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1 (INS1007) is an oral reversible inhibitor of dipeptidyl peptidase 1 (DPP-1), an enzyme responsible fo
2 tudies, CTL generated from mice deficient in dipeptidyl peptidase 1 (DPP1) were used to investigate t
5 ke WTX, PALB2, and SQSTM1, we found that the dipeptidyl peptidase 3 (DPP3) protein binds KEAP1 via an
6 as a mediator of the therapeutic effects of dipeptidyl peptidase 4 (DPP-4) inhibition (vildagliptin)
7 n), was identified as a potent and selective dipeptidyl peptidase 4 (DPP-4) inhibitor with an excelle
8 perglycemic agents, including saxagliptin, a dipeptidyl peptidase 4 (DPP-4) inhibitor, are unclear.
9 antidiabetic incretin-based drugs, including dipeptidyl peptidase 4 (DPP-4) inhibitors and glucagon-l
10 rior trials have demonstrated CV safety of 3 dipeptidyl peptidase 4 (DPP-4) inhibitors but have inclu
11 on-like peptide 1 receptor (GLP-1) agonists, dipeptidyl peptidase 4 (DPP-4) inhibitors, peroxisome pr
12 outcomes with alogliptin, a new inhibitor of dipeptidyl peptidase 4 (DPP-4), as compared with placebo
13 omaltase, glucose transporter 2 (GLUT2), and dipeptidyl peptidase 4 (DPP-4), as well as that of the p
14 Previous analysis of mice lacking the enzyme dipeptidyl peptidase 4 (DPP4(-/-) mice), a biomedically
15 ted proteins such as the tetraspanin CD9 and dipeptidyl peptidase 4 (DPP4) along with multiple endoso
16 due to reduced levels of the virus receptor, dipeptidyl peptidase 4 (DPP4) and higher basal levels of
18 r (Gipr)-deficient mice receiving background dipeptidyl peptidase 4 (DPP4) inhibitor treatment were c
19 like peptide 1 receptor (GLP1R) agonists and dipeptidyl peptidase 4 (DPP4) inhibitors, can also reduc
20 like peptide-1 (GLP-1) receptor agonists and dipeptidyl peptidase 4 (DPP4) inhibitors, with the risk
23 MERS-CoV to the cell surface entry receptor dipeptidyl peptidase 4 (DPP4) occurs via S1(B) We now de
24 th Jamaican fruit bat (Artibeus jamaicensis) dipeptidyl peptidase 4 (DPP4) receptor and MERS-CoV repl
25 avirus (MERS-CoV) binds to cellular receptor dipeptidyl peptidase 4 (DPP4) via the spike (S) protein
27 ions with the MERS-CoV cell surface receptor dipeptidyl peptidase 4 (DPP4), and evolutionary mechanis
28 receptor for MERS-CoV has been identified as dipeptidyl peptidase 4 (DPP4), the mouse DPP4 homologue
29 Taken together, our results point toward dipeptidyl peptidase 4 (DPP4)-dependent endosomal uptake
31 , 4, 5, 13, and 14; sucrase isomaltase (SI); dipeptidyl peptidase 4 (Dpp4); glucose transporter type
34 hree different epitopes in the RBD and human dipeptidyl peptidase 4 (hDPP4) interface with subnanomol
35 V after adenovirus transduction of the human dipeptidyl peptidase 4 (hDPP4) receptor and then analyze
36 omozygous (+/+) and heterozygous (+/-) human dipeptidyl peptidase 4 (hDPP4) transgenic mice to study
38 etformin (sulfonylureas, thiazolidinediones, dipeptidyl peptidase 4 [DPP-4] inhibitors, glucagon-like
40 t cells were identified as a major source of dipeptidyl peptidase 4 and we also found that skin mast
42 Previous trial results have suggested that dipeptidyl peptidase 4 inhibitor (DPP4i) use might incre
43 ficacy of two clinically used T2D drugs: the dipeptidyl peptidase 4 inhibitor linagliptin and the sul
44 rdiovascular events of adding sitagliptin, a dipeptidyl peptidase 4 inhibitor, to usual care in patie
48 gh biguanides, sulfonylurea, glitazones, and dipeptidyl peptidase 4 inhibitors have variable effects
49 ingestion and is critical for the actions of dipeptidyl peptidase 4 inhibitors that enhance GLP-1 lev
50 ike peptide 1 mimetics, amylin mimetics, and dipeptidyl peptidase 4 inhibitors), in addition to diet
51 nd 330) that match the human sequence in the dipeptidyl peptidase 4 receptor, making mice susceptible
52 MERS-CoV antigen; double immunostaining with dipeptidyl peptidase 4 showed colocalization in scattere
55 der enzymes (lactase, sucrase-isomaltase and dipeptidyl peptidase 4) and visible subepithelial and sm
56 ss spectrometry analysis revealed that DPP4 (dipeptidyl peptidase 4) was selectively expressed on the
57 corresponding oxopeptides toward cleavage by dipeptidyl peptidase 4, the principal regulator of their
58 lmonary expression of the MERS-CoV receptor, dipeptidyl peptidase 4, was similar in marmosets and mac
67 glucosyltransferase); butyrylcholinesterase; dipeptidyl-peptidase 4 (CD26, adenosine deaminase comple
69 CoV spike (S) glycoprotein to sialosides and dipeptidyl-peptidase 4 (the attachment and entry recepto
73 te effects of treatment with vildagliptin on dipeptidyl peptidase-4 (DPP-4) activity, glucagon-like p
74 nes are terminated via enzymatic cleavage by dipeptidyl peptidase-4 (DPP-4) and through renal clearan
76 nguish FAP from other prolyl peptidases like dipeptidyl peptidase-4 (DPP-4) have not been developed.
77 (GLP-1) receptor agonists and inhibitors of dipeptidyl peptidase-4 (DPP-4) have shown pleiotropic ef
78 in this subgroup who also had baseline serum dipeptidyl peptidase-4 (DPP-4) higher than the populatio
79 od, crossover study in 24 patients with T2D, dipeptidyl peptidase-4 (DPP-4) inhibition and its glucos
80 bese mice (ob/ob), 45h was as effective as a dipeptidyl peptidase-4 (DPP-4) inhibitor at reducing pea
85 acological levels of GLP-1 activity, whereas dipeptidyl peptidase-4 (DPP-4) inhibitors increase conce
86 1 (GLP-1) secretion, on glucose lowering by dipeptidyl peptidase-4 (DPP-4) inhibitors is unclear.
89 ike peptide-1 receptor (GLP-1R) agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors represent 2 di
90 etformin, thiazolidinediones, sulfonylureas, dipeptidyl peptidase-4 (DPP-4) inhibitors, and sodium-gl
91 italized heart failure (hHF) associated with dipeptidyl peptidase-4 (DPP-4) inhibitors, creating unce
92 mpared with an active comparator drug class, dipeptidyl peptidase-4 (DPP-4) inhibitors, in patients w
94 bute to the mechanism by which inhibitors of dipeptidyl peptidase-4 (DPP-4) lower postprandial glucos
95 on of enzymatic degradation by inhibition of dipeptidyl peptidase-4 (DPP-4) promotes glycemic reducti
96 ears to prevent apoptosis, and inhibition of dipeptidyl peptidase-4 (DPP-4), which cleaves GLP-1, is
99 ulated genes, we identified the exopeptidase dipeptidyl peptidase-4 (DPP4) as a critical glucocortico
102 icyte interactions, as well as the effect of dipeptidyl peptidase-4 (DPP4) inhibitor on CD in endothe
104 viously disclosed azolopyrimidine containing dipeptidyl peptidase-4 (DPP4) inhibitors led us to focus
111 antidiabetic agents such as sulfonylureas or dipeptidyl peptidase-4 antagonists, which promote glucos
114 d-line glucose-lowering medication-including dipeptidyl peptidase-4 inhibitor (DPP4i), insulin, or th
115 dy, we compared the safety and efficacy of a dipeptidyl peptidase-4 inhibitor (sitagliptin) plus basa
116 analyses comparing empagliflozin versus the dipeptidyl peptidase-4 inhibitor class, and comparing so
117 ium-glucose cotransporter-2 inhibitor versus dipeptidyl peptidase-4 inhibitor classes also produced c
118 controlled cardiovascular safety trials, the dipeptidyl peptidase-4 inhibitor linagliptin demonstrate
119 analyses of HF and related outcomes with the dipeptidyl peptidase-4 inhibitor linagliptin versus plac
120 inhibitor dapagliflozin with and without the dipeptidyl peptidase-4 inhibitor saxagliptin, and the ef
121 adverse events for those associated with the dipeptidyl peptidase-4 inhibitor sitagliptin and the glu
124 creasing thiazolidinedione use and increased dipeptidyl peptidase-4 inhibitor use over time (P<0.001)
125 f newer antihyperglycemic medications in the dipeptidyl peptidase-4 inhibitor, glucagon-like peptide-
126 o assess the effectiveness of linagliptin, a dipeptidyl peptidase-4 inhibitor, in elderly patients wi
127 gonist, versus maximum approved doses of the dipeptidyl peptidase-4 inhibitor, sitagliptin, or the th
129 CI 1.15-1.76; six trials), intermediate with dipeptidyl peptidase-4 inhibitors (1.25, 1.08-1.45; two
130 rsus 4.9%), sulfonylurea (8.7% versus 6.9%), dipeptidyl peptidase-4 inhibitors (10.6% versus 7.5%), S
131 n compared with thiazolidinediones (TZDs) or dipeptidyl peptidase-4 inhibitors (DPP-4is) as a third a
132 ndings from preclinical studies suggest that dipeptidyl peptidase-4 inhibitors and proton-pump inhibi
133 ials supporting the cardiovascular safety of dipeptidyl peptidase-4 inhibitors and some glucagon-like
134 lucagon-like peptide-1 receptor agonists and dipeptidyl peptidase-4 inhibitors are commonly used for
136 ncretin system, GLP-1 receptor agonists, and dipeptidyl peptidase-4 inhibitors for 26 +/- 8 months be
138 1 analogs, alpha-glucosidase inhibitors, and dipeptidyl peptidase-4 inhibitors were associated with w
139 diones were used in 6.6% of HF patients, and dipeptidyl peptidase-4 inhibitors were used in 5.1%, wit
140 n-like peptide [GLP]-1 receptor agonists and dipeptidyl peptidase-4 inhibitors) have proven efficacy
144 essing enzyme corin and BNP-degrading enzyme dipeptidyl peptidase-4 were reduced in HF versus normal,
146 otentially by producing excessive amounts of Dipeptidyl peptidase-4, a protease that is a target of d
149 inally, combination of DGAT1 inhibition with dipeptidyl-peptidase-4 (DPP-4) inhibition led to further
152 nel subunit Kv4.2 with its auxiliary subunit dipeptidyl peptidase 6 (DPP6), and thereby modulates neu
153 racting proteins (KChIPs) and transmembrane, dipeptidyl peptidase 6 and 10 (DPP6/10) accessory subuni
157 We find that the hippocampal neurons lacking dipeptidyl-peptidase 6 show a sparser dendritic branchin
159 we employ knockdown and genetic deletion of dipeptidyl-peptidase 6 to reveal its importance for the
160 including dipeptidyl peptidase IV (DPP IV), dipeptidyl peptidase 8 (DPP8), fibroblast activation pro
162 3.98 x 10(-12)) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1
163 es inflammasome activation in the context of dipeptidyl peptidase 9 inhibition and could thereby incr
166 demonstrate that M1184V increases binding to dipeptidyl peptidase 9, which can account for its inhibi
169 types of EDTA-resistant protease activities: dipeptidyl peptidase and a 170-kDa gelatinase activity.
174 The binding kinetics and thermodynamics of dipeptidyl peptidase (DPP)-4 inhibitors (gliptins) were
176 l modification of chemokines mediated by the dipeptidyl peptidase DPP4 (CD26) has been shown to negat
177 administration of an inhibitor of the enzyme dipeptidyl-peptidase (DPP4i), which prevents the cleavag
180 ncy and high selectivity against the related dipeptidyl peptidases (DPPs) DPPIV, DPP9, DPPII, and pro
181 demonstrate that this effect is prevented by dipeptidyl peptidases (DPPs), which cleave NPY to its sh
182 ors that are selective for FAP over both the dipeptidyl peptidases (DPPs), with which it shares exope
183 f dipeptide production processes mediated by dipeptidyl-peptidases (DPPs) should be beneficial for th
184 rectly inhibits the activity of MMP20, KLK4, dipeptidyl peptidase I (DPPI) (an in vitro activator of
188 e injected TxA into ileal loops in PAR(2) or dipeptidyl peptidase I (DPPI) knockout mice or in wild-t
189 In this study, we show that the absence of dipeptidyl peptidase I (DPPI), a lysosomal cysteine prot
191 n inactivating mutation in the gene encoding dipeptidyl peptidase I, resulting in neutrophils lacking
192 aring features like propeptide processing by dipeptidyl peptidase I, storage, and release as an activ
193 ial of alpha-amylase, alpha-glucosidase, and dipeptidyl peptidase III (DPP III) enzyme activities.
195 glucagon-like peptide 1 (GLP1) mimetics and dipeptidyl peptidase inhibitors that enhance GLP1 recept
198 Binding of plasminogen type II (Pg 2) to dipeptidyl peptidase IV (DPP IV) on the surface of the h
199 method to a variety of proteases, including dipeptidyl peptidase IV (DPP IV), dipeptidyl peptidase 8
201 e synthesized and evaluated as inhibitors of dipeptidyl peptidase IV (DPP-4) for the treatment of typ
202 novel aminopiperidine-fused imidazopyridine dipeptidyl peptidase IV (DPP-4) inhibitor 1 has been dev
203 ered as potent, selective, and orally active dipeptidyl peptidase IV (DPP-4) inhibitors by extensive
204 les are rapidly inactivated by the action of dipeptidyl peptidase IV (DPP-4) which limits their use a
207 e synthesized and evaluated as inhibitors of dipeptidyl peptidase IV (DPP-IV) for the treatment of ty
208 e synthesized and evaluated as inhibitors of dipeptidyl peptidase IV (DPP-IV) for the treatment of ty
209 agon-like peptide-1 (GLP-1) degrading enzyme dipeptidyl peptidase IV (DPP-IV) have been shown to be e
211 acid linked l-cis-4,5-methanoprolinenitrile dipeptidyl peptidase IV (DPP-IV) inhibitors led to the i
212 ad angiotensin-I-converting enzyme (ACE) and dipeptidyl peptidase IV (DPP-IV) inhibitory activities,
213 tent angiotensin converting enzyme (ACE) and dipeptidyl peptidase IV (DPP-IV) inhibitory and oxygen r
215 ts (DOE) was used to optimise the release of dipeptidyl peptidase IV (DPP-IV) inhibitory peptides dur
216 of 72 dietary proteins to act as a source of dipeptidyl peptidase IV (DPP-IV) inhibitory peptides.
220 l screening was performed against the target dipeptidyl peptidase IV (DPP-IV) to identify good chemic
221 HSA), other components, such as the protease dipeptidyl peptidase IV (DPP-IV), possibly contribute to
227 epatocytes can give rise to SHPCs, rats with dipeptidyl peptidase IV (DPPIV) chimeric livers, which h
228 expression of CD26, especially its intrinsic dipeptidyl peptidase IV (DPPIV) enzyme activity, results
229 ine (C5-Pro-Pro) analogues was discovered as dipeptidyl peptidase IV (DPPIV) inhibitors as a potentia
231 as evaluated by injecting cell isolates from dipeptidyl peptidase IV (DPPIV) positive (DPPIV+) Fische
233 ddresses the hypothesis that the activity of dipeptidyl peptidase IV (DPPIV), an enzyme that inactiva
235 g the protocol of injecting hepatocytes from dipeptidyl peptidase IV (DPPIV)-positive donors into ret
236 ffects of HIR on engraftment of transplanted dipeptidyl peptidase IV (DPPIV)-positive hepatocytes in
240 proteins after enzymatic digestion, against dipeptidyl peptidase IV (DPPIV); an enzyme known to deac
243 tivities, among them primarily inhibition of dipeptidyl peptidase IV and angiotensin-converting enzym
245 assays based on F344 recipient rats lacking dipeptidyl peptidase IV enzyme activity to identify tran
247 vivo, but this effect was only detected with dipeptidyl peptidase IV inhibition, while mucosal respon
248 ulocyte-colony stimulating factor (G-CSF), a dipeptidyl peptidase IV inhibitor (DPP-4i), and a proton
251 tal liver cells were transplanted into adult dipeptidyl peptidase IV knockout mice and differentiated
253 vivo and mature into hepatocytes expressing dipeptidyl peptidase IV or fumarylacetoacetate hydrolase
254 ntained large clusters of sinusoids lined by dipeptidyl peptidase IV positive endothelial cells coexp
257 ts but does not inhibit close FAP homologues dipeptidyl peptidase IV, dipeptidyl peptidase 9, and pro
260 hepatocytes were transplanted into syngeneic dipeptidyl peptidase IV-deficient rats followed by histo
267 n, expression of sucrase isomaltase (SI) and dipeptidyl-peptidase IV (DPP-IV), two well known intesti
268 ow cytometry and histochemical estimation of dipeptidyl-peptidase IV enzyme activity of donor cells i
270 -glucosidase (37.8%), alpha-amylase (35.6%), dipeptidyl peptidase-IV (34.4%), reactive oxygen species
271 uggest a variety of bioactivities, including dipeptidyl peptidase-IV (DPP-IV) and angiotensin convert
272 wever, its rapid degradation by enzymes like dipeptidyl peptidase-IV (DPP-IV) and neutral endopeptida
273 f GLP-1 is short due to rapid degradation by dipeptidyl peptidase-IV (DPP-IV) and renal clearance.
274 P-1 is short because of rapid degradation by dipeptidyl peptidase-IV (DPP-IV) and renal clearance.
278 ate or propionate increased DBS, enhanced by dipeptidyl peptidase-IV (DPPIV) inhibition, at the same
279 s are a good source of natural inhibitors of dipeptidyl peptidase-IV and prolyl endopeptidase and cou
281 tivities and clinical variants, for example, dipeptidyl peptidase-IV inhibitor-associated noninflamma
282 d 1-beta-fructofuranosyl nystose) are potent dipeptidyl peptidase-IV inhibitors as well as peroxisome
283 ction of several serine proteases, including dipeptidyl peptidase-IV, neutrophil elastase, matrix met
285 yeast of Blastomyces dermatitidis elaborates dipeptidyl-peptidase IVA (DppIVA), a close mimic of the
288 , the Ca(2+) binding proteins KChIPs and the dipeptidyl peptidase-like proteins (DPPLs) DPP6 (also kn
291 cell-base experiments with Kv4.2 and several dipeptidyl-peptidase-like protein-6 (DPPX) plasmid const
292 metabotropic glutamate receptor 5 (mGluR5), dipeptidyl-peptidase-like protein-6 (DPPX), and gamma-am
293 mined the putative novel contribution of the dipeptidyl-peptidase-like protein-6 DPP6-S to the gamma
294 Kv channel-interacting proteins (KChIPs) and dipeptidyl-peptidase-like proteins (DPLs: DPP6 or DPPX,
295 hannel interacting proteins (KChIPs) and the dipeptidyl-peptidase-like proteins (DPPLs) DPPX (DPP6) a
296 ulating the biophysical properties of Kv4.2: dipeptidyl-peptidase-like type II transmembrane proteins
298 marked TSS energy for both endopeptidase and dipeptidyl peptidase substrates, and structural modeling