PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
33338714-6	2021	Therefore, this study aimed was to investigate the functional components in the seed pomace ethanol extracts of C. oleifera Abel (CPE) and Oolong tea (OPE) and to evaluate the ameliorative effects of CPE and OPE on oxidative stress, inflammation, and vascular remodeling in l-NAME induced hypertensive C57BL/6J mice.	Ethanol	92-99	carboxypeptidase E	Mus musculus	130-133
33338714-9	2021	Moreover, CPE and OPE decreased the malondialdehyde concentration in the liver by over 33%, as well as levels of tumor necrosis factor-alpha, interleukin 6, and interleukin-1beta in the kidney and heart.	Malondialdehyde	36-51	carboxypeptidase E	Mus musculus	10-13
32995694-9	2020	Treatment of preosteoblastic cells with intact or mutated recombinant CPE led to a transient accumulation of small lipid droplets, increased oxidative phosphorylation, and increased cellular dependence on fatty acids as fuel for energy production.	Fatty Acids	205-216	carboxypeptidase E	Mus musculus	70-73
33414376-9	2021	Subsequently, treatment of the HT22cpe-/- cells with NF-alpha1-CPE or CPE-E342Q equivalently activated ERK signaling and increased BCL2 expression to protect these neurons against H2O2-or glutamate-induced cytotoxicity.	Hydrogen Peroxide	180-184	carboxypeptidase E	Mus musculus	63-66
33414376-9	2021	Subsequently, treatment of the HT22cpe-/- cells with NF-alpha1-CPE or CPE-E342Q equivalently activated ERK signaling and increased BCL2 expression to protect these neurons against H2O2-or glutamate-induced cytotoxicity.	Glutamic Acid	188-197	carboxypeptidase E	Mus musculus	63-66
33152480-4	2021	CPE-decorated liposomes undergo efficient in vitro endocytosis, and delivered doxorubicin to the cell nuclei.	Doxorubicin	78-89	carboxypeptidase E	Mus musculus	0-3
32422353-10	2020	CPE enhanced acute GLP-1 secretion 6.4-16.3-fold from GLUTag cells at both low (1.1 mM) and high (16.7 mM) glucose (P < 0.01) concentrations.	Glucose	107-114	carboxypeptidase E	Mus musculus	0-3
29476513-4	2018	Because CPE removes C-terminal Lys and Arg residues from peptide-processing intermediates, organisms lacking CPE show a large decrease in the levels of the mature forms of most neuropeptides and peptide hormones, and a very large increase in the levels of the processing intermediates that contain C-terminal Lys and/or Arg (i.e., the CPE substrates).	Lysine	31-34	carboxypeptidase E	Mus musculus	8-11
32163602-3	2020	The molecular weight of CPH and the degraded P. haitanensis polysaccharide (DCPH) were measured to be 524 and 217 kDa, respectively.	DCPH	76-80	carboxypeptidase E	Mus musculus	24-27
32163602-4	2020	GC-MS spectrometry results showed that CPH and DCPH were mainly composed of galactose.	Galactose	76-85	carboxypeptidase E	Mus musculus	39-42
32163602-5	2020	In vitro antioxidant assays indicated that DCPH possessed improved radical scavenging activity and ferric iron reducing power when compared to those of CPH.	ferric sulfate	99-110	carboxypeptidase E	Mus musculus	44-47
32163602-6	2020	In H2 O2 -treated RAW264.7 cells, DCPH was also found to be more effective in reducing the generation of malondialdehyde and reactive oxygen species than CPH.	Hydrogen Peroxide	3-8	carboxypeptidase E	Mus musculus	35-38
32163602-6	2020	In H2 O2 -treated RAW264.7 cells, DCPH was also found to be more effective in reducing the generation of malondialdehyde and reactive oxygen species than CPH.	Malondialdehyde	105-120	carboxypeptidase E	Mus musculus	35-38
32163602-6	2020	In H2 O2 -treated RAW264.7 cells, DCPH was also found to be more effective in reducing the generation of malondialdehyde and reactive oxygen species than CPH.	Reactive Oxygen Species	125-148	carboxypeptidase E	Mus musculus	35-38
29476513-4	2018	Because CPE removes C-terminal Lys and Arg residues from peptide-processing intermediates, organisms lacking CPE show a large decrease in the levels of the mature forms of most neuropeptides and peptide hormones, and a very large increase in the levels of the processing intermediates that contain C-terminal Lys and/or Arg (i.e., the CPE substrates).	Lysine	31-34	carboxypeptidase E	Mus musculus	109-112
29476513-4	2018	Because CPE removes C-terminal Lys and Arg residues from peptide-processing intermediates, organisms lacking CPE show a large decrease in the levels of the mature forms of most neuropeptides and peptide hormones, and a very large increase in the levels of the processing intermediates that contain C-terminal Lys and/or Arg (i.e., the CPE substrates).	Lysine	31-34	carboxypeptidase E	Mus musculus	109-112
29476513-4	2018	Because CPE removes C-terminal Lys and Arg residues from peptide-processing intermediates, organisms lacking CPE show a large decrease in the levels of the mature forms of most neuropeptides and peptide hormones, and a very large increase in the levels of the processing intermediates that contain C-terminal Lys and/or Arg (i.e., the CPE substrates).	Arginine	39-42	carboxypeptidase E	Mus musculus	8-11
29476513-4	2018	Because CPE removes C-terminal Lys and Arg residues from peptide-processing intermediates, organisms lacking CPE show a large decrease in the levels of the mature forms of most neuropeptides and peptide hormones, and a very large increase in the levels of the processing intermediates that contain C-terminal Lys and/or Arg (i.e., the CPE substrates).	Arginine	39-42	carboxypeptidase E	Mus musculus	109-112
29476513-4	2018	Because CPE removes C-terminal Lys and Arg residues from peptide-processing intermediates, organisms lacking CPE show a large decrease in the levels of the mature forms of most neuropeptides and peptide hormones, and a very large increase in the levels of the processing intermediates that contain C-terminal Lys and/or Arg (i.e., the CPE substrates).	Arginine	39-42	carboxypeptidase E	Mus musculus	109-112
29476513-4	2018	Because CPE removes C-terminal Lys and Arg residues from peptide-processing intermediates, organisms lacking CPE show a large decrease in the levels of the mature forms of most neuropeptides and peptide hormones, and a very large increase in the levels of the processing intermediates that contain C-terminal Lys and/or Arg (i.e., the CPE substrates).	Lysine	309-312	carboxypeptidase E	Mus musculus	8-11
29476513-4	2018	Because CPE removes C-terminal Lys and Arg residues from peptide-processing intermediates, organisms lacking CPE show a large decrease in the levels of the mature forms of most neuropeptides and peptide hormones, and a very large increase in the levels of the processing intermediates that contain C-terminal Lys and/or Arg (i.e., the CPE substrates).	Lysine	309-312	carboxypeptidase E	Mus musculus	109-112
29476513-4	2018	Because CPE removes C-terminal Lys and Arg residues from peptide-processing intermediates, organisms lacking CPE show a large decrease in the levels of the mature forms of most neuropeptides and peptide hormones, and a very large increase in the levels of the processing intermediates that contain C-terminal Lys and/or Arg (i.e., the CPE substrates).	Lysine	309-312	carboxypeptidase E	Mus musculus	109-112
29476513-4	2018	Because CPE removes C-terminal Lys and Arg residues from peptide-processing intermediates, organisms lacking CPE show a large decrease in the levels of the mature forms of most neuropeptides and peptide hormones, and a very large increase in the levels of the processing intermediates that contain C-terminal Lys and/or Arg (i.e., the CPE substrates).	Arginine	320-323	carboxypeptidase E	Mus musculus	8-11
29476513-4	2018	Because CPE removes C-terminal Lys and Arg residues from peptide-processing intermediates, organisms lacking CPE show a large decrease in the levels of the mature forms of most neuropeptides and peptide hormones, and a very large increase in the levels of the processing intermediates that contain C-terminal Lys and/or Arg (i.e., the CPE substrates).	Arginine	320-323	carboxypeptidase E	Mus musculus	109-112
29476513-4	2018	Because CPE removes C-terminal Lys and Arg residues from peptide-processing intermediates, organisms lacking CPE show a large decrease in the levels of the mature forms of most neuropeptides and peptide hormones, and a very large increase in the levels of the processing intermediates that contain C-terminal Lys and/or Arg (i.e., the CPE substrates).	Arginine	320-323	carboxypeptidase E	Mus musculus	109-112
29476513-5	2018	These CPE substrates can be purified on an anhydrotrypsin-agarose affinity resin, which specifically binds peptides with C-terminal basic residues.	Sepharose	58-65	carboxypeptidase E	Mus musculus	6-9
28386642-7	2017	The CPE-KO mice showed normal postsynaptic AMPA response to kainate application in hippocampal slices and dissociated neurons.	Kainic Acid	60-67	carboxypeptidase E	Mus musculus	4-7
27321121-6	2016	In addition, the HFD+CPH group had significantly decreased liver total cholesterol and triglyceride levels compared with those in the HFD group.	Cholesterol	71-82	carboxypeptidase E	Mus musculus	17-24
27321121-6	2016	In addition, the HFD+CPH group had significantly decreased liver total cholesterol and triglyceride levels compared with those in the HFD group.	Triglycerides	87-99	carboxypeptidase E	Mus musculus	17-24
26987021-7	2016	At levels of 50 and 100 mug/mL, CPE significantly inhibited preadipocyte lipid accumulation by 35% and 50%, respectively, and by 22% and 36% when combined with 15 mM Leu.	Leucine	166-169	carboxypeptidase E	Mus musculus	32-35
23825125-6	2013	After mild CRS (1 h/d for 7 d), CPE protein and mRNA were significantly elevated in the hippocampal CA3 region, compared to naive littermates.	3-cresol	11-14	carboxypeptidase E	Mus musculus	32-35
26705481-3	2015	We used 1-hydroxy-3-carboxy-2,2,5,5-tetramethylpyrrolidine (CPH) as a reporter for one-electron oxidations, e.g. free radical-mediated oxidations; the one-electron oxidation product of CPH, 3-carboxy-2,2,5,5-tetramethyl-1-pyrrolidinyloxy (CP ), is a nitroxide free radical that is relatively persistent in vivo and detectable by EPR.	1-hydroxy-2,2,5,5-tetramethylpyrrolidine-3-carboxylic acid	8-58	carboxypeptidase E	Mus musculus	60-63
26705481-3	2015	We used 1-hydroxy-3-carboxy-2,2,5,5-tetramethylpyrrolidine (CPH) as a reporter for one-electron oxidations, e.g. free radical-mediated oxidations; the one-electron oxidation product of CPH, 3-carboxy-2,2,5,5-tetramethyl-1-pyrrolidinyloxy (CP ), is a nitroxide free radical that is relatively persistent in vivo and detectable by EPR.	1-hydroxy-2,2,5,5-tetramethylpyrrolidine-3-carboxylic acid	8-58	carboxypeptidase E	Mus musculus	185-188
26705481-3	2015	We used 1-hydroxy-3-carboxy-2,2,5,5-tetramethylpyrrolidine (CPH) as a reporter for one-electron oxidations, e.g. free radical-mediated oxidations; the one-electron oxidation product of CPH, 3-carboxy-2,2,5,5-tetramethyl-1-pyrrolidinyloxy (CP ), is a nitroxide free radical that is relatively persistent in vivo and detectable by EPR.	2,2,5,5-Tetramethyl-3-carboxypyrrolidinooxy	190-237	carboxypeptidase E	Mus musculus	60-63
26705481-3	2015	We used 1-hydroxy-3-carboxy-2,2,5,5-tetramethylpyrrolidine (CPH) as a reporter for one-electron oxidations, e.g. free radical-mediated oxidations; the one-electron oxidation product of CPH, 3-carboxy-2,2,5,5-tetramethyl-1-pyrrolidinyloxy (CP ), is a nitroxide free radical that is relatively persistent in vivo and detectable by EPR.	Hydroxylamine	250-259	carboxypeptidase E	Mus musculus	60-63
25645504-5	2015	Active immunization of mice with r-Cpae generated high circulating serum IgG (systemic), significantly increased intestinal mucosal s-IgA antibody titres and resulted in substantial protection to the immunized animals (100% and 75% survival) with reduced tissue morbidity when administered with 5xLD(100) doses of alphaC (intramuscular) and CPE (intra-gastric gavage) respectively.	r-cpae	33-39	carboxypeptidase E	Mus musculus	341-344
25203099-7	2014	At 16 weeks of age, CPE(fat/fat) mice develop severe obesity, hyperglycemia, elevated serum triglycerides and leptin, and increased blood neutrophil counts.	Triglycerides	92-105	carboxypeptidase E	Mus musculus	20-23
23825125-7	2013	In addition, luciferase reporter assays identified a functional glucocorticoid regulatory element within the cpe promoter that mediated the up-regulation of CPE expression in primary hippocampal neurons following dexamethasone treatment, suggesting that circulating plasma glucocorticoids could evoke a similar effect on CPE in the hippocampus in vivo.	Dexamethasone	213-226	carboxypeptidase E	Mus musculus	109-112
23825125-7	2013	In addition, luciferase reporter assays identified a functional glucocorticoid regulatory element within the cpe promoter that mediated the up-regulation of CPE expression in primary hippocampal neurons following dexamethasone treatment, suggesting that circulating plasma glucocorticoids could evoke a similar effect on CPE in the hippocampus in vivo.	Dexamethasone	213-226	carboxypeptidase E	Mus musculus	157-160
23825125-7	2013	In addition, luciferase reporter assays identified a functional glucocorticoid regulatory element within the cpe promoter that mediated the up-regulation of CPE expression in primary hippocampal neurons following dexamethasone treatment, suggesting that circulating plasma glucocorticoids could evoke a similar effect on CPE in the hippocampus in vivo.	Dexamethasone	213-226	carboxypeptidase E	Mus musculus	321-324
23442571-1	2013	Cpe(fat/fat) mice have a point mutation in carboxypeptidase E (Cpe), an exopeptidase that removes C-terminal basic amino acids from intermediates to produce bioactive peptides.	Amino Acids, Basic	109-126	carboxypeptidase E	Mus musculus	0-3
23442571-1	2013	Cpe(fat/fat) mice have a point mutation in carboxypeptidase E (Cpe), an exopeptidase that removes C-terminal basic amino acids from intermediates to produce bioactive peptides.	Amino Acids, Basic	109-126	carboxypeptidase E	Mus musculus	43-61
23442571-1	2013	Cpe(fat/fat) mice have a point mutation in carboxypeptidase E (Cpe), an exopeptidase that removes C-terminal basic amino acids from intermediates to produce bioactive peptides.	Amino Acids, Basic	109-126	carboxypeptidase E	Mus musculus	63-66
22678994-6	2013	Polymethoxylated flavones such as nobiletin and tangeretin were found as the active compounds responsible for CPE effects on  Psim .	polymethoxylated flavones	0-25	carboxypeptidase E	Mus musculus	110-113
22678994-6	2013	Polymethoxylated flavones such as nobiletin and tangeretin were found as the active compounds responsible for CPE effects on  Psim .	nobiletin	34-43	carboxypeptidase E	Mus musculus	110-113
22678994-6	2013	Polymethoxylated flavones such as nobiletin and tangeretin were found as the active compounds responsible for CPE effects on  Psim .	tangeretin	48-58	carboxypeptidase E	Mus musculus	110-113
22678994-7	2013	Neuronal viability was significantly increased in a dose-dependent manner by CPE treatment in H2 O2 -stimulated HT-22 cells as an in vitro neuronal insult model.	Hydrogen Peroxide	94-99	carboxypeptidase E	Mus musculus	77-80
22678994-8	2013	CPE treatment significantly inhibited H2 O2 -induced apoptotic processes such as chromatin condensation, caspase 3 activation and anti-poly (ADP-ribose) polymerase (PARP) cleavage.	Hydrogen Peroxide	38-43	carboxypeptidase E	Mus musculus	0-3
22678994-9	2013	CPE treatment significantly blocked mitochondrial calcium overload in H2 O2 -stimulated HT-22 neurons as indicated by rhod-2 acetoxymethyl ester.	Calcium	50-57	carboxypeptidase E	Mus musculus	0-3
22678994-9	2013	CPE treatment significantly blocked mitochondrial calcium overload in H2 O2 -stimulated HT-22 neurons as indicated by rhod-2 acetoxymethyl ester.	Hydrogen Peroxide	70-75	carboxypeptidase E	Mus musculus	0-3
22678994-9	2013	CPE treatment significantly blocked mitochondrial calcium overload in H2 O2 -stimulated HT-22 neurons as indicated by rhod-2 acetoxymethyl ester.	acetoxymethyl ester	125-144	carboxypeptidase E	Mus musculus	0-3
25346878-0	2012	Carbamazepine Prevents Hippocampal Neurodegeneration in Mice Lacking the Neuroprotective Protein, Carboxypetidase E. Carboxypeptidase E (CPE) has recently been described as a neuroprotective protein, and in mice devoid of CPE, a complete loss of the hippocampal CA3 neurons is observed.	Carbamazepine	0-13	carboxypeptidase E	Mus musculus	117-135
25346878-0	2012	Carbamazepine Prevents Hippocampal Neurodegeneration in Mice Lacking the Neuroprotective Protein, Carboxypetidase E. Carboxypeptidase E (CPE) has recently been described as a neuroprotective protein, and in mice devoid of CPE, a complete loss of the hippocampal CA3 neurons is observed.	Carbamazepine	0-13	carboxypeptidase E	Mus musculus	137-140
25346878-0	2012	Carbamazepine Prevents Hippocampal Neurodegeneration in Mice Lacking the Neuroprotective Protein, Carboxypetidase E. Carboxypeptidase E (CPE) has recently been described as a neuroprotective protein, and in mice devoid of CPE, a complete loss of the hippocampal CA3 neurons is observed.	Carbamazepine	0-13	carboxypeptidase E	Mus musculus	222-225
19369449-4	2009	Thus Ncbe/Nbcn2 mediates the DIDS-sensitive Na(+)-dependent pH(i) recovery in the CPE.	4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid	29-33	carboxypeptidase E	Mus musculus	82-85
25346878-6	2012	Daily treatment with carbamazepine, an antiepileptic agent, in 2 week old CPE KO mice for 2 weeks prevented the neurodegeneration, despite the weaning process at 3 weeks.	Carbamazepine	21-34	carboxypeptidase E	Mus musculus	74-77
25346878-9	2012	This degeneration was prevented by carbamazepine suggesting that the stress associated with weaning caused epileptic-like events in the CPE KO mice.	Carbamazepine	35-48	carboxypeptidase E	Mus musculus	136-139
21983135-4	2012	Substitution of Asn and Ser at positions 309 and 313, respectively, with alanine increased the affinity of C-CPE for claudin-4.	Asparagine	16-19	carboxypeptidase E	Mus musculus	109-112
21983135-4	2012	Substitution of Asn and Ser at positions 309 and 313, respectively, with alanine increased the affinity of C-CPE for claudin-4.	Serine	24-27	carboxypeptidase E	Mus musculus	109-112
21983135-4	2012	Substitution of Asn and Ser at positions 309 and 313, respectively, with alanine increased the affinity of C-CPE for claudin-4.	Alanine	73-80	carboxypeptidase E	Mus musculus	109-112
21983135-11	2012	These findings suggest that the alanine-substituted C-CPE mutant shows promise as a claudin-targeted mucosal vaccine.	Alanine	32-39	carboxypeptidase E	Mus musculus	54-57
20655338-1	2010	Carboxypeptidase E (CPE) is an exopeptidase that removes C-terminal basic amino acids from a variety of bioactive peptides.	Amino Acids, Basic	68-85	carboxypeptidase E	Mus musculus	0-18
20655338-1	2010	Carboxypeptidase E (CPE) is an exopeptidase that removes C-terminal basic amino acids from a variety of bioactive peptides.	Amino Acids, Basic	68-85	carboxypeptidase E	Mus musculus	20-23
20655338-5	2010	ACTH was released in a regulated fashion from CPE-depleted cells in response to two secretagogues, 8-bromo-cyclic AMP and corticotrophin-releasing hormone.	8-Bromo Cyclic Adenosine Monophosphate	99-117	carboxypeptidase E	Mus musculus	46-49
20492353-3	2010	Additionally, we found K(+)-stimulated glutamate secretion from hypothalamic embryonic neurons was impaired in CPE-KO mice.	Glutamic Acid	39-48	carboxypeptidase E	Mus musculus	111-114
22247830-4	2010	Aqueous extract (CPA) significantly inhibited writhes at the dose of 75 and 150 mg/kg body weight, while ethanol extract (CPE) produced significant protection at the dose of 150 mg/kg body weight.	Ethanol	105-112	carboxypeptidase E	Mus musculus	122-125
22247830-5	2010	However, in tail flick method only the ethanol extract (CPE) showed significant central analgesic action, while aqueous extract was totally ineffective.	Ethanol	39-46	carboxypeptidase E	Mus musculus	56-59
18202146-2	2008	Here we uncover a mechanism in which the cytoplasmic tail of transmembrane carboxypeptidase E (CPE) found in proopiomelanocotin (POMC)/ACTH vesicles interacts with microtubule-based motors to control transport of these vesicles to the release site in pituitary cells.	proopiomelanocotin	109-127	carboxypeptidase E	Mus musculus	75-93
18550819-3	2008	The most significantly altered protein in both human islets and MIN6 beta-cells treated with palmitate was carboxypeptidase E (CPE).	Palmitates	93-102	carboxypeptidase E	Mus musculus	107-125
18550819-3	2008	The most significantly altered protein in both human islets and MIN6 beta-cells treated with palmitate was carboxypeptidase E (CPE).	Palmitates	93-102	carboxypeptidase E	Mus musculus	127-130
18202146-2	2008	Here we uncover a mechanism in which the cytoplasmic tail of transmembrane carboxypeptidase E (CPE) found in proopiomelanocotin (POMC)/ACTH vesicles interacts with microtubule-based motors to control transport of these vesicles to the release site in pituitary cells.	proopiomelanocotin	109-127	carboxypeptidase E	Mus musculus	95-98
18202146-2	2008	Here we uncover a mechanism in which the cytoplasmic tail of transmembrane carboxypeptidase E (CPE) found in proopiomelanocotin (POMC)/ACTH vesicles interacts with microtubule-based motors to control transport of these vesicles to the release site in pituitary cells.	pomc	129-133	carboxypeptidase E	Mus musculus	75-93
18202146-2	2008	Here we uncover a mechanism in which the cytoplasmic tail of transmembrane carboxypeptidase E (CPE) found in proopiomelanocotin (POMC)/ACTH vesicles interacts with microtubule-based motors to control transport of these vesicles to the release site in pituitary cells.	pomc	129-133	carboxypeptidase E	Mus musculus	95-98
17587672-2	2007	CPE, crude polysaccharide extract isolated from the rhizome of C. xanthorrhiza using 0.1 N NaOH, consisted of arabinose (18.69%), galactose (14.0%), glucose (50.67%), mannose (12.97%), rhamnose (2.73%), and xylose (0.94%), with an average molecular weight of 33,000 Da.	Polysaccharides	11-25	carboxypeptidase E	Mus musculus	0-3
17587672-5	2007	CPE significantly increased the phagocytosis of macrophages and the release of NO, H2O2, TNF-alpha, and PGE2 in a dose-dependent manner, and showed a similar activity to lipopolysaccharide (LPS).	Hydrogen Peroxide	83-87	carboxypeptidase E	Mus musculus	0-3
17587672-5	2007	CPE significantly increased the phagocytosis of macrophages and the release of NO, H2O2, TNF-alpha, and PGE2 in a dose-dependent manner, and showed a similar activity to lipopolysaccharide (LPS).	Dinoprostone	104-108	carboxypeptidase E	Mus musculus	0-3
17587672-2	2007	CPE, crude polysaccharide extract isolated from the rhizome of C. xanthorrhiza using 0.1 N NaOH, consisted of arabinose (18.69%), galactose (14.0%), glucose (50.67%), mannose (12.97%), rhamnose (2.73%), and xylose (0.94%), with an average molecular weight of 33,000 Da.	Sodium Hydroxide	91-95	carboxypeptidase E	Mus musculus	0-3
17587672-2	2007	CPE, crude polysaccharide extract isolated from the rhizome of C. xanthorrhiza using 0.1 N NaOH, consisted of arabinose (18.69%), galactose (14.0%), glucose (50.67%), mannose (12.97%), rhamnose (2.73%), and xylose (0.94%), with an average molecular weight of 33,000 Da.	Arabinose	110-119	carboxypeptidase E	Mus musculus	0-3
17587672-2	2007	CPE, crude polysaccharide extract isolated from the rhizome of C. xanthorrhiza using 0.1 N NaOH, consisted of arabinose (18.69%), galactose (14.0%), glucose (50.67%), mannose (12.97%), rhamnose (2.73%), and xylose (0.94%), with an average molecular weight of 33,000 Da.	Galactose	130-139	carboxypeptidase E	Mus musculus	0-3
17587672-2	2007	CPE, crude polysaccharide extract isolated from the rhizome of C. xanthorrhiza using 0.1 N NaOH, consisted of arabinose (18.69%), galactose (14.0%), glucose (50.67%), mannose (12.97%), rhamnose (2.73%), and xylose (0.94%), with an average molecular weight of 33,000 Da.	Glucose	149-156	carboxypeptidase E	Mus musculus	0-3
17587672-2	2007	CPE, crude polysaccharide extract isolated from the rhizome of C. xanthorrhiza using 0.1 N NaOH, consisted of arabinose (18.69%), galactose (14.0%), glucose (50.67%), mannose (12.97%), rhamnose (2.73%), and xylose (0.94%), with an average molecular weight of 33,000 Da.	Mannose	167-174	carboxypeptidase E	Mus musculus	0-3
17587672-2	2007	CPE, crude polysaccharide extract isolated from the rhizome of C. xanthorrhiza using 0.1 N NaOH, consisted of arabinose (18.69%), galactose (14.0%), glucose (50.67%), mannose (12.97%), rhamnose (2.73%), and xylose (0.94%), with an average molecular weight of 33,000 Da.	Rhamnose	185-193	carboxypeptidase E	Mus musculus	0-3
17587672-2	2007	CPE, crude polysaccharide extract isolated from the rhizome of C. xanthorrhiza using 0.1 N NaOH, consisted of arabinose (18.69%), galactose (14.0%), glucose (50.67%), mannose (12.97%), rhamnose (2.73%), and xylose (0.94%), with an average molecular weight of 33,000 Da.	Xylose	207-213	carboxypeptidase E	Mus musculus	0-3
17177860-5	2006	We also show that absence of CPE causes a sporadic but striking placental phenotype characterized by an increase in giant and glycogen cell numbers and giant cell hypertrophy.	Glycogen	126-134	carboxypeptidase E	Mus musculus	29-32
16002559-4	2006	Airway responsiveness to intravenous methacholine, measured by forced oscillation, was increased in Cpe(fat) vs. wild-type mice after air exposure.	Methacholine Chloride	37-49	carboxypeptidase E	Mus musculus	100-103
16002559-5	2006	In addition, compared with air exposure, airway responsiveness was increased 24 h after O3 exposure (2 ppm for 3 h) in Cpe(fat) but not in wild-type mice.	Ozone	88-90	carboxypeptidase E	Mus musculus	119-122
14975454-1	2004	1-Acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine (ACP) is a unique probe for in vivo measurements of reactive oxygen species (ROS), because it is hydrolyzed by esterase to a hydroxylamine form (CP-H), which is oxidized to an electron spin resonance-detectable nitroxyl radical (CP) by a reaction with superoxide anion radical, etc.	1-acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine	0-52	carboxypeptidase E	Mus musculus	198-202
16219686-1	2005	Secretogranin III (SgIII) and carboxypeptidase E (CPE) bind specifically to cholesterol-rich secretory granule (SG) membranes.	Cholesterol	76-87	carboxypeptidase E	Mus musculus	30-48
16219686-1	2005	Secretogranin III (SgIII) and carboxypeptidase E (CPE) bind specifically to cholesterol-rich secretory granule (SG) membranes.	Cholesterol	76-87	carboxypeptidase E	Mus musculus	50-53
16219686-5	2005	The Cpe fat pituitary exhibited elevated levels of SgIII and CgA, which suggests that they compensate for a sorting function of CPE for POMC and its intermediates to ACTH.	acth	166-170	carboxypeptidase E	Mus musculus	4-7
16219686-5	2005	The Cpe fat pituitary exhibited elevated levels of SgIII and CgA, which suggests that they compensate for a sorting function of CPE for POMC and its intermediates to ACTH.	acth	166-170	carboxypeptidase E	Mus musculus	128-131
16219686-8	2005	We suggest that SgIII and CPE form the separate functional sorting complex by anchoring to cholesterol-rich SG membranes, and POMC-derived peptides are transferred from CPE to SgIII, and subsequently to CgA.	Cholesterol	91-102	carboxypeptidase E	Mus musculus	26-29
14715715-2	2004	These animals have a point mutation in carboxypeptidase E (CPE), an exopeptidase that removes C-terminal basic amino acids from peptide intermediates.	Amino Acids, Basic	105-122	carboxypeptidase E	Mus musculus	39-57
14715715-2	2004	These animals have a point mutation in carboxypeptidase E (CPE), an exopeptidase that removes C-terminal basic amino acids from peptide intermediates.	Amino Acids, Basic	105-122	carboxypeptidase E	Mus musculus	59-62
14975454-1	2004	1-Acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine (ACP) is a unique probe for in vivo measurements of reactive oxygen species (ROS), because it is hydrolyzed by esterase to a hydroxylamine form (CP-H), which is oxidized to an electron spin resonance-detectable nitroxyl radical (CP) by a reaction with superoxide anion radical, etc.	1-acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine	54-57	carboxypeptidase E	Mus musculus	198-202
14975454-1	2004	1-Acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine (ACP) is a unique probe for in vivo measurements of reactive oxygen species (ROS), because it is hydrolyzed by esterase to a hydroxylamine form (CP-H), which is oxidized to an electron spin resonance-detectable nitroxyl radical (CP) by a reaction with superoxide anion radical, etc.	Reactive Oxygen Species	130-133	carboxypeptidase E	Mus musculus	198-202
14975454-3	2004	We investigated the pharmacokinetics of ACP in mice by examining the time course of the tissue distribution of ACP, CP-H, and CP after intravenous or intraperitoneal injection of ACP.	1-acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine	40-43	carboxypeptidase E	Mus musculus	116-120
14975454-6	2004	ACP was hydrolyzed to CP-H in the liver and kidney predominantly, and the first-pass effect of liver on the hydrolysis of ACP was very large.	1-acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine	0-3	carboxypeptidase E	Mus musculus	22-26
14975454-7	2004	A homogeneous biodistribution of CP-H was obtained 10 min after the injection of ACP regardless of the injection route, and concentrations remained stable over at least 20 min.	1-acetoxy-3-carbamoyl-2,2,5,5-tetramethylpyrrolidine	81-84	carboxypeptidase E	Mus musculus	33-37
12587273-0	2002	[Effect of testosterone and progesterone on carboxypeptidase H activity during stress in mice].	Testosterone	11-23	carboxypeptidase E	Mus musculus	44-62
12403651-11	2003	We conclude that the sorting of CPE to the regulated secretory pathway in endocrine cells is mediated by lipid rafts, and that the C-terminal four residues of CPE, i.e. Thr(431)-Leu-Asn-Phe(434), are required for raft association and sorting.	Threonine	169-172	carboxypeptidase E	Mus musculus	159-162
12403651-11	2003	We conclude that the sorting of CPE to the regulated secretory pathway in endocrine cells is mediated by lipid rafts, and that the C-terminal four residues of CPE, i.e. Thr(431)-Leu-Asn-Phe(434), are required for raft association and sorting.	phenylalanyl-leucyl-leucyl-arginyl-asparagine	178-185	carboxypeptidase E	Mus musculus	159-162
12403651-11	2003	We conclude that the sorting of CPE to the regulated secretory pathway in endocrine cells is mediated by lipid rafts, and that the C-terminal four residues of CPE, i.e. Thr(431)-Leu-Asn-Phe(434), are required for raft association and sorting.	Phenylalanine	186-189	carboxypeptidase E	Mus musculus	159-162
12270926-11	2002	Recombinant CPE or carboxypeptidase D can convert synthetic TRH-[Gly(4)-Lys(5)] and TRH-[Gly(4)-Lys(5)-Arg(6)] to TRH-[Gly(4)].	Glycine	65-68	carboxypeptidase E	Mus musculus	12-15
12270926-11	2002	Recombinant CPE or carboxypeptidase D can convert synthetic TRH-[Gly(4)-Lys(5)] and TRH-[Gly(4)-Lys(5)-Arg(6)] to TRH-[Gly(4)].	4)-lys	69-75	carboxypeptidase E	Mus musculus	12-15
12270926-11	2002	Recombinant CPE or carboxypeptidase D can convert synthetic TRH-[Gly(4)-Lys(5)] and TRH-[Gly(4)-Lys(5)-Arg(6)] to TRH-[Gly(4)].	Glycine	64-68	carboxypeptidase E	Mus musculus	12-15
12270926-11	2002	Recombinant CPE or carboxypeptidase D can convert synthetic TRH-[Gly(4)-Lys(5)] and TRH-[Gly(4)-Lys(5)-Arg(6)] to TRH-[Gly(4)].	Lysine	72-75	carboxypeptidase E	Mus musculus	12-15
12270926-11	2002	Recombinant CPE or carboxypeptidase D can convert synthetic TRH-[Gly(4)-Lys(5)] and TRH-[Gly(4)-Lys(5)-Arg(6)] to TRH-[Gly(4)].	Arginine	103-106	carboxypeptidase E	Mus musculus	12-15
12270926-11	2002	Recombinant CPE or carboxypeptidase D can convert synthetic TRH-[Gly(4)-Lys(5)] and TRH-[Gly(4)-Lys(5)-Arg(6)] to TRH-[Gly(4)].	Glycine	89-92	carboxypeptidase E	Mus musculus	12-15
12587273-0	2002	[Effect of testosterone and progesterone on carboxypeptidase H activity during stress in mice].	Progesterone	28-40	carboxypeptidase E	Mus musculus	44-62
12587273-1	2002	It was found that testosterone propionate (3 mg/kg of body weight) and progesterone (1 mg/kg of body weight) partially prevent an augmentation of the carboxypeptidase H activity in the mouse pituitary gland under stress caused by a single intraperitoneal administration of olive oil.	Testosterone Propionate	18-41	carboxypeptidase E	Mus musculus	150-168
12587273-1	2002	It was found that testosterone propionate (3 mg/kg of body weight) and progesterone (1 mg/kg of body weight) partially prevent an augmentation of the carboxypeptidase H activity in the mouse pituitary gland under stress caused by a single intraperitoneal administration of olive oil.	Progesterone	71-83	carboxypeptidase E	Mus musculus	150-168
10896946-7	2000	Cholesterol depletion resulted in dissociation of CPE from secretory granule membranes and decreased the binding of prohormones to membranes.	Cholesterol	0-11	carboxypeptidase E	Mus musculus	50-53
10896946-9	2000	We propose that the sorting receptor function of CPE necessitates its interaction with glycosphingolipid-cholesterol rafts at the TGN, thereby anchoring it in position to bind to its prohormone cargo.	Glycosphingolipids	87-104	carboxypeptidase E	Mus musculus	49-52
10896946-9	2000	We propose that the sorting receptor function of CPE necessitates its interaction with glycosphingolipid-cholesterol rafts at the TGN, thereby anchoring it in position to bind to its prohormone cargo.	Cholesterol	105-116	carboxypeptidase E	Mus musculus	49-52
10979568-0	2000	[Effect of testosterone on carboxypeptidase H activity in the murine hypothalamus and hypophysis].	Testosterone	11-23	carboxypeptidase E	Mus musculus	27-45
10870222-0	2000	[Effect of testosterone and progesterone on carboxypeptidase H activity in the hypothalamo-hypophyseal-gonadal axis and the adrenal gland in mice].	Testosterone	11-23	carboxypeptidase E	Mus musculus	44-62
10870222-0	2000	[Effect of testosterone and progesterone on carboxypeptidase H activity in the hypothalamo-hypophyseal-gonadal axis and the adrenal gland in mice].	Progesterone	28-40	carboxypeptidase E	Mus musculus	44-62
10870222-1	2000	Testosterone propionate decreased activity of carboxypeptidase H in the male mongrel mice pituitary gland, activity of the CP H in testicles, and increased these parameters in 4 hours after treatment.	Testosterone Propionate	0-23	carboxypeptidase E	Mus musculus	46-64
10870222-1	2000	Testosterone propionate decreased activity of carboxypeptidase H in the male mongrel mice pituitary gland, activity of the CP H in testicles, and increased these parameters in 4 hours after treatment.	Testosterone Propionate	0-23	carboxypeptidase E	Mus musculus	123-127
10870222-3	2000	Progesterone increased the CP H activity in female pituitary gland and decreased it in adrenal gland and hypothalamus.	Progesterone	0-12	carboxypeptidase E	Mus musculus	27-31
10870222-4	2000	The role of the CP H in the effects of the sex steroids on the function of peptidergic systems is discussed.	Steroids	47-55	carboxypeptidase E	Mus musculus	16-20
10979568-1	2000	Effects of single intraperitoneal administration of testosterone propionate (3 or 30 mg/kg body weight) on activity of carboxypeptidase H in pituitary body and hypothalamus of female white mouse were studied.	Testosterone Propionate	52-75	carboxypeptidase E	Mus musculus	119-137
10979568-2	2000	It was found that testosterone propionate treatment (3 and 30 mg/kg body weight) increased the carboxypeptidase H activity in pituitary through 0.5 hour and it decreased one in 24 hours after treatment.	Testosterone Propionate	18-41	carboxypeptidase E	Mus musculus	95-113
10979568-3	2000	The carboxypeptidase H activity in hypothalamus was lower as compared with control animals in 24 hours after testosterone propionate treatment in the dose 3 mg/kg body weight.	Testosterone Propionate	109-132	carboxypeptidase E	Mus musculus	4-22
10979568-4	2000	However, the carboxypeptidase H activity in hypothalamus was lower in 0.5 and 24 hours and it was higher in 4 h after testosterone propionate treatment in the dose 30 mg/kg body weight as compared with the control.	Testosterone Propionate	118-141	carboxypeptidase E	Mus musculus	13-31
10979568-5	2000	These data suggest that testosterone affects the carboxypeptidase H activity by changing the level of enzyme gene expression.	Testosterone	24-36	carboxypeptidase E	Mus musculus	49-67
10657504-3	1999	Dopamine inhibited forskolin-stimulated accumulation of cAMP in the intermediate lobe of Cpe(fat)/ Cpe(fat)mice, showing that their dopamine receptors were fully functional.	Dopamine	0-8	carboxypeptidase E	Mus musculus	89-92
10477916-7	1999	These results suggest that CPE cells may be a suitable in vitro model for further studies on the cellular pathways involved in radioprotection by misoprostol in particular and prostaglandins in general.	Misoprostol	146-157	carboxypeptidase E	Mus musculus	27-30
10477916-7	1999	These results suggest that CPE cells may be a suitable in vitro model for further studies on the cellular pathways involved in radioprotection by misoprostol in particular and prostaglandins in general.	Prostaglandins	176-190	carboxypeptidase E	Mus musculus	27-30
10657504-3	1999	Dopamine inhibited forskolin-stimulated accumulation of cAMP in the intermediate lobe of Cpe(fat)/ Cpe(fat)mice, showing that their dopamine receptors were fully functional.	Dopamine	0-8	carboxypeptidase E	Mus musculus	99-102
10657504-3	1999	Dopamine inhibited forskolin-stimulated accumulation of cAMP in the intermediate lobe of Cpe(fat)/ Cpe(fat)mice, showing that their dopamine receptors were fully functional.	Colforsin	19-28	carboxypeptidase E	Mus musculus	89-92
10657504-3	1999	Dopamine inhibited forskolin-stimulated accumulation of cAMP in the intermediate lobe of Cpe(fat)/ Cpe(fat)mice, showing that their dopamine receptors were fully functional.	Colforsin	19-28	carboxypeptidase E	Mus musculus	99-102
10657504-3	1999	Dopamine inhibited forskolin-stimulated accumulation of cAMP in the intermediate lobe of Cpe(fat)/ Cpe(fat)mice, showing that their dopamine receptors were fully functional.	Cyclic AMP	56-60	carboxypeptidase E	Mus musculus	89-92
10657504-3	1999	Dopamine inhibited forskolin-stimulated accumulation of cAMP in the intermediate lobe of Cpe(fat)/ Cpe(fat)mice, showing that their dopamine receptors were fully functional.	Cyclic AMP	56-60	carboxypeptidase E	Mus musculus	99-102
10657504-6	1999	In the anterior pituitary of Cpe(fat)/ Cpe(fat)mice, a 1.6-fold increase in basal release of POMC was accompanied by a similar increase in [(35)S]-methionine incorporation into POMC, although POMC mRNA levels were unchanged.	Methionine	147-157	carboxypeptidase E	Mus musculus	29-32
10657504-6	1999	In the anterior pituitary of Cpe(fat)/ Cpe(fat)mice, a 1.6-fold increase in basal release of POMC was accompanied by a similar increase in [(35)S]-methionine incorporation into POMC, although POMC mRNA levels were unchanged.	Methionine	147-157	carboxypeptidase E	Mus musculus	39-42
10221600-0	1998	Adult carboxypeptidase E-deficient fat/fat mice have a near-total depletion of brain CCK 8 accompanied by a massive accumulation of glycine and arginine extended CCK: identification of CCK 8 Gly as the immediate precursor of CCK 8 in rodent brain.	Glycine	132-139	carboxypeptidase E	Mus musculus	6-24
10221600-0	1998	Adult carboxypeptidase E-deficient fat/fat mice have a near-total depletion of brain CCK 8 accompanied by a massive accumulation of glycine and arginine extended CCK: identification of CCK 8 Gly as the immediate precursor of CCK 8 in rodent brain.	Arginine	144-152	carboxypeptidase E	Mus musculus	6-24
10221600-1	1998	Cholecystokinin (CCK) amide concentrations were reduced over 85% in all the major brain regions of carboxypeptidase E (Cpe)(fat)/Cpe(fat) mice in comparison to control mice.	Amides	22-27	carboxypeptidase E	Mus musculus	99-117
10221600-1	1998	Cholecystokinin (CCK) amide concentrations were reduced over 85% in all the major brain regions of carboxypeptidase E (Cpe)(fat)/Cpe(fat) mice in comparison to control mice.	Amides	22-27	carboxypeptidase E	Mus musculus	119-122
10221600-0	1998	Adult carboxypeptidase E-deficient fat/fat mice have a near-total depletion of brain CCK 8 accompanied by a massive accumulation of glycine and arginine extended CCK: identification of CCK 8 Gly as the immediate precursor of CCK 8 in rodent brain.	Glycine	191-194	carboxypeptidase E	Mus musculus	6-24
10221600-1	1998	Cholecystokinin (CCK) amide concentrations were reduced over 85% in all the major brain regions of carboxypeptidase E (Cpe)(fat)/Cpe(fat) mice in comparison to control mice.	Amides	22-27	carboxypeptidase E	Mus musculus	129-132
9291640-9	1997	Calcium deposits were detected by von Kossa staining in 14-day MDFC cultures treated with CPE.	Calcium	0-7	carboxypeptidase E	Mus musculus	90-93
10221600-2	1998	Using an radioimmunoassay (RIA) specific for glycine-extended CCK (CCK Gly), low levels of CCK Gly were detected in control (0.65 ng/g tissue) and were even lower in Cpe(fat)/Cpe(fat) (0.246 ng/g) mice brain extracts.	Glycine	45-52	carboxypeptidase E	Mus musculus	166-169
10221600-2	1998	Using an radioimmunoassay (RIA) specific for glycine-extended CCK (CCK Gly), low levels of CCK Gly were detected in control (0.65 ng/g tissue) and were even lower in Cpe(fat)/Cpe(fat) (0.246 ng/g) mice brain extracts.	Glycine	45-52	carboxypeptidase E	Mus musculus	175-178
10221600-3	1998	After treatment with carboxypeptidase B, the level of CCK Gly in Cpe(fat)/Cpe(fat) in these brain extracts was elevated to 33.5 ng/g, about 51-fold higher than in control.	Glycine	58-61	carboxypeptidase E	Mus musculus	65-68
10221600-3	1998	After treatment with carboxypeptidase B, the level of CCK Gly in Cpe(fat)/Cpe(fat) in these brain extracts was elevated to 33.5 ng/g, about 51-fold higher than in control.	Glycine	58-61	carboxypeptidase E	Mus musculus	74-77
10221600-5	1998	These results demonstrate that CPE is required for the correct processing of arginine- and glycine-extended CCK in all major regions of the mouse brain.	Arginine	77-85	carboxypeptidase E	Mus musculus	31-34
10221600-5	1998	These results demonstrate that CPE is required for the correct processing of arginine- and glycine-extended CCK in all major regions of the mouse brain.	Glycine	91-98	carboxypeptidase E	Mus musculus	31-34
9275097-3	1997	In contrast, using an antiserum specific for CCK Gly Arg Arg, Cpe(fat)/Cpe(fat) mice brain had about 13-fold higher levels of this peptide relative to controls, while levels were identical in mutant and control duodenal tissue.	Glycine	49-52	carboxypeptidase E	Mus musculus	62-65
9275097-3	1997	In contrast, using an antiserum specific for CCK Gly Arg Arg, Cpe(fat)/Cpe(fat) mice brain had about 13-fold higher levels of this peptide relative to controls, while levels were identical in mutant and control duodenal tissue.	Arginine	57-60	carboxypeptidase E	Mus musculus	62-65
9275097-3	1997	In contrast, using an antiserum specific for CCK Gly Arg Arg, Cpe(fat)/Cpe(fat) mice brain had about 13-fold higher levels of this peptide relative to controls, while levels were identical in mutant and control duodenal tissue.	Glycine	49-52	carboxypeptidase E	Mus musculus	71-74
9275097-3	1997	In contrast, using an antiserum specific for CCK Gly Arg Arg, Cpe(fat)/Cpe(fat) mice brain had about 13-fold higher levels of this peptide relative to controls, while levels were identical in mutant and control duodenal tissue.	Arginine	57-60	carboxypeptidase E	Mus musculus	71-74
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	Glycine	24-27	carboxypeptidase E	Mus musculus	39-42
9275097-3	1997	In contrast, using an antiserum specific for CCK Gly Arg Arg, Cpe(fat)/Cpe(fat) mice brain had about 13-fold higher levels of this peptide relative to controls, while levels were identical in mutant and control duodenal tissue.	Arginine	53-56	carboxypeptidase E	Mus musculus	62-65
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	Glycine	24-27	carboxypeptidase E	Mus musculus	48-51
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	Arginine	32-35	carboxypeptidase E	Mus musculus	39-42
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	Arginine	28-31	carboxypeptidase E	Mus musculus	39-42
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	Arginine	28-31	carboxypeptidase E	Mus musculus	48-51
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	Arginine	32-35	carboxypeptidase E	Mus musculus	39-42
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	Arginine	32-35	carboxypeptidase E	Mus musculus	48-51
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	Arginine	32-35	carboxypeptidase E	Mus musculus	48-51
8662840-12	1996	Pulse-chase analysis using dispersed pituitary cells from C57BLKS/Lt-Cpefat/Cpefat mutant mice shows similar results; Pro202-CPE produced in these cells was not secreted but rather was degraded within 5 h. Immunofluorescence analysis of epitope-tagged CPE revealed Ser202CPE to be present primarily in secretory vesicles, whereas Pro202CPE was localized to the endoplasmic reticulum and not the secretory vesicle-like structures.	ser202cpe	265-274	carboxypeptidase E	Mus musculus	125-128
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	dibasic	99-106	carboxypeptidase E	Mus musculus	39-42
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	dibasic	99-106	carboxypeptidase E	Mus musculus	48-51
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	Arginine	32-35	carboxypeptidase E	Mus musculus	39-42
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	Arginine	32-35	carboxypeptidase E	Mus musculus	48-51
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	Arginine	32-35	carboxypeptidase E	Mus musculus	39-42
9275097-5	1997	The accumulation of CCK Gly Arg Arg in Cpe(fat)/Cpe(fat) brains provides definitive proof that the dibasic cleavage of the carboxyl terminus of pro CCK occurs on the carboxyl terminal of the dibasic, between the Arg and Ser as well as confirming that amidated CCK 8 in brain originates from CCK 8 Gly Arg Arg rather than from larger amidated peptides like CCK 22 or CCK 33.	Arginine	32-35	carboxypeptidase E	Mus musculus	48-51
9173892-5	1997	Stimulation of AtT-20 cells with either forskolin or phorbol 12-myristate 13-acetate induces the secretion of wild-type CPE and of CPE lacking the pro region to similar extents, indicating a similar efficiency of sorting of the mutant.	Colforsin	40-49	carboxypeptidase E	Mus musculus	120-123
9173892-5	1997	Stimulation of AtT-20 cells with either forskolin or phorbol 12-myristate 13-acetate induces the secretion of wild-type CPE and of CPE lacking the pro region to similar extents, indicating a similar efficiency of sorting of the mutant.	Colforsin	40-49	carboxypeptidase E	Mus musculus	131-134
9173892-5	1997	Stimulation of AtT-20 cells with either forskolin or phorbol 12-myristate 13-acetate induces the secretion of wild-type CPE and of CPE lacking the pro region to similar extents, indicating a similar efficiency of sorting of the mutant.	Tetradecanoylphorbol Acetate	53-84	carboxypeptidase E	Mus musculus	120-123
9173892-5	1997	Stimulation of AtT-20 cells with either forskolin or phorbol 12-myristate 13-acetate induces the secretion of wild-type CPE and of CPE lacking the pro region to similar extents, indicating a similar efficiency of sorting of the mutant.	Tetradecanoylphorbol Acetate	53-84	carboxypeptidase E	Mus musculus	131-134
9173892-9	1997	In contrast, confocal microscopy indicates that the majority of the propeptide is removed from CPE, and that this cleavage occurs in the trans-Golgi network or soon after sorting into the secretory vesicles.	propeptide	68-78	carboxypeptidase E	Mus musculus	95-98
8643504-10	1996	Inclusion of carboxypeptidase E (CPE) in the reaction greatly diminished the inhibitory potency of the CT peptide against PC2, in line with the notion that the CT peptide cleavage product is not inhibitory after the removal of terminal lysines by CPE.	Lysine	236-243	carboxypeptidase E	Mus musculus	33-36
8522057-4	1996	In addition to that of proinsulin, the biosynthesis of the two proinsulin conversion endopeptidases, PC2 and PC3, was coordinately glucose regulated in MIN6 cells, whereas that of the exopeptidase, carboxypeptidase H, was unaffected by glucose.	Glucose	236-243	carboxypeptidase E	Mus musculus	198-216
8051069-8	1994	The secretion of albumin with the C-terminal region of CPE was stimulated by a phorbol ester and by forskolin, although the magnitude of the stimulation was smaller than the effect of these compounds on the secretion of CPE.	Phorbol Esters	79-92	carboxypeptidase E	Mus musculus	55-58
8051069-8	1994	The secretion of albumin with the C-terminal region of CPE was stimulated by a phorbol ester and by forskolin, although the magnitude of the stimulation was smaller than the effect of these compounds on the secretion of CPE.	Colforsin	100-109	carboxypeptidase E	Mus musculus	55-58
8376994-4	1993	Following a 15-min pulse with [35S]Met, both soluble and membrane-bound forms of CPE were identified, indicating that the posttranslational processing event that generates these forms of CPE occurs in the endoplasmic reticulum or early Golgi apparatus.	Sulfur-35	31-34	carboxypeptidase E	Mus musculus	81-84
8376994-4	1993	Following a 15-min pulse with [35S]Met, both soluble and membrane-bound forms of CPE were identified, indicating that the posttranslational processing event that generates these forms of CPE occurs in the endoplasmic reticulum or early Golgi apparatus.	Sulfur-35	31-34	carboxypeptidase E	Mus musculus	187-190
8376994-10	1993	This enzyme, which removes the C-terminal region of CPE, is partially inhibited by EDTA and phenylmethylsulfonyl fluoride and is activated by CaCl2.	Edetic Acid	83-87	carboxypeptidase E	Mus musculus	52-55
8376994-10	1993	This enzyme, which removes the C-terminal region of CPE, is partially inhibited by EDTA and phenylmethylsulfonyl fluoride and is activated by CaCl2.	Phenylmethylsulfonyl Fluoride	92-121	carboxypeptidase E	Mus musculus	52-55
8376994-10	1993	This enzyme, which removes the C-terminal region of CPE, is partially inhibited by EDTA and phenylmethylsulfonyl fluoride and is activated by CaCl2.	Calcium Chloride	142-147	carboxypeptidase E	Mus musculus	52-55
1327723-6	1992	Upon stimulation with a beta-adrenergic agonist, a phorbol ester, a calcium ionophore, or forskolin, the secretion of DCE activity was increased; this rise was parallel to the secretion of CPE activity and ACTH.	Phorbol Esters	51-64	carboxypeptidase E	Mus musculus	189-192
8473886-0	1993	Differential effects of a phorbol ester on carboxypeptidase E in cultured astrocytes and AtT-20 cells, a neuroendocrine cell line.	Phorbol Esters	26-39	carboxypeptidase E	Mus musculus	43-61
8473886-2	1993	The secretion of CPE enzymatic activity from astrocytes has been shown previously to be increased approximately twofold by treatment with tetradecanoylphorbol 13-acetate (TPA), a phorbol ester.	tetradecanoylphorbol 13-acetate	138-169	carboxypeptidase E	Mus musculus	17-20
8473886-2	1993	The secretion of CPE enzymatic activity from astrocytes has been shown previously to be increased approximately twofold by treatment with tetradecanoylphorbol 13-acetate (TPA), a phorbol ester.	Tetradecanoylphorbol Acetate	171-174	carboxypeptidase E	Mus musculus	17-20
8473886-2	1993	The secretion of CPE enzymatic activity from astrocytes has been shown previously to be increased approximately twofold by treatment with tetradecanoylphorbol 13-acetate (TPA), a phorbol ester.	Phorbol Esters	179-192	carboxypeptidase E	Mus musculus	17-20
8473886-3	1993	In this study, metabolic labeling with [35S]Met was utilized to examine the effect of TPA on the biosynthesis of CPE protein in cultured astrocytes and in AtT-20 cells, a pituitary-derived cell line.	Tetradecanoylphorbol Acetate	86-89	carboxypeptidase E	Mus musculus	113-116
8473886-4	1993	Treatment of astrocytes with 0.1 micrograms/ml TPA for 24 h caused an 80% increase in the level of radiolabeled CPE in both the media and the cells, indicating that the synthesis of CPE was stimulated by the TPA.	Tetradecanoylphorbol Acetate	47-50	carboxypeptidase E	Mus musculus	112-115
8473886-4	1993	Treatment of astrocytes with 0.1 micrograms/ml TPA for 24 h caused an 80% increase in the level of radiolabeled CPE in both the media and the cells, indicating that the synthesis of CPE was stimulated by the TPA.	Tetradecanoylphorbol Acetate	47-50	carboxypeptidase E	Mus musculus	182-185
8473886-4	1993	Treatment of astrocytes with 0.1 micrograms/ml TPA for 24 h caused an 80% increase in the level of radiolabeled CPE in both the media and the cells, indicating that the synthesis of CPE was stimulated by the TPA.	Tetradecanoylphorbol Acetate	208-211	carboxypeptidase E	Mus musculus	112-115
8473886-4	1993	Treatment of astrocytes with 0.1 micrograms/ml TPA for 24 h caused an 80% increase in the level of radiolabeled CPE in both the media and the cells, indicating that the synthesis of CPE was stimulated by the TPA.	Tetradecanoylphorbol Acetate	208-211	carboxypeptidase E	Mus musculus	182-185
8473886-5	1993	AtT-20 cells also secreted more radiolabeled CPE in response to TPA, but this increase was offset by a proportional decrease in the cellular level of radiolabeled CPE, and synthesis of CPE was not stimulated in this cell line.	Tetradecanoylphorbol Acetate	64-67	carboxypeptidase E	Mus musculus	45-48
8473886-6	1993	Northern blot analysis demonstrated that 0.1 micrograms/ml TPA elevated CPE mRNA by approximately 50% in cultured astrocytes but not in AtT-20 cells.	Tetradecanoylphorbol Acetate	59-62	carboxypeptidase E	Mus musculus	72-75
8473886-7	1993	Quantitative in situ hybridization studies demonstrated that the TPA-induced increase in CPE mRNA expression was largely due to increases in the number of cells expressing CPE mRNA, although for astrocytes from some brain regions the average level of CPE mRNA per cell was also elevated by TPA.	Tetradecanoylphorbol Acetate	65-68	carboxypeptidase E	Mus musculus	89-92
8473886-7	1993	Quantitative in situ hybridization studies demonstrated that the TPA-induced increase in CPE mRNA expression was largely due to increases in the number of cells expressing CPE mRNA, although for astrocytes from some brain regions the average level of CPE mRNA per cell was also elevated by TPA.	Tetradecanoylphorbol Acetate	65-68	carboxypeptidase E	Mus musculus	172-175
8473886-7	1993	Quantitative in situ hybridization studies demonstrated that the TPA-induced increase in CPE mRNA expression was largely due to increases in the number of cells expressing CPE mRNA, although for astrocytes from some brain regions the average level of CPE mRNA per cell was also elevated by TPA.	Tetradecanoylphorbol Acetate	65-68	carboxypeptidase E	Mus musculus	172-175
8473886-7	1993	Quantitative in situ hybridization studies demonstrated that the TPA-induced increase in CPE mRNA expression was largely due to increases in the number of cells expressing CPE mRNA, although for astrocytes from some brain regions the average level of CPE mRNA per cell was also elevated by TPA.	Tetradecanoylphorbol Acetate	290-293	carboxypeptidase E	Mus musculus	89-92
1327723-6	1992	Upon stimulation with a beta-adrenergic agonist, a phorbol ester, a calcium ionophore, or forskolin, the secretion of DCE activity was increased; this rise was parallel to the secretion of CPE activity and ACTH.	Calcium	68-75	carboxypeptidase E	Mus musculus	189-192
1327723-6	1992	Upon stimulation with a beta-adrenergic agonist, a phorbol ester, a calcium ionophore, or forskolin, the secretion of DCE activity was increased; this rise was parallel to the secretion of CPE activity and ACTH.	Colforsin	90-99	carboxypeptidase E	Mus musculus	189-192
1573389-9	1992	CPE secretion is stimulated two- to threefold by prolonged treatment (3-48 h) with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) but not by treatment with other secretagogues that stimulate CPE secretion from AtT-20 cells (forskolin, isoproterenol, A23187, and vasoactive intestinal peptide) or short (less than 3 h) exposure to TPA.	Phorbol Esters	87-100	carboxypeptidase E	Mus musculus	0-3
1573389-9	1992	CPE secretion is stimulated two- to threefold by prolonged treatment (3-48 h) with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) but not by treatment with other secretagogues that stimulate CPE secretion from AtT-20 cells (forskolin, isoproterenol, A23187, and vasoactive intestinal peptide) or short (less than 3 h) exposure to TPA.	Tetradecanoylphorbol Acetate	101-137	carboxypeptidase E	Mus musculus	0-3
1573389-9	1992	CPE secretion is stimulated two- to threefold by prolonged treatment (3-48 h) with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) but not by treatment with other secretagogues that stimulate CPE secretion from AtT-20 cells (forskolin, isoproterenol, A23187, and vasoactive intestinal peptide) or short (less than 3 h) exposure to TPA.	Tetradecanoylphorbol Acetate	139-142	carboxypeptidase E	Mus musculus	0-3
1573389-9	1992	CPE secretion is stimulated two- to threefold by prolonged treatment (3-48 h) with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) but not by treatment with other secretagogues that stimulate CPE secretion from AtT-20 cells (forskolin, isoproterenol, A23187, and vasoactive intestinal peptide) or short (less than 3 h) exposure to TPA.	Tetradecanoylphorbol Acetate	139-142	carboxypeptidase E	Mus musculus	205-208
1573389-9	1992	CPE secretion is stimulated two- to threefold by prolonged treatment (3-48 h) with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) but not by treatment with other secretagogues that stimulate CPE secretion from AtT-20 cells (forskolin, isoproterenol, A23187, and vasoactive intestinal peptide) or short (less than 3 h) exposure to TPA.	Colforsin	238-247	carboxypeptidase E	Mus musculus	0-3
1573389-9	1992	CPE secretion is stimulated two- to threefold by prolonged treatment (3-48 h) with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) but not by treatment with other secretagogues that stimulate CPE secretion from AtT-20 cells (forskolin, isoproterenol, A23187, and vasoactive intestinal peptide) or short (less than 3 h) exposure to TPA.	Isoproterenol	249-262	carboxypeptidase E	Mus musculus	0-3
1573389-9	1992	CPE secretion is stimulated two- to threefold by prolonged treatment (3-48 h) with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) but not by treatment with other secretagogues that stimulate CPE secretion from AtT-20 cells (forskolin, isoproterenol, A23187, and vasoactive intestinal peptide) or short (less than 3 h) exposure to TPA.	Calcimycin	264-270	carboxypeptidase E	Mus musculus	0-3
1573389-9	1992	CPE secretion is stimulated two- to threefold by prolonged treatment (3-48 h) with the phorbol ester 12-O-tetradecanoylphorbol 13-acetate (TPA) but not by treatment with other secretagogues that stimulate CPE secretion from AtT-20 cells (forskolin, isoproterenol, A23187, and vasoactive intestinal peptide) or short (less than 3 h) exposure to TPA.	Tetradecanoylphorbol Acetate	344-347	carboxypeptidase E	Mus musculus	0-3
34432857-0	2021	Activation of Cph1 causes ss(1,3)-glucan unmasking in Candida albicans and attenuates virulence in mice in a neutrophil-dependent manner.	ss(1,3)-glucan	26-40	carboxypeptidase E	Mus musculus	14-18
34432857-8	2021	In an effort to understand the mechanism by which Ste11DeltaN467 causes unmasking, transcriptomics were used to reveal that several components in the Cek1 MAPK pathway were upregulated, including the transcription factor CPH1 and the cell wall sensor DFI1.	ste11deltan467	50-64	carboxypeptidase E	Mus musculus	221-225
34432857-9	2021	In this report we show that a cph1DeltaDelta mutation restored ss(1,3)-glucan exposure to wild-type levels in the STE11DeltaN467 strain, confirming that Cph1 is the transcription factor mediating Ste11DeltaN467-induced unmasking.	ste11deltan467	196-210	carboxypeptidase E	Mus musculus	153-157
2784437-8	1989	Treatment of AtT20 cells with dexamethasone decreased the levels of both carboxypeptidase H and preproopiomelanocortin (POMC) mRNAs by approximately 30%.	Dexamethasone	30-43	carboxypeptidase E	Mus musculus	73-91
35618016-3	2022	In the present study, we tested if CPE is a rate-limiting enzyme in neuropeptide production using CpeNeo mice, which contain a neomycin cassette within the Cpe gene that eliminates enzyme expression.	Neomycin	127-135	carboxypeptidase E	Mus musculus	35-38
35618016-5	2022	Removal of the neomycin cassette with Flp recombinase under a germline promoter restored expression of CPE activity and resulted in normal behavioral and physiological properties, including levels of neuropeptides.	Neomycin	15-23	carboxypeptidase E	Mus musculus	103-106
35268078-7	2022	Compared to the NEG, the CPE decreased to 22% of the ROS generation and significantly increased cell viability in vitro.	ros	53-56	carboxypeptidase E	Mus musculus	25-28
35268078-11	2022	Such protection can be explained by the anti-oxidative capacity of CPE, likely due to its bioactives, including naringin (7.74 mg/g CPE).	naringin	112-120	carboxypeptidase E	Mus musculus	67-70
35268078-11	2022	Such protection can be explained by the anti-oxidative capacity of CPE, likely due to its bioactives, including naringin (7.74 mg/g CPE).	naringin	112-120	carboxypeptidase E	Mus musculus	132-135