Collectively, this study identifies Wnt/DPP4 axis as a key driver of extracellular matrix homeos
58 these compounds displayed not only increased DPP4 binding activity but also significantly reduced hum
59            These RBD mutants with diminished DPP4 binding also led to virus attenuation, suggesting t
60 tively, these mutations were found to reduce DPP4 binding and viral entry into target cells.
61 ss-neutralization involving occlusion of the DPP4 binding site, highlighting its potential as a broad
62 m337, and m338, targeting the receptor (CD26/DPP4) binding domain (RBD) of the MERS-CoV spike glycopr
63 e RBD has identified several residues at the DPP4-binding surface that serve as neutralizing epitopes
64 ion, and siRNA-mediated knockdowns of GR and DPP4 blocked dexamethasone-induced THP1-MPhi migration.
65 bodies against the gelatin-binding domain of DPP4 blocked the local gelatin degradation by endothelia
66  D510G and I529T reduce S protein binding to DPP4 but show that this reduction only translates into d
67 rated by the protease dipeptidylpeptidase 4 (DPP4), can act as chemokine antagonist.
68                    We demonstrate that mouse DPP4 cannot support MERS-CoV infection.
69 oteinases, including dipeptidyl peptidase 4 (DPP4), carboxypeptidase E (CPE) and prostate specific an
70 LD-related proteins like ADIPOQ, APOC, APOE, DPP4, CAT, GC, HP, CETP, SERPINA1, COLA1, PIGR, IGHD, SA
71 mokines mediated by the dipeptidyl peptidase DPP4 (CD26) has been shown to negatively regulate lympho
72 IL), KIT (CD117), IL2RA (CD25), CD27, CXCR3, DPP4 (CD26), GPR183, and MHC class II transcripts and pr
73 ression of the enzyme dipeptidylpeptidase-4 (DPP4)/CD26 by endothelial cells activates NPY-mediated s
74      Cells marked by dipeptidyl peptidase-4 (DPP4)/CD26 expression are highly proliferative, multipot
75                      Dipeptidyl peptidase 4 (DPP4, CD26) is a protease that cleaves selected amino ac
76                      Dipeptidyl peptidase 4 (DPP4, CD26), a type II transmembrane ectopeptidase, is t
77                     Dipeptidyl peptidase IV (DPP4/CD26) and seprase/fibroblast activation protein alp
78 h an increase in dipeptidylpeptidase 4/CD26 (DPP4/CD26), an enzyme that truncates the neurotransmitte
79    Transforming growth factor-beta maintains DPP4+ cell identity and inhibits adipogenic commitment o
80  of DPP4 substrates and the reduced ratio of DPP4 cleaved peptide to intact substrate peptide.
81                                              DPP4 cleaved within the N-termini of the CSFs granulocyt
82                         Dipeptidylpeptidase (DPP4) cleaves a wide variety of substrates, including th
83                                          The DPP4 colocalized with membrane-bound ADA on human DCs an
84 ble to MERS-CoV, whereas expression of human DPP4 containing the five hamster DPP4 amino acids did no
85                        Expression of hamster DPP4 containing the five human DPP4 amino acids rendered
86                          We suggest that the DPP4-CXCL10 axis inhibits antiviral innate and adaptive
87                     Dipeptidyl peptidase IV (DPP4) deactivates glucose-regulating hormones such as GL
88  microfragments from dipeptidyl peptidase 4 (DPP4)-deficient rats were transplanted into syngeneic no
89 similar phenotype was observed in homozygous DPP4-deficient mice, emphasizing the role of DPP4 in reg
90 on, Gata4 generates similar amounts of epCam+Dpp4- definitive endoderm enriched for Cxcr4, FoxA2, Fox
91 results point toward dipeptidyl peptidase 4 (DPP4)-dependent endosomal uptake and subsequent infectio
92 ion, whereas expression of hamster or ferret DPP4 did not.
93     Mass spectrometry analysis revealed that DPP4 (dipeptidyl peptidase 4) was selectively expressed
94 ism of these viruses in bats, we studied the DPP4 distribution in the respiratory and extra-respirato
95 uding mouse, ferret, hamster, and guinea pig DPP4, do not.
96 e are not susceptible to MERS because murine dpp4 does not serve as a receptor.
97 gipain gene-disrupted mutants indicated that DPP4, DPP5, DPP7, and DPP11 together with Arg- and Lys-g
98 tidase (DPP) 4 family includes four enzymes, DPP4, DPP8, DPP9 and fibroblast activation protein (FAP)
99 se of experiments showing that inhibition of DPP4 enhances SDF-1-mediated progenitor cell survival, e
100      Small molecule-based inhibition of CD26/DPP4 enzymatic activity during wound healing results in
101 RU-486 and by GR siRNA transfection and that DPP4 enzyme activity is reduced by DPP4 inhibitors.
102 llectively our findings dissociate levels of DPP4 enzyme activity, sDPP4 and biomarkers of inflammati
103 ns in protein levels by Western blotting and Dpp4 enzyme activity.
104  S protein of MERS-CoV specifically bound to DPP4-expressing cells and soluble DPP4 protein and induc
105 verexpression of DPP4 in HeLa cells rendered DPP4-expressing EVs that were no longer taken up by othe
106 highlight differences in the distribution of DPP4 expression among MERS-CoV susceptible species, whic
107 r biopsy specimens revealed a correlation of DPP4 expression and DNA methylation to stages of hepatos
108 te that glucocorticoids directly up-regulate DPP4 expression and thereby induce migration in macropha
109 and rodents demonstrated increased levels of DPP4 expression in DC/macrophage cell populations from v
110          In the insectivorous bats, however, DPP4 expression in epithelial cells of the respiratory t
111                                          The DPP4 expression increased during monocyte differentiatio
112 ionally, we show that glucocorticoid-induced DPP4 expression is blocked by the GR antagonist RU-486 a
113                                      Hepatic DPP4 expression is elevated in subjects with ectopic fat
114  was increased only in animals with elevated Dpp4 expression.
115                                              DPP4 family inhibitors have been used for the treatment
116 PP4 lacked an analogous effect, the combined DPP4/FAP inhibitor linagliptin, but not the FAP-specific
117 were identified (SERPINB2, CNTNAP4, DENND4B, DPP4, FGFBP2, MIGA2, POLE, SNRNP40, TOP2B, and ZDHHC18)
118 g/ml, respectively, likely by competing with DPP4 for binding to the S glycoprotein.
119 e identified a novel mechanism involving the DPP4 gelatin-binding domain of the DPP4-seprase complex
120 liver is facilitated by demethylation of the Dpp4 gene early in life.
121            We found that GR directly induces DPP4 gene expression by binding to two glucocorticoid-re
122 ase isomaltase (SI); dipeptidyl peptidase 4 (Dpp4); glucose transporter type 2 (Glut2); and villin we
123 he levels of the differentiation markers SI, Dpp4, Glut2, and villin.
124 lating frequency, we unexpectedly found that DPP4 has a more general role in regulating colony-stimul
125                                              DPP4 has a number of nonenzymatic functions that involve
126 e developed transgenic mice expressing human DPP4 (hDPP4) under the control of the surfactant protein
127  as dipeptidyl peptidase 4 (DPP4), the mouse DPP4 homologue does not allow virus entry into cells.
128 trol, revealed when endogenous mechanisms of DPP4 immunoregulation are inhibited.
129 ase and cystic fibrosis, exhibited increased DPP4 immunostaining in alveolar epithelia (type I and II
130 infection of cells expressing high levels of DPP4.IMPORTANCE MERS-CoV has pandemic potential, and it
131  a distinct mechanism by which inhibition of DPP4 improves anti-tumor responses.
132 hat the preferential spatial localization of DPP4 in alveolar regions may explain why MERS is charact
133 ferating cells, as ectopic overexpression of DPP4 in HeLa cells rendered DPP4-expressing EVs that wer
134                                 Knockdown of DPP4 in human DCs, but not pharmacologic inhibition of t
135        We believe that the potential role of DPP4 in modification of many regulatory proteins, and th
136                          Expression of human DPP4 in nonsusceptible BHK and ferret cells enabled MERS
137 ing glucose-induced transcription of hepatic Dpp4 In older mice, hepatic triglyceride content was inc
138  peptide substrates support a broad role for DPP4 in proline-containing peptide catabolism and streng
139   Here, we assessed the nonenzymatic role of DPP4 in regulating dendritic cell (DC)/macrophage-mediat
140 DPP4-deficient mice, emphasizing the role of DPP4 in regulating these behaviors.
141 ed collagens (gelatin), suggesting a role of DPP4 in the cell invasive phenotype.
142               The preferential expression of DPP4 in the intestinal tract of insectivorous bats, sugg
143 data show that glucose-induced expression of Dpp4 in the liver is facilitated by demethylation of the
144                          The distribution of DPP4 in the respiratory tract tissues of humans and came
145            Here, we investigated the role of DPP4 in this observed species tropism.
146 ed the transcriptional regulation of hepatic Dpp4 in young mice prone to diet-induced obesity.
147    Given the role of Dipeptidyl Peptidase-4 (DPP4) in glucose homeostasis, we further demonstrate tha
148 nzymes targeted by new diabetes medications (DPP4), indicating new genetic influences on hippocampal
149                             Dpp4 knockout or DPP4 inhibition enhanced CSF activities both in vitro an
150                                              DPP4 inhibition enhanced engraftment in mice without com
151 lating hormones such as GLP-1 and GIP, thus, DPP4 inhibition has become a useful therapy for type 2 d
152                                              DPP4 inhibition has recently been used in a clinical tri
153 mation, and impaired ventricular function to DPP4 inhibition in preclinical studies.
154                       Surprisingly, systemic DPP4 inhibition increases plasma levels of inflammatory
155                                    Prolonged DPP4 inhibition increases plasma levels of sDPP4, and in
156 t with this maladaptive role, the effects of DPP4 inhibition seem to exert a protective role in cardi
157 t source of plasma sDPP4 following catalytic DPP4 inhibition.
158  non-GLP-1RA (aHR, 1.29; 95% CI, 1.17-1.42), DPP4 inhibitor (aHR, 1.36; 95% CI, 1.17-1.58), SGLT2 inh
159 was reversed in cells that were treated with DPP4 inhibitor along with pro-CD.
160  agonist liraglutide or the highly selective DPP4 inhibitor MK-0626.
161                        Administration of the DPP4 inhibitor sitagliptin resulted in higher concentrat
162 vestigated alone and in combination with the DPP4 inhibitor sitagliptin; these only modestly increase
163 xamide (24s), emerged as a potent, selective DPP4 inhibitor that displayed excellent PK profiles and
164 tment of cord blood cells, and an endogenous DPP4 inhibitor tissue factor pathway inhibitor has been
165 ion, and this was significantly reduced with DPP4 inhibitor treatment.
166  rats, which were significantly changed with DPP4 inhibitor treatment.
167 tes for heart failure (HF) among a subset of DPP4 inhibitor-treated subjects with diabetes.
168 -/-) mice or mice receiving an orally active DPP4 inhibitor.
169 y potent, selective, and orally bioavailable DPP4 inhibitor.
170 ell as the effect of dipeptidyl peptidase-4 (DPP4) inhibitor on CD in endothelial-pericyte interactio
171 receiving background dipeptidyl peptidase 4 (DPP4) inhibitor treatment were characterized as a model
172 alogue) or enhancer (dipeptidyl peptidase 4 [DPP4] inhibitor).
173                  In this paper, we show that DPP4 inhibitors also induced cell death in multiple huma
174 10 000 person-years in 36 897 patients using DPP4 inhibitors and 4 per 10 000 person-years in 10 684
175 nce of an inverse association between use of DPP4 inhibitors and GLP-1 mimetics and the onset of Park
176                                   The use of DPP4 inhibitors and/or GLP-1 mimetics is associated with
177 se in individuals treated with glitazones or DPP4 inhibitors and/or GLP-1 receptor agonists to indivi
178                                 As these two DPP4 inhibitors are known to have off-target effects aga
179                                              DPP4 inhibitors are modestly effective in reducing HbA1c
180                                      Indeed, DPP4 inhibitors are widely used in clinical practice as
181 events per 10 000 person years) treated with DPP4 inhibitors developed thyroid cancer.
182                                        Thus, DPP4 inhibitors may be used as potential adjuvant therap
183                           GLP1R agonists and DPP4 inhibitors might also attenuate oxidative stress, f
184 eview the science of DPP4 and the effects of DPP4 inhibitors on the cardiovascular system.
185 ics, 6861 of whom were prescribed GTZ and/or DPP4 inhibitors prior to using GLP-1 mimetics.
186  vs placebo and insulin, respectively) while DPP4 inhibitors were weight neutral.
187 es and -0.74% [95% CI, -0.85% to -0.62%] for DPP4 inhibitors) and were noninferior to other hypoglyce
188 ce for adverse effects, especially among the DPP4 inhibitors, and continued evaluation in longer-term
189                                   Among five DPP4 inhibitors, only two of them, vildagliptin and saxa
190 eridine-constrained phenethylamines as novel DPP4 inhibitors.
191  and that DPP4 enzyme activity is reduced by DPP4 inhibitors.
192 tin-based therapies, dipeptidyl peptidase-4 (DPP4) inhibitors and glucagon-like peptide-1 (GLP-1) ana
193                     Dipeptidyl peptidase IV (DPP4) inhibitors are emerging as a new class of therapeu
194                Dipeptidyl peptidase-4 (CD26, DPP4) inhibitors are the most widely used incretin-based
195 yrimidine containing dipeptidyl peptidase-4 (DPP4) inhibitors led us to focus on an imidazolopyrimidi
196                      Dipeptidyl peptidase-4 (DPP4) inhibitors used for the treatment of type 2 diabet
197 (GLP1R) agonists and dipeptidyl peptidase 4 (DPP4) inhibitors, can also reduce blood pressure, body w
198 eceptor agonists and dipeptidyl peptidase 4 (DPP4) inhibitors, with the risk of Parkinson's disease o
199                                          The DPP4 interaction with ADA in human DC/macrophages was co
200                   The data further show that DPP4 is a novel marker of HIF-1 induction.
201           Immunoprecipitation confirmed that DPP4 is displayed on the surface of eHAV produced in cel
202                                        Human DPP4 is ubiquitously expressed in epithelial and endothe
203                                      Indeed, DPP4 is upregulated in proinflammatory states including
204 r, whether increased dipeptidyl peptidase 4 (DPP4) is involved in the pathogenesis or is rather a con
205                      Dipeptidyl peptidase 4 (DPP4) is the receptor for cell binding and entry.
206        Upon inoculation with MERS-CoV, human DPP4 knockin (KI) mice supported virus replication in th
207                                              Dpp4 knockout or DPP4 inhibition enhanced CSF activities
208 s from FAP-null mice, and, while knockout of DPP4 lacked an analogous effect, the combined DPP4/FAP i
209 le of the liver in participation to systemic DPP4 levels.
210 tion of surface CD26 (dipeptidyl peptidase 4/DPP4) levels.
211 mice with humanized exons 10-12 of the mouse Dpp4 locus.
212 xpressed in PTC, such as MET, LGALS3, KRT19, DPP4, MDK, TIMP1, and FN1.
213                                        Mouse DPP4 (mDPP4) does not support MERS-CoV entry; however, c
214 pike and the mouse host cell receptor, mouse DPP4 (mDPP4).
215 timulated macrophage mobility; unexpectedly, DPP4 mediated the glucocorticoid-induced macrophage migr
216 S1(B) We now demonstrate that in addition to DPP4, MERS-CoV binds to sialic acid (Sia).
217  binding energy (- 10.2 kcal/mol) toward the DPP4-MERS-CoV spike complex by disrupting the key electr
218  cardiovascular function in young euglycemic Dpp4(-/-) mice and in older, high fat-fed, diabetic C57B
219                             Young euglycemic Dpp4(-/-) mice exhibited a cardioprotective response aft
220 er radiation or chemotherapy was enhanced in Dpp4(-/-) mice or mice receiving an orally active DPP4 i
221 we utilize these substrates and tissues from DPP4(-/-) mice to improve the coverage of the peptidomic
222 e lacking the enzyme dipeptidyl peptidase 4 (DPP4(-/-) mice), a biomedically relevant peptidase, usin
223                      Dipeptidyl peptidase-4 (DPP4) modulates inflammation by enzymatic cleavage of im
224  2, tissue inhibitor of metalloproteinase 1, Dpp4, nitric oxide synthase 2 (Nos2), interleukin 1beta
225  degradation protein dipeptidyl peptidase 4 (DPP4) no significant association with either GLP-1 or -2
226 ry structure, GraphPAC discovers clusters in DPP4, NRP1 and other proteins not identified by existing
227 rface entry receptor dipeptidyl peptidase 4 (DPP4) occurs via S1(B) We now demonstrate that in additi
228 ed on the ability of MERS-CoV to utilize the DPP4 of common Middle East livestock species, such as ca
229 ng energies of MERS-CoV spike protein RBD to DPP4 of human (susceptible) or hamster (nonsusceptible)
230 redicted the ability of MERS-CoV to bind the DPP4s of camel, goat, cow, and sheep.
231 ch, the potential of MERS-CoV to utilize the DPP4s of common Middle Eastern livestock was investigate
232                            Expression of the DPP4s of these species on BHK cells supported MERS-CoV r
233 ial implications of the modifying effects of DPP4 on a large number of cytokines and other growth-reg
234                 The widespread expression of DPP4 on blood vessels, myocardium, and myeloid cells and
235                 The nonenzymatic function of DPP4 on DC may play a role in potentiation of inflammati
236 to diminished viral entry when expression of DPP4 on target cells is low.
237          In sum, the selective expression of DPP4 on the surface of senescent cells enables their pre
238 ADS-CoV did not use human coronavirus ACE-2, DPP4, or CD13 receptors for docking and entry.
239 ) infection, suggesting that other mammalian DPP4 orthologs may also support infection.
240 ng the virus-receptor interactions for these DPP4 orthologs will help in the development of additiona
241 man DPP4 support MERS-CoV infection, several DPP4 orthologs, including mouse, ferret, hamster, and gu
242                       The sequences of these DPP4 peptide substrates support a broad role for DPP4 in
243 echanism by the peptides was investigated by DPP4-peptide inhibition kinetics, molecular docking and
244           We show that the MERS-CoV receptor DPP4 plays a pivotal role in the observed species tropis
245 us work revealed that glycosylation of mouse DPP4 plays a role in blocking MERS-CoV infection.
246                                              DPP4 plays a role in regulating the activity of CSFs and
247 ized with the understanding of the role that DPP4 plays in prolonging the half-life of incretins such
248 rmal hepatic architecture and development of DPP4-positive vessels, indicating angiogenesis and revas
249 (ADCC) assays revealed that the cell surface DPP4 preferentially sensitized senescent, but not dividi
250    This suggests, together with the abundant DPP4 presence in the respiratory tract, that these speci
251                                     Notably, DPP4+ progenitors reside in the reticular interstitium,
252 ticoid-responsive elements (GREs) within the DPP4 promoter.
253 y bound to DPP4-expressing cells and soluble DPP4 protein and induced significant neutralizing antibo
254 ied five amino acid residues involved in the DPP4-RBD interaction.
255 at glycosylation is a major factor impacting DPP4 receptor function.
256 alizing monoclonal antibodies (MAbs) and the DPP4 receptor, and high immunogenicity, able to elicit S
257 rtibeus jamaicensis) dipeptidyl peptidase 4 (DPP4) receptor and MERS-CoV replicated efficiently in Ja
258                      We constructed chimeric DPP4 receptors that have the virus-binding domains of in
259 gins with virus spike (S) protein binding to DPP4 receptors.
260 coagulation factors; silencing or inhibiting DPP4 reduced these factors and increased cell death.
261 s to discuss the recent literature regarding DPP4 regulation, as well as the variety of molecules it
262                The TGF-beta/NPY/Y5R axis and DPP4 represent attractive therapeutic targets for contro
263 ng the key electrostatic interaction between DPP4 residue K267 and viral residue D539.
264 d subsequently identified the amino acids in DPP4 responsible for this restriction.
265 associations included one SNP at 2q24 within DPP4 (rs6741949; P = 2.9 x 10(-7)) and nine SNPs at 9p33
266 lving the DPP4 gelatin-binding domain of the DPP4-seprase complex that facilitates the local degradat
267 nsight into the number of proteins that have DPP4 sites, and how DPP4 truncation may alter hematopoie
268           These results provide insight into DPP4 species-specific differences impacting MERS-CoV hos
269           These results provide insight into DPP4 species-specific differences impacting MERS-CoV hos
270 significantly increased Slfn3 expression and Dpp4-specific activity compared with GFP-expressing viru
271 low, and in doing so, discover over 70 renal DPP4 substrates (up from 7 at the beginning of our optim
272 DPP4 was associated with the accumulation of DPP4 substrates and the reduced ratio of DPP4 cleaved pe
273 ach identified a handful of novel endogenous DPP4 substrates.
274                       This includes an epCam+Dpp4+ subtype of visceral endoderm.
275                  While bat, camel, and human DPP4 support MERS-CoV infection, several DPP4 orthologs,
276 s been identified as dipeptidyl peptidase 4 (DPP4), the mouse DPP4 homologue does not allow virus ent
277  are restricted to infection at the level of DPP4, the MERS-CoV receptor, we generated mice with huma
278 ted the spatial and cellular localization of DPP4 to evaluate an association MERS clinical disease.
279               Homozygosity mapping uncovered DPP4, TRHR, and MLF1 as novel candidate susceptibility g
280 matopoietic cells, and subsequent effects of DPP4-truncated proteins on multiple aspects of steady-st
281                      The reduced activity of DPP4-truncated versus full-length human GM-CSF was mecha
282 er of proteins that have DPP4 sites, and how DPP4 truncation may alter hematopoiesis based on the pro
283                                              DPP4 truncation of certain chemokines, colony-stimulatin
284 l length vs. truncated state, has shown that DPP4 truncation of colony-stimulating factors (CSFs) alt
285 ating factors with either proven or putative DPP4 truncation sites on hematopoietic cells, and subseq
286 ke (S) protein binds to the cellular protein DPP4 via its receptor binding domain (RBD) and mediates
287 to cellular receptor dipeptidyl peptidase 4 (DPP4) via the spike (S) protein receptor-binding domain
288 RS-CoV, our transgenic mice expressing hCD26/DPP4 viral receptor uniformly succumbed to death within
289                                              DPP4 was also found in a subset of mononuclear leukocyte
290 er identified that the reduced expression of DPP4 was associated with the accumulation of DPP4 substr
291 g domain (RBD) of MERS-CoV spike protein and DPP4 was determined by crystallography.
292                           In the parenchyma, DPP4 was found principally in type I and II cells and al
293                                  Among them, DPP4 was found to selectively prevent uptake by prolifer
294 ady at 6 weeks of age, expression of hepatic Dpp4 was increased in mice with high weight gain, indepe
295                     In the frugivorous bats, DPP4 was present in epithelial cells of both the respira
296                                              DPP4 was rarely detected in the surface epithelium from
297 he MERS-CoV receptor dipeptidyl peptidase 4 (DPP4) was identified and the specific interaction of the
298                      Dipeptidyl peptidase-4 (DPP4) was recently identified as its receptor.
299 mucosal mRNA levels of Slfn3, SI, Glut2, and Dpp4 were all substantially higher in the rat jejunum th
300                    Expression and release of DPP4 were markedly higher in the liver compared with adi

 
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