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isoleucine/nekrosis
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Substitution of methionine 435 with leucine, isoleucine, and serine in tumor necrosis factor alpha converting enzyme inactivates ectodomain shedding activity.
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Tumor necrosis factor alpha (TNF-alpha) converting enzyme (TACE) is a zinc metalloprotease that has emerged as a general sheddase, which is responsible for ectodomain release of numerous membrane proteins, including the proinflammatory cytokine TNF-alpha, the leukocyte adhesin L-selectin and
Tumour necrosis factor-related apoptosis-inducing ligand induces apoptosis in canine hemangiosarcoma cells in vitro.
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Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) is an apoptosis-inducing cytokine that shows potential therapeutic value for human neoplasms, and is effective in some canine tumours; however, its potential for killing canine hemangiosarcoma (HSA) cells is unknown. Thus, we evaluated
An isoleucine-zipper motif enhances costimulation of human soluble trimeric GITR ligand.
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Glucocorticoid-induced tumor-necrosis factor receptor (GITR) and its ligand, GITRL, play significant roles in regulating immune responses. It is clear that human soluble GITRL (hsGITRL) transduces signal activity through multiple oligomerization states. To develop human soluble trimeric GITRL
Biological and physicochemical evaluation of the conformational stability of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
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Tumor necrosis factor (TNF)-related, apoptosis-inducing ligand (Apo2L/TRAIL) has a unique homotrimeric structure, and its conformational stability is essential for its apoptotic activity. The conformational stability of a modified version of TRAIL(114-281) with two additional domains of histidine
N-methyl-4-isoleucine cyclosporine attenuates CCl -induced liver fibrosis in rats by interacting with cyclophilin B and D.
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OBJECTIVE
N-methyl-4-isoleucine cyclosporine (NIM811), a new analogue of cyclosporine A, can inhibit collagen deposition in vitro and reduce liver necrosis in a bile-duct-ligation animal model. However, whether NIM811 effects on CCl(4) -induced rat liver fibrosis, and the related mechanism has not
Delineating the molecular basis of the inactivity of tissue inhibitor of metalloproteinase-2 against tumor necrosis factor-alpha-converting enzyme.
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Tumor necrosis factor-alpha (TNF-alpha)-converting enzyme (TACE, ADAM-17) is a zinc-dependent ADAM (a disintegrin and metalloproteinase) metalloproteinase (MP) of the metzincin superfamily. The enzyme regulates the shedding of a variety of cell surface-anchored molecules such as cytokines, growth
A novel mutation (T61I) in the gene encoding tumour necrosis factor receptor superfamily 1A (TNFRSF1A) in a Japanese patient with tumour necrosis factor receptor-associated periodic syndrome (TRAPS) associated with systemic lupus erythematosus.
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OBJECTIVE
To identify potential mutations in the tumour necrosis factor receptor superfamily 1A gene (TNFRSF1A) in a Japanese female patient with recurrent fever complicated by systemic lupus erythematosus (SLE), and in her family members.
METHODS
DNA sequencing of exons 1-10 of the TNFRSF1A gene
Orally administered angiotensin-converting enzyme-inhibitors captopril and isoleucine-proline-proline have distinct effects on local renin-angiotensin system and corticosterone synthesis in dextran sulfate sodium-induced colitis in mice.
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The effects of angiotensin-converting enzyme (ACE) inhibition by an antihypertensive drug, captopril, and milk casein-derived ACE-inhibiting bioactive tripeptide isoleucine-proline-proline (Ile-Pro-Pro), on local renin-angiotensin system (RAS) and glucocorticoid production in the intestine were
Trimer form of tumor necrosis factor-related apoptosis inducing ligand induces apoptosis in canine cell lines derived from mammary tumors.
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We evaluated the cytotoxic effect of isoleucine-zipper tumor necrosis factor-related apoptosis inducing ligand (izTRAIL) against cell lines, B101592, Cha, and C090115, derived from canine mammary gland tumors. These cells were derived from three dogs diagnosed with mammary adenoma or carcinoma. All
Novel mitochondrial transition pore inhibitor N-methyl-4-isoleucine cyclosporin is a new therapeutic option in acute pancreatitis.
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Hepatic mitochondrial enzyme activity and serum amino acid composition in rats treated with tumor necrosis factor.
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The biochemical integrity of hepatocellular mitochondria was investigated in rats treated with small doses of human recombinant tumor necrosis factor-alpha (Hur-TNF;50-100 micrograms/kg/d injected intraperitoneally for 5 d) by measuring the activities of three mitochondrial enzymes, glutamate
Metabolic indices related to leaf marginal necrosis associated with potassium deficiency in tomato using GC/MS metabolite profiling
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To clarify the physiological factors associated with the development of tomato leaf marginal necrosis associated with potassium deficiency, tomato leaf blades prior to development of the symptoms were collected, and profiles of water-soluble metabolites were analyzed using gas chromatography-mass
Minocycline and N-methyl-4-isoleucine cyclosporin (NIM811) mitigate storage/reperfusion injury after rat liver transplantation through suppression of the mitochondrial permeability transition.
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Graft failure after liver transplantation may involve mitochondrial dysfunction. We examined whether prevention of mitochondrial injury would improve graft function. Orthotopic rat liver transplantation was performed after 18 hours' cold storage in University of Wisconsin solution and treatment with
NIM811 (N-methyl-4-isoleucine cyclosporine), a mitochondrial permeability transition inhibitor, attenuates cholestatic liver injury but not fibrosis in mice.
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Cholestasis causes hepatocyte death, possibly because of mitochondrial injury. This study investigated whether NIM811 (N-methyl-4-isoleucine cyclosporine), an inhibitor of the mitochondrial permeability transition (MPT), attenuates cholestatic liver injury in vivo. Cholestasis was induced in mice by
Effects of tumor necrosis factor alpha on skeletal muscle amino acid metabolism studied in-vivo.
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OBJECTIVE
The present study was performed to determine the chronology of the effects of a single 50 ug subcutaneous dose of TNF on food intake, weight gain, and skeletal muscle protein metabolism in normal rats. Earlier work demonstrated that a single subcutaneous dose of 50 ug of tumor necrosis
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