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Relevant bibliographies by topics / Leupeptin

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Academic literature on the topic 'Leupeptin'

Author: Grafiati

Published: 5 June 2025

Last updated: 1 August 2025

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Journal articles on the topic "Leupeptin"

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Yoshinari, Mototaka, and Alvin Taurog. "Physiological role of thiol proteases in thyroid hormone secretion." Acta Endocrinologica 113, no. 2 (1986): 261–67. http://dx.doi.org/10.1530/acta.0.1130261.

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Abstract. To determine the physiological role of the thiol proteases in T4 and T3 release from thyroglobulin, experiments were performed with 131I-prelabelled rat thyroid lobes incubated in vitro in the presence and absence of leupeptin, an inhibitor of thiol proteases. Basal secretion of [131I]T4 and [131I]T3 from rat thyroid lobes prelabelled in vivo was quite low, but in the presence of 10 mU/ml bovine TSH a marked stimulatory effect was observed. The stimulatory effect of TSH was completely abolished by leupeptin. This was associated with marked inhibition of lysosomal proteolytic activity

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KIM, In Seop, Young Bae KIM, and Kye Joon LEE. "Characterization of the leupeptin-inactivating enzyme from Streptomyces exfoliatus SMF13 which produces leupeptin." Biochemical Journal 331, no. 2 (1998): 539–45. http://dx.doi.org/10.1042/bj3310539.

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Leupeptin-inactivating enzyme (LIE) was purified from Streptomyces exfoliatusSMF13 by ammoniumm sulphate fractionation of cell-free culture broth, ultrafiltration, anion-exchange chromatography on DEAE–Sephadex A-50 and gel filtration chromatography on Sephadex G-75. The molecular mass of the purified enzyme was measured as 34700 Da and the N-terminal amino acid sequence was APTPPDIPLANVPA. Acetyl-leucine, leucine and argininal were identified as the products of leupeptin inactivated by the LIE, indicating that leupeptin is inactivated by hydrolysis of peptide bond between leucine and leucine

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BADALAMENTE, MARIE A., L. C. HURST, S. B. PAUL, and A. STRACHER. "Enhancement of Neuromuscular Recovery after Nerve Repair in Primates." Journal of Hand Surgery 12, no. 2 (1987): 211–17. http://dx.doi.org/10.1016/0266-7681_87_90015-5.

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This investigation describes the use of the calcium-activated protease inhibitor, leupeptin, as an adjunctive therapy to the microsurgical repair of median nerves in a primate model. Our results indicate that leupeptin facilitates morphological recovery in denervated thenar muscles and in distal sensory and mixed motor-sensory nerve trunks and functional recovery measured by motor nerve conduction velocity. Toxicological testing of leupeptin showed that, when administered at a dose of 12mg/kg, intramuscularly, once daily, haematological and clotting profiles were not adversely affected.

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Noda, Toru, Mary L. Bronson, Shang-Ming Yu, and Marilyn G. Farquhar. "The 215 KD mannose-6-phosphate receptor is involved in crinophagy but not in autophagy." Proceedings, annual meeting, Electron Microscopy Society of America 48, no. 3 (1990): 932–33. http://dx.doi.org/10.1017/s0424820100162223.

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Autophagy and crinophagy represent the two major pathways for digestion of intracellular material via lysosomes have been described. Though both phenomena involve in corporation of cell organelles into lysosomes and thus degradation by lysosomal enzymes, the process by which autophagic and crinophagic vacuoles acquire lysosomal enzymes remains to be clarified. The aim of this work is to find out if mannose-6-phosphate (M6P) receptors are involved in this process. As a typical working model, we used hepatocytes of leupeptin-treated rats for autophagy (Fig. 1) and mammotrophs of female rats trea

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Zachgo, S., B. Dobberstein, and G. Griffiths. "A block in degradation of MHC class II-associated invariant chain correlates with a reduction in transport from endosome carrier vesicles to the prelysosome compartment." Journal of Cell Science 103, no. 3 (1992): 811–22. http://dx.doi.org/10.1242/jcs.103.3.811.

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Invariant chain (Ii) associated with MHC class II molecule is processed proteolytically via several distinct intermediates during its intracellular transport through endosomal compartments. Leupeptin added to the culture medium blocks processing of Ii, prevents its dissociation from the class II molecules and leads to an intracellular accumulation of a 22 kDa intermediate form of Ii. We show here that leupeptin has a very general effect on protein transport in the endocytic pathway. When added to Mel Juso cells leupeptin reduces the transport of endocytosed material from multivesicular body-li

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Subramanyam, Sarvepalli B., Aparna Tipirneni, Nazih Youssef, Generoso G. Gascon, and Pinar T. Ozand. "Biochemical Heterogeneity of Infantile Central Nervous System Spongy Degeneration." Journal of Child Neurology 7, no. 1_suppl (1992): S22—S25. http://dx.doi.org/10.1177/08830738920070010411.

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Aspartoacylase, the enzyme whose activity is deficient in infantile central nervous system spongy degeneration (Canavan-Van Bogaert-Bertrand disease), is detected as an approximately 59-kD protein in the Sephadex G-200 filtration of normal fibroblast extracts. The enzyme activity in homogenates of fibroblasts is protected by leupeptin, a protease inhibitor. In the absence of leupeptin, 90% of aspartoacylase activity is lost. In some patients with infantile spongy degeneration, no activity (less than 2%) can be detected. In some other patients with residual activity in fibroblasts, two separate

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Yamashita, Kouwa, Keiko Watanabe, Hideki Takayama, et al. "Assay of plasma leupeptin using the reversible binding of leupeptin to bovine pancreatic trypsin." Analytical Biochemistry 156, no. 2 (1986): 503–7. http://dx.doi.org/10.1016/0003-2697(86)90285-x.

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Freeman, Stuart J., and Nigel A. Brown. "Comparative effects of cathepsin inhibitors on rat embryonic development in vitro. Evidence that cathepsin D is unimportant in the proteolytic function of yolk sac." Development 86, no. 1 (1985): 271–81. http://dx.doi.org/10.1242/dev.86.1.271.

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The effects of two proteinase inhibitors, leupeptin and pepstatin on the development of 9·5-day rat conceptuses in vitro has been studied. All cultures were of 48 h duration and the inhibitors were present throughout the entire period. When pepstatin was added to the culture medium (5–25 μg/ml) conceptuses developed and grew to an extent that did not differ from untreated controls. However, leupeptin (l–4 μg/ml) caused severe growth retardation and abnormal development of conceptuses. The effects of the two inhibitors on the hydrolysis of 125I-labelled BSA and haemoglobin by homogenates of 10·

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Selsby, Joshua, Klara Pendrak, Monica Zadel, et al. "Leupeptin-based inhibitors do not improve the mdx phenotype." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 299, no. 5 (2010): R1192—R1201. http://dx.doi.org/10.1152/ajpregu.00586.2009.

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Calpain activation has been implicated in the disease pathology of Duchenne muscular dystrophy. Inhibition of calpain has been proposed as a promising therapeutic target, which could lessen the protein degradation and prevent progressive fibrosis. At the same time, there are conflicting reports as to whether elevation of calpastatin, an endogenous calpain inhibitor, alters pathology. We compared the effects of pharmacological calpain inhibition in the mdx mouse using leupeptin and a proprietary compound (C101) that linked the inhibitory portion of leupeptin to carnitine (to increase uptake int

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Al, Z., and C. M. Cohen. "Phorbol 12-myristate 13-acetate-stimulated phosphorylation of erythrocyte membrane skeletal proteins is blocked by calpain inhibitors: possible role of protein kinase M." Biochemical Journal 296, no. 3 (1993): 675–83. http://dx.doi.org/10.1042/bj2960675.

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Human erythrocytes contain cytosolic protein kinase C (PKC) which, when activated by phorbol 12-myristate 13-acetate (PMA), induces the phosphorylation of the membrane skeletal proteins band 4.1, band 4.9 and adducin. We found that brief treatments of erythrocytes with PMA resulted in a decrease in cytosolic PKC content and in the transient appearance in the cytosol of a Ca(2+)- and phospholipid-independent 55 kDa fragment of PKC, called PKM. Prolonged treatment with PMA resulted in the complete and irreversible loss of erythrocyte PKC. To investigate the possible role of calpain in this proce

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Dissertations / Theses on the topic "Leupeptin"

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Clark, S. A. "The mechanism of uptake and intracellular fate of leupeptin in rat yolk sacs." Thesis, Keele University, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376309.

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Schroeder, Ewald. "Structural studies of #mu#-calpain, a novel calpain substrate, and a papain-leupeptin complex." Thesis, University of Oxford, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.386677.

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Fuska, Jana. "The effect of ammonium chloride and leupeptin on the concentration of prosaposin in endosomes and lysosomes of Marshall cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape10/PQDD_0025/MQ50770.pdf.

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Singh, Raja Balraj. "Attenuation of abnormalities in sarcoplasmic reticulum of the ischemic reperfused heart by leupeptin." 2003. http://hdl.handle.net/1993/20020.

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Book chapters on the topic "Leupeptin"

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Mehlhorn, Heinz. "Leupeptin." In Encyclopedia of Parasitology. Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-43978-4_4009.

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Mehlhorn, Heinz. "Leupeptin." In Encyclopedia of Parasitology. Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27769-6_4009-1.

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Kovats, Erwin, Josef Karner, Günter Ollenschläger, Judith Karner, Annette Simmel, and Erich Roth. "Increased Mortality in Septic Rats after Leupeptin Application." In Advances in Experimental Medicine and Biology. Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-1057-0_65.

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Tsuzuki, Kayo, Ryo Fukatsu, Yuji Takamaru, Nobuhiro Fujii, and Naohiko Takahata. "Amyloidogenic Fragments of Amyloid Precursor Protein in Cells Cultured under Leupeptin." In Alzheimer’s and Parkinson’s Diseases. Springer US, 1995. http://dx.doi.org/10.1007/978-1-4757-9145-7_19.

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Takauchi, Shigeru, and Koho Miyoshi. "Degeneration of Neuronal Processes in Rats Induced by the Protease Inhibitor Leupeptin." In Basic, Clinical, and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases. Springer New York, 1990. http://dx.doi.org/10.1007/978-1-4684-5844-2_15.

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Hashimoto, Yoko. "Gelatin Zymography Using Leupeptin for the Detection of Various Cathepsin L Forms." In Methods in Molecular Biology. Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-6934-0_16.

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Porta, Eduardo A., Alberto J. Monserrat, Alejandro Berra, and Modesto C. Rubio. "Effects of Lovastatin and Leupeptin on Ceroidogenesis of Vitamin E-Deficient And-Supplemented Young Rats." In Lipofuscin and Ceroid Pigments. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4899-5339-1_13.

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Suhar, A., V. Turk, M. Korbelik, D. Petrovic, J. Skrk, and P. Schauer. "The role of cathepsins H and B, and inhibitors leupeptin and CPI in proliferative activities of non-malignant cells in culture." In Cysteine Proteinases and their Inhibitors, edited by Vito Turk. De Gruyter, 1986. http://dx.doi.org/10.1515/9783110846836-031.

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Enna, S. J., and David B. Bylund. "Leupeptin." In xPharm: The Comprehensive Pharmacology Reference. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.63280-5.

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Conference papers on the topic "Leupeptin"

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Lipinski, B., J. Ewaskiewicz, S. Niewiarowski, and A. Z. Budzynski. "STRUCTURE AND FUNCTIONAL PROPERTIES OF A FIBRINOGEN EERIVATIVE FORMED BY LIMITED PROTEOLYSIS WITH RED BLOOD CELL." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643329.

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Normal human plasma contains, in addition to fibrinogen (Mr 340,000), two major thranbin-coagulable fibrinogen derivative of Mr 320,000 and 300,000. Previous investigations demonstrated that these derivatives do not originate from plasmic cleavages, however, no enzyme(s) responsible for the cleavages have been identified. The purpose of this study was to investigate a possible role of red blood cells (RBC) in the formation of these physiologic fibrinogen derivatives. RBC ghosts were prepared from ACD blood obtained from normal donors after removal of leukocytes and platelets. Purified human fi

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Selak, M. A., M. Chignard, and J. B. Smith. "CHARACTERIZATION OF A NEUTROPHIL CPYMOTRYPSIN-LIKE ENZYME THAT ACTIVATES PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643157.

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Communication between neutrophils and platelets was previously investigated by measuring platelet aggregation, serotonin release and changes in cytosolic free calcium subsequent to specific stimulation of neutrophils by fMet-Leu-Phe (FMLP) in a suspension of both cell types. The addition of the chemotactic peptide was shown to elicit secondary platelet activation as a consequence of primary stimulation of neutrophils. Cell-free supernatants from FMLP-stimulated neutrophils were capable of inducing platelet activation thus demonstrating that a factor released bv neutrophils was responsible for

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Puri, R. N., F. Zhou, H. Bradford, E. J. Gustafson, R. F. Colman, and R. W. Colman. "HIGH MOLECULAR WEIGHT KININOGEN SPECIFICALLY BLOCKS THROMBIN-INDUCED AGGREGATION BY INHIBITING PLATELET CALPAIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643860.

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We have previously shown that platelet-aggregation induced by alpha-thrombin (1.7 nM) involves complete cleavage of the surface membrane polypeptide, Mr = 100 kDa (MP 100) labeled by FSBA in intact platelets. The failure to cleave MP100 in membrane preparations or in platelets treated with metabolic inhibitors or leupeptin, suggested that thrombin was acting by activating platelet calpain. Since high molecular weight kininogen (HMWK) is the most potent plasma inhibitor of calpain(s), we now report that HMWK inhibited thrombin-induced aggregation in a dose-dependent manner over a range of plasm

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Wallace, Robert W., E. Ann Tallant, and Lynn M. Brumley. "POSSIBLE ROLE FOR THE CA2+-DEPENDENT PROTEASE (CALPAIN I) AS AN IRREVERSIBLE ACTIVATOR OF CA2+/CALMODULIN-MEDIATED REACTIONS IN THE HUMAN PLATELET." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644528.

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Calmodulin (CaM)-binding proteins have been identified in human platelets using Western blotting techniques and 125I-CaM. Ten proteins of 245, 225. 175, 150, 90. 82(2), 60 and 41(2) kilodaltons (kDa) bind 125I-CaM in a Ca2+-dependent manner; the binding is blocked by both trifluoperazine and nonradiolabeled CaM. The 225 and 90 kDa proteins are labeled by antisera against myosin light chain kinase (MLCK); the 60 kDa and one of the 82 kDa proteins have been identified as the CaM-dependent phosphatase (calcineurin) and caldesmon. The other proteins are presumed to be other Ca2+/CaM regulated enzy

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NAKAMURA, Shin. "MONOCYTE/MACROPHAGE TISSUE FACTOR: ROLE OF ITS N-GLYCOSYLATED CARBOHYDRATE MOIETY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643286.

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Monocytes/macrophages and related cells are known to generate tissue factor (TF) , a membrane associated lipid-glycoprotein complex, following activation with LPS or other stimuli. Monkey (M. fuscata) mononuclear leukocytes (MNL, 3 × 106/ml) cultured with LPS (lµg/ml) in FCS-free RPMI medium were stimulated to produce the glycoprotein (TF-Apo). After a lag period of 2 h the TF-Apo production was initiated, and its accumulation reached the plateau after 12 h and then declined to approximately half of the maximum level after 24 h. A time course of the TF activity was strictly in accord with that

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Aakhus, A. M., N. O. Solum, and I. Hagen. "EFFECTS OF SOME ORGANIC SOLVENTS ON GP lb AND ACTIN-BINDING PROTEIN IN BLOOD PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643511.

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Effects on filamentous proteins appear to be a central phenomenon in the neuronal toxic effects of organic solvents. We have therefore compared the effects of some organic solvents (particularly isopropylalcohol, IPA) to the previously observed effects of dibucaine (DBC) on platelet cytoskeletal proteins. Incubation of platelets with 6% IPA at 37° C, like DBC, initiates a degradation of actin-binding protein (ABP) as substrate for a calcium activated protease (CAP), shown by SDS-PAGE. IPA leads to an increase followed by a decrease in bovine von Willebrand factor-induced agglutination. The dec

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Sakon, M., Y. Uemura, K. Suga, T. Tsujinaka, J. Kambayashi, and T. Mori. "STUDIES ON PHOSPHATASES IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644494.

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Activation of platelets by various agonists has been ascribed to be associated with phosphorylation and dephosphorylation of specific proteins such as 20K and 47K polypeptide. Although protein kinases such as myosin light chain kinase and C kinase have been extensively studied, little information is currently available on platelet phosphatases, which may play a crucial role in the regulation of stimulus-linked protein phosphorylation. Thereby, the present study was conducted to know some characters of platelet phosphatases. Glycerol loaded platelets prepared from human platelet concentrates we

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Fujimura, K., T. Fujimoto, M. Takemoto, K. Oda, S. Maehama, and A. Kuramoto. "INTERACTION OF MEMBRANE GLYCOPROTEIN GPIIb AND Ilia WITH CYTOSKELETAL PROTEINS DURING PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643515.

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Experiments were designed and performed to analyse the cytoskeleton assembly and the interaction of glycoprotein (GP)IIb, IIIa and cytoskeletal proteins during platelet activation. A23187 stimulated 125I labeled platelets were solubilised with Triton X-100 solution and centrifuged. The insoluble fraction were analysed by two dimensional electrophoresis and the soluble fraction were fractionated with 5-25% sucrose gradient centrifugation and analysed by SDS PAGE. In Triton X-100 insoluble fraction, high molecular weight protein fraction(MW > 106) was present after stimulation which were cons

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