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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.
22 Sitagliptin therapy for 12 months reduces DPP4 activity yet does not increase markers of inflammat
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
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
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.
34 ce of a novel protease complex consisting of DPP4 and seprase in human endothelial cells that were ac
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
42 including increased expression of IL6, TNF, DPP4, and IL8, as well as elevated SA-beta-gal activity.
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
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
56 er, NPY conversion by dipeptidylpeptidase 4 (DPP4) augmented Y5R activation and function in liver can
58 these compounds displayed not only increased DPP4 binding activity but also significantly reduced hum
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
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
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
84 ble to MERS-CoV, whereas expression of human DPP4 containing the five hamster DPP4 amino acids did no
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
94 ism of these viruses in bats, we studied the DPP4 distribution in the respiratory and extra-respirato
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
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
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
112 ionally, we show that glucocorticoid-induced DPP4 expression is blocked by the GR antagonist RU-486 a
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)
119 e identified a novel mechanism involving the DPP4 gelatin-binding domain of the DPP4-seprase complex
122 ase isomaltase (SI); dipeptidyl peptidase 4 (Dpp4); glucose transporter type 2 (Glut2); and villin we
124 lating frequency, we unexpectedly found that DPP4 has a more general role in regulating colony-stimul
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.
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
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
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
143 data show that glucose-induced expression of Dpp4 in the liver is facilitated by demethylation of the
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
151 lating hormones such as GLP-1 and GIP, thus, DPP4 inhibition has become a useful therapy for type 2 d
156 t with this maladaptive role, the effects of DPP4 inhibition seem to exert a protective role in cardi
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
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
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
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
177 se in individuals treated with glitazones or DPP4 inhibitors and/or GLP-1 receptor agonists to indivi
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
192 tin-based therapies, dipeptidyl peptidase-4 (DPP4) inhibitors and glucagon-like peptide-1 (GLP-1) ana
195 yrimidine containing dipeptidyl peptidase-4 (DPP4) inhibitors led us to focus on an imidazolopyrimidi
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
204 r, whether increased dipeptidyl peptidase 4 (DPP4) is involved in the pathogenesis or is rather a con
208 s from FAP-null mice, and, while knockout of DPP4 lacked an analogous effect, the combined DPP4/FAP i
215 timulated macrophage mobility; unexpectedly, DPP4 mediated the glucocorticoid-induced macrophage migr
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
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
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)
231 ch, the potential of MERS-CoV to utilize the DPP4s of common Middle Eastern livestock was investigate
233 ial implications of the modifying effects of DPP4 on a large number of cytokines and other growth-reg
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
243 echanism by the peptides was investigated by DPP4-peptide inhibition kinetics, molecular docking 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
253 y bound to DPP4-expressing cells and soluble DPP4 protein and induced significant neutralizing antibo
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
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
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
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
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.
280 matopoietic cells, and subsequent effects of DPP4-truncated proteins on multiple aspects of steady-st
282 er of proteins that have DPP4 sites, and how DPP4 truncation may alter hematopoiesis based on the pro
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
290 er identified that the reduced expression of DPP4 was associated with the accumulation of DPP4 substr
294 ady at 6 weeks of age, expression of hepatic Dpp4 was increased in mice with high weight gain, indepe
297 he MERS-CoV receptor dipeptidyl peptidase 4 (DPP4) was identified and the specific interaction of the
299 mucosal mRNA levels of Slfn3, SI, Glut2, and Dpp4 were all substantially higher in the rat jejunum th