Relevant bibliographies by topics / Peptidase inhibitor 16

Academic literature on the topic 'Peptidase inhibitor 16'

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Published: 10 December 2022
Last updated: 28 January 2023

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Journal articles on the topic "Peptidase inhibitor 16"

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Cwiklinski, Krystyna, Orla Drysdale, Jesús López Corrales, Yolanda Corripio-Miyar, Carolina De Marco Verissimo, Heather Jewhurst, David Smith, Richard Lalor, Tom N. McNeilly, and John P. Dalton. "Targeting Secreted Protease/Anti-Protease Balance as a Vaccine Strategy against the Helminth Fasciola hepatica." Vaccines 10, no. 2 (January 20, 2022): 155. http://dx.doi.org/10.3390/vaccines10020155.

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The liver fluke Fasciola hepatica is an economically important global pathogen of humans and their livestock. To facilitate host invasion and migration, F. hepatica secretes an abundance of cathepsin peptidases but prevents excessive damage to both parasite and host tissues by co-secreting regulatory peptidase inhibitors, cystatins/stefins and Kunitz-type inhibitors. Here, we report a vaccine strategy aimed at disrupting the parasite’s protease/anti-protease balance by targeting these key inhibitors. Our vaccine cocktail containing three recombinant stefins (rFhStf-1, rFhStf-2, rFhStf-3) and a Kunitz-type inhibitor (rFhKT1) formulated in adjuvant Montanide 61VG was assessed in two independent sheep trials. While fluke burden was not reduced in either trial, in Trial 1 the vaccinated animals showed significantly greater weight gain (p < 0.05) relative to the non-vaccinated control group. In both trials we observed a significant reduction in egg viability (36–42%). Multivariate regression analyses showed vaccination and increased levels of IgG2 antibodies specific for the F. hepatica peptidase inhibitors were positive indicators for increased weight gain and levels of haemoglobin within the normal range at 16 weeks post-infection (wpi; p < 0.05). These studies point to the potential of targeting peptidase inhibitors as vaccine cocktails for fasciolosis control in sheep.
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Bai, T. R., and A. M. Bramley. "Effect of an inhibitor of nitric oxide synthase on neural relaxation of human bronchi." American Journal of Physiology-Lung Cellular and Molecular Physiology 264, no. 5 (May 1, 1993): L425—L430. http://dx.doi.org/10.1152/ajplung.1993.264.5.l425.

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This study examines the roles of peptides and nitric oxide (NO) as mediators of inhibitory nonadrenergic, noncholinergic (NANCi) neurons in human and guinea pig airways in vitro. Tissues were contracted with 0.3 microM methacholine (MCh) and relaxation studied before and after the addition of the peptidase alpha-chymotrypsin (alpha-CT) (2 U/ml) and NG-nitro-L-arginine methyl ester (L-NAME 0.1-1.1 mM), an inhibitor of NO synthase, the enzyme catalyzing the formation of NO. alpha-CT alone, in comparison to parallel time controls, inhibited control relaxation to electrical field stimulation (EFS) by 29.2 +/- 8.6% in guinea pig tracheae (n = 9), whereas a small augmentation of relaxation was observed in human bronchi (n = 7). L-NAME inhibited the NANCi response in both guinea pig tracheae and human bronchi: in guinea pig tracheae, maximal inhibition of the alpha-CT-insensitive relaxation was 59.3 +/- 11.5% (SE, P = 0.003) at low frequencies (4-16 Hz) and 28.6 +/- 8.9% (P = 0.08) at 32 Hz; in human bronchi, the maximal inhibition was 37.7 +/- 9.3% (P = 0.008) at 8 or 16 Hz, and 37.9 +/- 5.9% (P = 0.005) at 32 Hz. Inhibition was greater after repeated baseline EFS for 90 min before initiation of contraction with MCh and addition of L-NAME (59.8 +/- 13.9% after repeated baseline EFS, n = 4; vs. 34.9 +/- 6.2% without repeated baseline EFS, n = 9, P = 0.025). Relaxant responses to sodium nitroprusside, vasoactive intestinal peptide, and isoproterenol were not affected by L-NAME. L-Arginine (10 mM), a precursor of NO, partially reversed the effect of L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)
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Martínez-Guitián, Marta, Juan C. Vázquez-Ucha, Joshua Odingo, Tanya Parish, Margarita Poza, Richard D. Waite, German Bou, David W. Wareham, and Alejandro Beceiro. "Synergy between Colistin and the Signal Peptidase Inhibitor MD3 Is Dependent on the Mechanism of Colistin Resistance in Acinetobacter baumannii." Antimicrobial Agents and Chemotherapy 60, no. 7 (May 2, 2016): 4375–79. http://dx.doi.org/10.1128/aac.00510-16.

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ABSTRACTSynergy between colistin and the signal peptidase inhibitor MD3 was tested against isogenic mutants and clinical pairs ofAcinetobacter baumanniiisolates. Checkerboard assays and growth curves showed synergy against both colistin-susceptible strains (fractional inhibitory concentration index [FICindex] = 0.13 to 0.24) and colistin-resistant strains with mutations inpmrBand phosphoethanolamine modification of lipid A (FICindex= 0.14 to 0.25) but not against colistin-resistant Δlpxstrains with loss of lipopolysaccharide (FICindex= 0.75 to 1). A colistin/MD3 combination would need to be targeted to strains with specific colistin resistance mechanisms.
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Lupsa, Nikolett, Barbara Érsek, Andor Horváth, András Bencsik, Eszter Lajkó, Pálma Silló, Ádám Oszvald, et al. "Skin‐homing CD8 + T cells preferentially express GPI‐anchored peptidase inhibitor 16, an inhibitor of cathepsin K." European Journal of Immunology 48, no. 12 (November 9, 2018): 1944–57. http://dx.doi.org/10.1002/eji.201847552.

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Lin, Kun-Der, Chao-Hung Chen, Hsing-Yi Lin, Mei-Yueh Lee, Yu-Li Lee, Wei-Wen Hung, He-Jiun Jiang, Pi-Jung Hsiao, and Shyi-Jang Shin. "Dipeptidyl peptidase-4 inhibitor prevents diabetic nephropathy through STRA6 signaling." Diabetes Research and Clinical Practice 120 (October 2016): S61. http://dx.doi.org/10.1016/s0168-8227(16)31050-6.

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Apaijai, Nattayaporn, Tharnwimol Inthachai, Suree Lekawanvijit, Siriporn C. Chattipakorn, and Nipon Chattipakorn. "Effects of dipeptidyl peptidase-4 inhibitor in insulin-resistant rats with myocardial infarction." Journal of Endocrinology 229, no. 3 (June 2016): 245–58. http://dx.doi.org/10.1530/joe-16-0096.

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Adverse cardiac remodeling after myocardial infarction (MI) leads to progressive heart failure. Obese-insulin resistance increases risks of MI and heart failure. Although dipeptidyl peptidase-4 (DPP4) inhibitor is known to exert cardioprotection, its effects on adverse remodeling after MI in obese-insulin-resistant rats are unclear. We hypothesized that DPP4 inhibitor reduces adverse left ventricular (LV) remodeling and LV dysfunction in obese-insulin-resistant rats with MI. Rats were fed either normal diet (ND) or high-fat diet (HFD) for 12 weeks to induce obese-insulin resistance, followed by left anterior descending coronary artery ligation to induce MI. Then, rats in each dietary group were divided into five subgroups to receive vehicle, enalapril (10mg/kg/day), metformin (30mg/kg/day), DPP4 inhibitor vildagliptin (3mg/kg/day), or combined metformin and vildagliptin for 8 weeks. Heart rate variability (HRV), LV function, pathological and biochemical studies for LV remodeling, and cardiomyocyte apoptosis were determined. Obese-insulin-resistant rats had severe insulin resistance and LV dysfunction. HFD rats had a higher mortality rate than ND rats, and all treatments reduced the mortality rate in obese-insulin-resistant rats. Although all drugs improved insulin resistance, HRV, LV function as well as reduced cardiac hypertrophy and fibrosis, vildagliptin effectively reduced cardiomyocyte cross-sectional areas more than enalapril and was related to markedly decreased ERK1/2 phosphorylation. In ND rats with MI, metformin neither improved LV ejection fraction nor reduced cardiac fibrosis. The infarct size and transforming growth factor-β expression were not different among groups. In obese-insulin-resistant rats with chronic MI, DPP4 inhibitor vildagliptin exerts better cardioprotection than enalapril in attenuating adverse LV remodeling.
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Regn, Michael, Bernhard Laggerbauer, Claudia Jentzsch, Deepak Ramanujam, Andrea Ahles, Sonja Sichler, Julia Calzada-Wack, et al. "Peptidase inhibitor 16 is a membrane-tethered regulator of chemerin processing in the myocardium." Journal of Molecular and Cellular Cardiology 99 (October 2016): 57–64. http://dx.doi.org/10.1016/j.yjmcc.2016.08.010.

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DIN, KHUZMA, AMIZA MAT AMIN, FISAL AHMAD, AMIN ISMAIL, and ADAWIYAH SURIZA SHUIB. "IN SILICO ANALYSIS OF EDIBLE BIRD’S NEST PROTEINS AS POTENTIAL PRECURSORS FOR BIOACTIVE PEPTIDES." Malaysian Applied Biology 51, no. 2 (June 29, 2022): 53–62. http://dx.doi.org/10.55230/mabjournal.v51i2.1997.

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The present study aimed to perform an in silico evaluation of edible bird’s nest protein as potential precursors of bioactive peptides, as well as to determine whether such peptides can be released by selected proteolytic enzymes. Six edible bird’s nest (EBN) protein sequences from a previous study were chosen as potential precursors to produce bioactive peptides via in silico method using the BIOPEP database. AMCase protein sequences gave the highest number of bioactivities (16 to 18) and nucleobindin-2 protein gave the lowest number of bioactivities (9) among the other protein sequences. It was found that the most potential bioactive peptides from EBN proteins are angiotensin-converting enzyme (ACE) inhibitors and dipeptidyl peptidase-IV (DPPIV) inhibitors. Furthermore, in silico proteolysis using six selected enzymes was employed to release both dominant bioactivities in EBN proteins, which were ACE and DPP-IV inhibitors. This study shows that a combination of enzymes, chymotrypsin, and papain, produced the highest number of activities for both ACE and DPP-IV inhibitor peptides with the frequency of occurrence of bioactive peptides of 0.0968 and 0.1104, respectively. The toxic prediction tool, ToxinPred, found that all EBN peptides derived by in silico analysis were non-toxic. The current study proposed that EBN can serve as a potential source of bioactive peptides.
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Chen, Q., Y. Miao, and K. Jiang. "Peptidase Inhibitor 16 Promote Proliferation and Metastasis in Pancreatic Ductal Adenocarcinoma via Oligoadenylate Synthetase L." HPB 24 (2022): S258. http://dx.doi.org/10.1016/j.hpb.2022.05.542.

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Danilov, Alexey V., Olga V. Danilova, Andreas K. Klein, and Brigitte T. Huber. "Dipeptidyl Peptidase 2 - A Pro-Survival Molecule in Chronic Lymphocytic Leukemia." Blood 108, no. 11 (November 16, 2006): 4964. http://dx.doi.org/10.1182/blood.v108.11.4964.4964.

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Abstract Chronic lymphocytic leukemia (CLL) is a unique malignancy characterized by persistent accumulation of quiescent B-cells. Disruption of survival pathways leads to apoptosis and renders CLL cells sensitive to chemotherapeutic agents. As clinical outcomes in CLL are heterogeneous, it is important to better predict prognosis in each individual case of the disease. In this respect, detection of somatic mutations in the immunoglobulin variable heavy chain (IgVH) genes has become the gold standard. Overexpression of ZAP-70 (Zeta-chain associated protein kinase - 70 kDa) by CLL cells correlates with unmutated IgVH genes and predicts poor outcome in B-CLL. Dipeptidyl Peptidase 2 (DPP2) is a newly discovered serine protease which maintains lymphocytes in a quiescent state (G0). In this study we investigated whether DPP2 is involved in cell cycle control in B-CLL. 38 patients with B-CLL and 20 healthy controls were included in the study. Median age of CLL patients was 67 years. Median time from diagnosis to enrollment in the study was 102 months. 21 patients (55.3%) received treatment before enrollment in the study. Standard Ficoll-Hypaque techniques were used to isolate peripheral blood mononuclear cells (PBMC) from healthy donors and CLL patients. CLL cells were isolated to &gt;98% purity by means of a MoFlo using CD19−specific antibodies. Cells were treated with Val-boro-Pro, a pan-inhibitor of DPP, or with DPP2-specific inhibitor (DSI), incubated for 16 hours and stained with propidium iodide and Annexin V. Expression of CD38 was assessed by flow cytometry, DPP2 and ZAP-70 - by real-time reverse-transcription polymerase chain reaction, Bcl-2 and p27 - by western blot analysis. We report that CLL B-cells expressed higher levels of DPP2 mRNA than normal B-cells. Inhibition of DPP2 in PBMC with VbP or DSI resulted in caspase-dependent apoptosis. In individuals with CLL, death of B-lymphocytes (and rescue by caspase inhibitors) was observed in 22 cases (57.9%). In the remaining 16 cases (42.1%) malignant B-cells did not undergo apoptosis upon inhibition of DPP2 with either VbP or DSI. We found that CLL cells resistant to DPP2 inhibition-induced apoptosis expressed higher levels of ZAP-70. Meanwhile, protein levels of p27 (cell cycle inhibitor) were decreased in resistant CLL. These patients exhibited worse disease prognosis such as shorter treatment-free period (p&lt;0.001), frequent episodes of treatment failure and faster disease progression. Between the two groups, we identified no differences in expression of Bcl-2. CLL B-cells express higher levels of DPP2, a serine protease involved in maintenance of G0 which may serve as a survival factor in CLL B-cells. Resistance vs. susceptibility to DPP2 inhibition-induced apoptosis can be employed as a prognostic factor in CLL.
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Dissertations / Theses on the topic "Peptidase inhibitor 16"

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Pullaniparambil, Mohandas Arunesh. "Characterisation of PI16+ T helper cells." Thesis, 2015. http://hdl.handle.net/2440/103501.

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CD4 T cells, a major component of the immune system, are a heterogeneous population comprising cells with known and unknown function in both health and disease. Biomarkers that identify pathogenic T cell subsets enable early diagnosis and may also provide leads for therapeutic intervention. Peptidase inhibitor 16 (PI16), a recently discovered biomarker by the Barry lab, for a functionally distinct subset of regulatory T cells, is also expressed in T helper cells. However, the characteristics of PI16 expressing T helper cells have not been previously studied. This thesis investigates the molecular and functional characteristics of PI16+ T helper (Th) cells in health and disease. A high proportion of PI16+ Th cells express the chemokine receptors CCR4 and CCR6 in comparison with PI16- Th cells, indicating ability to respond to chemotactic stimuli, which was confirmed by in-vitro migration assays. Upon in-vitro stimulation, PI16+ Th cells express high levels of the Th17 transcription factor, ROR-γt, and produce more pro-inflammatory cytokines, including IL-17A, TNF, but less IFN-γ in comparison with PI16- Th cells. In the steady state, PI16+ Th cells express high levels of FAS receptor and low levels of CD38 and CXCR5, indicating a mature phenotype. Microarray analysis showed 649 genes were differentially expressed between PI16+ and PI16- Th cells and pathway analysis of the gene profile of PI16+ Th cells indicates a potential role in cell-mediated immune response, migration and inflammatory response. Intriguingly, nearly all PI16+ Th cells are memory (CD45RO+) cells, but not all memory cells are PI16+. Hence, PI16- cells are a mixture of CD45RA+ and CD45RO+. In order to exclude the possibility that the distinct characteristics of PI16+ Th cells are simply due to their differing memory status, this study further compares the functional and phenotypical difference between purified PI16+ memory and PI16- memory Th cells. PI16+ cells may mimic the properties of long-term resting memory T cells by their high expression of Integrin β1, Hepatic leukemia factor and Clusterin and low expression of Tyrosine kinase and CCL5. In addition, high expression of histamine H₄ receptor, Angiotensin converting enzyme 1 and Galectin-1 in PI16+ cells in comparison with PI16- memory Th cells may indicate their potential role in inflammation. Intracellular phosphoprotein analysis showed altered kinetics of STAT signalling by PI16+ cells in response to cytokine stimuli, compared with PI16- cells. Upon stimulation, PI16+ cells secrete more IL-2 than PI16- cells, indicating a potential autocrine driven proliferation status, which was confirmed by proliferation assay. However, PI16+ Th are more apoptotic on the one hand but resistant to suppression by Treg compared with PI16- mem Th cells on the other hand. A chemokine receptor profiling based method to segregate Th1, Th2, Th17 and Th22 subsets indicates, all the subsets express PI16 at varying proportions, but the Th22 subset almost uniformly expresses PI16. In order to further investigate the role of PI16+ Th cells in disease, a suite of pilot clinical studies were performed including rheumatoid arthritis (RA), juvenile idiopathic arthritis, scleroderma, asthma, chronic sinusitis and type I diabetes. The preliminary data indicate that in the peripheral blood of sinusitis and RA patients, the proportion of PI16+ Th cells were higher compared with healthy controls. In the peripheral blood of RA and scleroderma patients, higher numbers of CD45RA+PI16+ Th cells were present while these are almost undetectable in healthy control, which may indicate the peripheral expansion of this subset. In conclusion, PI16 may be a biomarker for long-term memory Th cells with potent effector functions. Preliminary clinical studies on the role of PI16+ Th cells in autoimmune / inflammatory diseases provide promising first data warranting further investigation on the functional role of the PI16+ CD4+ CD25- cells to determine whether or not they represent a novel lineage.
Thesis (Ph.D.) (Research by Publication) -- University of Adelaide, School of Paediatrics and Reproductive Health, 2015.
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Book chapters on the topic "Peptidase inhibitor 16"

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Kim, Yoo Hyung, and Young Min Cho. "Dipeptidyl Peptidase-4 Inhibitors." In Stroke Revisited, 143–54. Singapore: Springer Singapore, 2021. http://dx.doi.org/10.1007/978-981-16-5123-6_12.

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Pu, Jing, Qian Wang, and Shibo Jiang. "Peptide-Based HIV Entry Inhibitors." In Advances in Experimental Medicine and Biology, 15–26. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8702-0_2.

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Harms, Mirja, Manuel Hayn, Fabian Zech, Frank Kirchhoff, and Jan Münch. "Endogenous Peptide Inhibitors of HIV Entry." In Advances in Experimental Medicine and Biology, 65–85. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8702-0_5.

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Wang, Huan, and Chao Wang. "Peptide-Based Dual HIV and Coronavirus Entry Inhibitors." In Advances in Experimental Medicine and Biology, 87–100. Singapore: Springer Singapore, 2022. http://dx.doi.org/10.1007/978-981-16-8702-0_6.

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Dugave, C., C. Clavaud, J. Le Gal, R. Thai, and M. Moutiez. "Dynamic Combinatorial Assembly of Peptide-Rhenium Coordinates: Application to the Selection of hCyp-18 inhibitors from a Library of 12 × 16 Components." In Advances in Experimental Medicine and Biology, 3–4. New York, NY: Springer New York, 2009. http://dx.doi.org/10.1007/978-0-387-73657-0_1.

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Gilbert, Matthew, and Amy Shah. "Case 16: A Case of Euglycemic Diabetic Ketoacidosis After Initiation of Ketogenic Diet in a Patient With Type 2 Diabetes on a Sodium–Glucose Cotransporter 2 (SGLT2) Inhibitor." In Diabetes In Practice: Case Studies with Commentary, 62–65. American Diabetes Association, 2021. http://dx.doi.org/10.2337/9781580407663.16.

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A 52-year-old Caucasian female with a past medical history of well-controlled type 2 diabetes, hypertension, and dyslipidemia presented to the emergency department with a 3-day history of severe headache associated with nausea, neck pain, and photophobia. Her outpatient diabetes regimen consisted of metformin 1,000 mg twice a day, linagliptin (a dipeptidyl peptidase-4 [DPP-4] inhibitor) 5 mg daily, and empagliflozin (a sodium–glucose cotransporter 2 [SGLT2] inhibitor) 25 mg daily. She reported starting a ketogenic diet 4 months before admission with an objective 17-lb weight loss after she had prior success with extremely low-carbohydrate/ketogenic diets in the past.
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Kemp, Bruce E., Heung-Chin Cheng, and Donal A. Walsh. "[16] Peptide inhibitors of CAMP-dependent protein kinase." In Methods in Enzymology, 173–83. Elsevier, 1988. http://dx.doi.org/10.1016/0076-6879(88)59018-3.

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"Synthesis and Reactivity of Peptides - Substrates and Inhibitors of Thrombin." In Proceedings of the Fifth USSR-FRG Symposium on Chemistry of Peptides and Proteins, Odessa, USSR, May 16–20, 1985, 339–50. De Gruyter, 1986. http://dx.doi.org/10.1515/9783110858846-032.

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"Semisynthetic Conversion of the Bovine Trypsin Inhibitor (Kunitz) into an Efficient Leukocyte-Elastase Inhibitor by Specific Valine for Lysine Substitution in the Reactive Site." In Proceedings of the Fifth USSR-FRG Symposium on Chemistry of Peptides and Proteins, Odessa, USSR, May 16–20, 1985, 105–18. De Gruyter, 1986. http://dx.doi.org/10.1515/9783110858846-014.

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"Sequence Homology Between Phospholipase and its Inhibitor in Snake Venom. The Primary Structure of the Inhibitor of Vipoxin from the Venom of the Bulgarian Viper (Vipera ammodytes ammodytes, serpentes)." In Proceedings of the Fifth USSR-FRG Symposium on Chemistry of Peptides and Proteins, Odessa, USSR, May 16–20, 1985, 167–76. De Gruyter, 1986. http://dx.doi.org/10.1515/9783110858846-018.

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Conference papers on the topic "Peptidase inhibitor 16"

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Yoshioka, Y., M. Mitsuhashi, A. Kato, D. Kanai, A. Suda, and S. Nagaoka. "AB1166 The association of the early onset of remitting seronegative symmetrical synovitis with pitting oedema (RS3PE) syndrome with dipeptidyl peptidase-4 (DPP4) inhibitor." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.2829.

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Ryu, Jung Su, and Drazen Raucher. "Abstract 2072: Inhibition of breast cancer stem cells by Hedgehog-inhibitory peptide conjugated with Elastin-like biopolymers." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-2072.

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Zhang, Gan, Adam Herskovits, Nissim Levy, and Guillermo Gerona-Navarro. "Abstract PO-008: Bithioether Stapled Peptides as Allosteric Inhibitors of PRC2 function." In Abstracts: AACR Special Virtual Conference on Epigenetics and Metabolism; October 15-16, 2020. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.epimetab20-po-008.

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Moore, Terry W., Thomas E. Speltz, Sean W. Fanning, Christopher G. Mayne, Jonna Frasor, Geoffrey L. Greene, and Emad Tajkhorshid. "Abstract 3104: Stapled peptide inhibitors of the estrogen receptor/steroid receptor coactivator interaction." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3104.

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Lee, Jeong-Won, Jae Ryoung Hwang, Young-Jae Cho, Yoo-Young Lee, Chel Hun Choi, Duk-Soo Bae, and Byoung-Gie Kim. "Abstract 3384: IGFBP5-derived peptide as a novel angiogenesis inhibitor for treatment of ovarian cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3384.

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Du, Zhenjiao, and Yonghui Li. "Quantitative Structure-activity Relationship Study on Antioxidant Dipeptides." In 2022 AOCS Annual Meeting & Expo. American Oil Chemists' Society (AOCS), 2022. http://dx.doi.org/10.21748/cpyc1755.

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Antioxidative peptides have attracted increasing interest of researchers and consumers. Compared to wet chemistry methods, quantitative structure-activity relationship (QSAR) analysis as a in silicon method can be more efficient and cost effective and has been successfully applied to activity prediction of angiotensin I-converting enzyme inhibitory activity and bitterness of peptides. However, there are only few QSAR studies on antioxidative activity, particularly for dipeptides which have demonstrated ideal absorption ability in intestinal compared to larger peptides. This study aimed to conduct a comprehensive QSAR analysis between simple structure dipeptides and their antioxidative activity based on available results. 16 common amino acid descriptors were adopted and combined with partial least squares regression (PLSR) for modelling of ABTS and ORAC antioxidant activities of 75 dipeptides from literatures. Two descriptors, namely G-scale and VSW, were selected for further optimization of PLSR models for ABTS activity and ORAC activity, respectively. The two models resulted in R2 of 0.846 and 0.865 and Q2 of 0.737 and 0.756, respectively. With 20 times permutation, the R2 intercepts were 0.142 and 0.198, demonstrating the robustness of the models. Further, based on the two established models, the ABTS and ORAC activities of totally 400 dipeptides were predicted for screening. Overall, only a few descriptors can achieve acceptable performance in antioxidative activity modeling of dipeptides. The N-terminal residues have greater contribution to both ABTS and ORAC activity. Specifically, hydrophobicity played an important role in ABTS activity. The W, Y, E and L amino acid in the N-terminal of a dipeptide are likely to result in higher ABTS activity and the W and Y in the N-terminal of a dipeptide are likely to lead to higher ORAC activity. This study provides important guidance for future protein hydrolysis for antioxidant peptides, design, and selection of physicochemical properties and regression methods for model development.
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Berndt, M. "STRUCTURE AND FUNCTION OF THE GLYCOPROTEIN Ib-IX COMPLEX." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643729.

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At high shear flow, the adhesion of platelets to the exposed vascular subendothelium requires von Willebrand factor (vWF) and is dependent upon a specific platelet membrane adhesion receptor, the human platelet membrane glycoprotein (GP) Ib-IX complex. Recent evidence suggests that vWFbinding to the GP Ib-IX complex plays an important role in other key aspects of hemostasis and thrombosis such as shear-induced platelet aggregation and the interaction of platelets with fibrin.Studies in our laboratory with a seriesof murine monoclonal antibodies directed against epitopes on GP lb, GP IX, or against complex-specificepitopes indicate that GP lb and GP IX exist in the intact platelet membrane as a native heterodimer complex(-25,000 copies/platelet). By analysis onSDS-polyacrylamide gels, GP lb has an apparent molecular weight of 170,000 and cnsists of two disulfide-linked subunits, GP Iba (Mr = 135,000) and GP Ibβ (Mr = 25,000),whilst GP IX has an equivalent molecularweight under both nonreducing and reducing conditions (Mr = 22,000).The ±-chain ofGP lb has a central macroglycopeptide core (Mr =90,000) which is highly glycosylated. At each end of themacroglycopeptide region is a domainsensitive to proteolytic cleavage. Cleavage at the end proximal to the platelet membrane, e.g. by calpain, Serratia marcescens metalloprotease and trypsin, generates two fragments :a Mr =130,000 highly glycosylated fragment termed glycocalicin anda membrane-associated region consisting ofa Mr -25,000 fragment that remains disulfide-linkedto GP Ibβ and associated with GP IX. In resting platelets, the membrane-associated region spans the lipid bilayer linking the GP Ib-IX complex to the platelet endoskeleton via actin-binding protein. This membrane-associated region also contains the domain(s) recognized by quinine/quinidine drug-dependent antibodies. Cleavage at the plasma end of the macroglycopeptide, e.g. by human leukocyte elastase, generates a poorly glycosylated Mr = 45,000 fragment of GP Ibα (peptide tail region) and a heavily glycosylated Mr = 100,000 fragment that remains disulfide-linked to GP Ibg and associated with GP IX. Platelets lacking the N-terminal peptide tail region of GP Iba fail to agglutinate with ristocetin and vWF and show a delayed response to a-thrombin.Polyclonal and monoclonal antibodies against this region also inhibit both these platelet responses suggesting that the peptide tail region contains the binding sites for both α-thrombinand vWF. Rotary shadowingelectron microscopy of purified GP Ib-IX complex shows the structure to be highlyasymmetric with each complex existing asa flexible rod with a globular domain at each end. The overall length of the complexwas =60 nm.The smaller globular domain (peptidetail region) has a diameter of =9nm; the larger globular domain (membrane-associated region), a diameter of =16 nmWe have recently examined whetherthe human platelet GP Ib-IX complex is the receptor for the ristocetin-dependent binding of vWF by reconstitution with the purified components using a solid-phasebead assay. Our approach was to indirectlybind and orientate the GP Ib-IX complex onthe beads via a monoclonal antibody directed against the membrane-associated region of the complex (FMC 25, epitope on GP IX).Immunobeads were chosen as the insoluble matrix because they are uniform in size (=10μm in diameter), impermeable,specifically designed for the coupling of IgG, and because, like platelets, the beads have a net negative charge atneutral pH.Specific binding of 125I-labelled human vWF tothe GP Ib-IX complex-coated immunobeads was strictly ristocetin-dependent with maximal binding occurring atristocetin concentrations >1 mg/ml. Ristocetin-dependent specificbinding of 125I-labelled vWF was saturable.Scatchardanalysis revealed a single classof binding sites for vWF with purified GP Ib-IX complex.Monoclonal antibodies against the Mr = 45,000 peptide tail region ofGP lb which stronglyinhibitthe ristocetin-dependent binding ofvWF toplatelets also strongly inhibited the ristocetin-dependent binding of vWFto the GP Ib-IX coated beads. Monoclonalantibody against either themacroglycopeptide or membrane-associated regions of the GPIb-IX complex did not inhibit the ristocetin-dependent binding of vWF to platelets or to the GP Ib-IX complex-coated beads. Similar functional correlations were obtained with anti-vWFmonoclonal antibodies. The reconstitutiondata therefore confirm the functional roleof the GP Ib-IX complex as a major plateletvWF receptor. The region ofthe vWF molecule involved in binding to the GP Ib-IX complex has been localized toa Mr =50,000 domain towards theN-terminal end of the vWF subunit. The reconstitution assay should prove useful in the further definition of active peptides of vWF that bind tothe human platelet GP Ib-IX complex.
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Katkoori, Venkat R., and Harvey L. Bumpers. "Abstract 937: Nef-M1 peptide inhibits oncogenic signaling and tumor angiogenesis in patient-derived xenografts of colorectal cancer." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-937.

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Huhn, Annissa J., Rachel M. Guerra, Gregory H. Bird, and Loren D. Walensky. "Abstract 3845: A novel selectivity determinant informs the development of next-generation stapled peptide inhibitors of anti-apoptotic BFL-1/A1." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-3845.

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Boylan, Kristin L. M., Rory D. Manion, Heena Shah, and Amy P. N. Skubitz. "Abstract A06: Synthetic peptides derived from the cell adhesion molecule Nectin-4 inhibit the formation of ovarian cancer 3D spheroids." In Abstracts: AACR Special Conference on Advances in Ovarian Cancer Research; September 13-16, 2019; Atlanta, GA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1557-3265.ovca19-a06.

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Reports on the topic "Peptidase inhibitor 16"

1

Baszler, Timothy, Igor Savitsky, Christopher Davies, Lauren Staska, and Varda Shkap. Identification of bovine Neospora caninum cytotoxic T-lymphocyte epitopes for development of peptide-based vaccine. United States Department of Agriculture, March 2006. http://dx.doi.org/10.32747/2006.7695592.bard.

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The goal of the one-year feasibility study was to identify specific cytotoxic T-lymphocyte (CTL) epitopes to Neosporacaninum in the natural bovine host in order to make progress toward developing an effective peptide-based vaccine against bovine neosporosis. We tested the hypothesis that: N. caninum SRS2 peptides contain immunogenicCTLepitope clusters cross-presented by multiple bovine MHC-I and MHC-IIhaplotypes. The specific objectives were: (1) Map bovine CTLepitopes of N. caninum NcSRS-2 and identify consensus MHC-I and class-II binding motifs; and (2) Determine if subunit immunization with peptides containing N. caninum-specificCTLepitopes cross-reactive to multiple bovine MHChaplotypes induces a CTL response in cattle with disparate MHChaplotypes. Neosporosis is a major cause of infectious abortion and congenital disease in cattle, persisting in cattle herds via vertical transmission.5 N. caninum abortions are reported in Israel; a serological survey of 52 Israeli dairy herds with reported abortions indicated a 31% infection rate in cows and 16% infection rate in aborted fetuses.9,14 Broad economic loss due to bovine neosporosis is estimated at $35,000,000 per year in California, USA, and $100,000,000 (Australian) per year in Australia and New Zealand.13 Per herd losses in a Canadian herd of 50 cattle are estimated more conservatively at $2,305 (Canadian) annually.4 Up to date practical measures to reduce losses from neosporosis in cattle have not been achieved. There is no chemotherapy available and, although progress has been made toward understanding immunity to Neospora infections, no efficacious vaccine is available to limit outbreaks or prevent abortions. Vaccine development to prevent N. caninum abortion and congenital infection remains a high research priority. To this end, our research group has over the past decade: 1) Identified the importance of T-lymphocyte-mediated immunity, particularly IFN-γ responses, as necessary for immune protection to congenital neosporosis in mice,1,2,10,11 and 2) Identified MHC class II restricted CD4+ CTL in Neosporainfected Holstein cattle,16 and 3) Identified NcSRS2 as a highly conserved surface protein associated with immunity to Neospora infections in mice and cattle.7,8,15 In this BARD-funded 12 month feasibility study, we continued our study of Neospora immunity in cattle and successfully completed T-lymphocyte epitope mapping of NcSRS2 surface protein with peptides and bovine immune cells,15 fulfilling objective 1. We also documented the importance of immune responses NcSRS2 by showing that immunization with native NcSRS2 reduces congenital Neospora transmission in mice,7 and that antibodies to NcSRS2 specifically inhibition invasion of placental trophoblasts.8 Most importantly we showed that T-lymphocyte responses similar to parasite infection, namely induction of activated IFN-γ secreting Tlymphocytes, could be induced by subunit immunization with NcSRS2 peptides containing the Neospora-specificCTLepitopes (Baszler et al, In preparation) fulfilling objective 2. Both DNA and peptide-based subunit approaches were tested. Only lipopeptide-based NcSRS2 subunits, modified with N-terminal linked palmitic acid to enhance Toll-like receptors 2 and 1 (TLR2-TLR1), stimulated robust antigen-specific T-lymphocyte proliferation, IFN-γ secretion, and serum antibody production across different MHC-IIhaplotypes. The discovery of MHC-II cross-reactive T-cellinducing parasite peptides capable of inducing a potentially protective immune response following subunit immunization in cattle is of significant practical importance to vaccine development to bovine neosporosis. In addition, our findings are more widely applicable in future investigations of protective T-cell, subunit-based immunity against other infectious diseases in outbred cattle populations.
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