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Description:
Interleukin-33 (IL-33; HF-NEV; IL-1F11), a member of the IL-1 family of cytokines, is expressed by many cell types following pro-inflammatory stimulation and is thought to be released upon cell lysis. IL-33 binds to and signals through ST2 (IL-1R1) and its stimulation recruits MYD88, IRAK, IRAK4 and TRAF6, followed by phosphorylation of ERK1 (MAPK3) / ERK2 (MAPK1), p38 (MAPK14) and JNK. The ability of IL-33 to target numerous immune cell types, like Th2-like cells, mast cells and B1 cells, and to induce cytokine and chemokine production underlines its potential in influencing the outcome of a wide range of diseases, such as arthritis, asthma, atopic allergy & anaphylaxis, cardiovascular disease/atherosclerosis, nervous system diseases and sepsis. IL-33 facilitates Treg expansion in vitro and in vivo. Recently, IL-33 has been involved in adipocyte differentiation. The biological activity of IL-33 at its receptor ST2 is rapidly terminated in the extracellular environment by its oxidation (formation of two disulfide bridges), resulting in an extensive conformational change that disrupts the ST2 binding site. Mutations at amino acids C208S/C232S protect IL-33 from oxidation and increase its activity.
Description:
Catabolite of thymine. Precursor for 3-Hydroxyisobutyric acid synthesis. Small molecule myokine. Browning inducer of white adipose tissue (WAT) into brown adipose tissue (BAT). PGC-1alpha-mediated and exercise-triggered nonadrenergic activator of the thermogenic program in WAT. Increases the expression of brown adipocyte-specific genes (browning) in white adipocytes and beta-oxidation in hepatocytes through a PPARalpha-mediated mechanism. Induces a brown adipose-like phenotype in human pluripotent stem cells and improves glucose homeostasis. Enhances fatty acid oxidation and reduces body weight in mice through an increased production of leptin by the white adipose tissue (WAT). Inhibits Agxt2-mediated metabolism of dimethylarginines. Partial agonist of the glycine receptor (GlyR).
Description:
The non-protein amino acid L-canavanine is an analog of L-arginine. Selective inducible nitric oxide synthase (iNOS; NOS II) inhibitor. Induces apoptotic cell death and shows antiproliferative and immunotoxic effects.
Description:
Reactant for: 1.Preparation of (aryl)oxadiazolobenzoxazinones via Suzuki-Miyaura reaction. 2.Copper-catalyzed oxidative amination of benzoxazoles and related azoles via C-H and C-N bond activation. 3.Synthesis of N-(alkoxyphenyl)-aminocarbonylbenzoic acid derivatives as protein tyrosine phophatase 1B inhibitors. 4. Preparation of lipophilic deoxy-xylulose-phosphate reductoisomerase inhibitors. 5.Synthesis of benzoxazole benzenesulfonamides as allosteric inhibitors of fructose-1,6-bisphosphatase.application:Reactant for:Preparation of (aryl)oxadiazolobenzoxazinones via Suzuki-Miyaura reactionCopper-catalyzed oxidative amination of benzoxazoles and related azoles via C-H and C-N bond activationSynthesis of N-(alkoxyphenyl)-aminocarbonylbenzoic acid derivatives as protein tyrosine phophatase 1B inhibitorsPreparation of lipophilic deoxy-xylulose-phosphate reductoisomerase inhibitorsSynthesis of benzoxazole benzenesulfonamides as allosteric inhibitors of fructose-1,6-bisphosphatase
Description:
Aldehyde dehydrogenases (ALDHs) mediate the NADP+-dependent oxidation of aldehydes into acids and play an important role in the detoxification of alcohol-derived acetaldehyde, as well as in lipid peroxidation and in the metabolism of corticosteroids, biogenic amines and neurotransmitters. ALDH9A1 (aldehyde dehydrogenase family 9 member A1), also known as E3, ALDH4, ALDH7, ALDH9 or TMABADH, is a 494 amino acid cytoplasmic protein that is highly expressed in adult liver, skeletal muscle, kidney and embryonic brain. ALDH9A1 converts gamma-trimethylaminobutyraldehyde into gamma-butyrobetaine and catalyzes the irreversible oxidation of a broad range of aldehydes to the corresponding acids in a NAD-dependent reaction.
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