目录号 | 产品详情 | 靶点 | |
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T1560 | Glucocorticoid Receptor Endogenous Metabolite | ||
Prednisolone (Hydroretrocortine) 是有口服活性的皮质类固醇和糖皮质激素。它的抗炎特性约为氢化可的松的四倍,同时减少了水和盐的保留。它能够用于眼部抗炎研究。 | |||
T14377 | Glucocorticoid Receptor | ||
AZD5423 是可吸入的非甾体糖皮质激素受体选择性调节剂,能够有效降改善轻度过敏性哮喘患者的过敏原诱导反应。 | |||
T82303 | |||
Glucocorticoid receptor agonist-1 phosphate Gly-Glu (TFA) 是用于抗体-药物偶联物 (Antibody-Drug Conjugates (ADCs)) 合成的可降解 Linker。 | |||
T15451 | Glucocorticoid Receptor | ||
GW-870086 是抗炎剂,是糖皮质激素受体激动剂,在 A549 细胞中,能够降低 NFκB 报告基因活性(pIC50: 10.1)。 | |||
T77835 | |||
Glucocorticoid receptor agonist-1 phosphate Gly-Glu-Br 为ADC linker,适用于ABBV-154、ABBV-927及ABBV-368或相似化合物的合成。 | |||
T74116 | |||
Glucocorticoid receptoragonist-1 Ala-Ala-Mal (化合物 88) 是一种糖皮质激素,是糖皮质激素受体激动剂。Glucocorticoid receptoragonist-1 Ala-Ala-Mal 可与Adalimumab 偶联制备ADC。 | |||
T77869 | |||
Glucocorticoid receptor agonist-2 Ala-Ala-Mal(化合物79)是ABBV-3373的活性对照,可用于合成抗炎ADC分子。 | |||
T1614 | Glucocorticoid Receptor Endogenous Metabolite | ||
Hydrocortisone (Cortisol) 是一种糖皮质激素,由肾上腺素皮质分泌。Hydrocortisone 激动糖皮质激素受体,可促进蛋白质分解代谢、糖异生、毛细血管壁稳定性、肾脏钙排泄,并抑制免疫和炎症反应。 | |||
T8777 | Glucocorticoid Receptor | ||
Beclometasone 是糖皮质激素受体激动剂。 | |||
T75130 | |||
Glucocorticoid receptor agonist-1 phosphate Ala-Ala-Br 作为一种Drug-linker conjugates for ADC,主要用于抗CD40抗体活性分子偶联物 (ADCs) 的合成, 充当反应试剂。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPY-04561 | SGK3 Protein, Human, Recombinant (His & GST) | Human | Baculovirus-Insect Cells | ||
Serine / threonine-protein kinase Sgk3, also known as Serum / glucocorticoid-regulated kinase 3, Serum / glucocorticoid-regulated kinase-like and SGK3, is a cytoplasmic vesicle protein that belongs to the protein kinase superfamily and AGC Ser/Thr protein kinase family. SGK3 contains one AGC-kinase C-terminal domain, one protein kinase domain and one PX (phox homology) domain. Two specific sites of SGK3, one in the kinase domain (Thr-32) and the other in the C-terminal regulatory region (Ser-486), is needed to be phosphorylated for its full activation. SGK3 is expressed in most tissues with highest levels in pancreas, kidney liver, heart and brain and lower levels in lung, placenta and skeletal muscle. SGK3 is involved in the activation of potassium channels. It mediates cell IL-3-dependent survival signals. SGK3 participates in the regulation of HERG by increasing HERG protein abundance in the plasma membrane and may thus modify the duration of the cardiac action potential. SGK3 is also a very important and characteristic molecule that plays a critical role in both hair follicle morphogenesis and hair cycling.
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TMPY-02248 | Myocilin Protein, Human, Recombinant (His) | Human | HEK293 | ||
Myocilin, also known as Trabecular meshwork-induced glucocorticoid response protein, MYOC, and GLC1A, is a protein that contains one olfactomedin-like domain. Myocilin / MYOC may participate in the obstruction of fluid outflow in the trabecular meshwork. Myocilin / MYOC is expressed in large amounts in various types of muscle, ciliary body, papillary sphincter, skeletal muscle, heart, and other tissues. Myocilin / MYOC is expressed predominantly in the retina. In normal eyes, it is found in the inner uveal meshwork region and the anterior portion of the meshwork. In contrast, in many glaucomatous eyes, it is found in more regions of the meshwork and appeared more intensively than in normal eyes, regardless of the type of clinical severity of glaucoma. Defects in Myocilin / MYOC may contribute to primary congenital glaucoma type 3A (GLC3A). Defects in MYOC may also contribute to this phenotype via digenic inheritance. GLC3A is an autosomal recessive form of primary congenital glaucoma (PCG). PCG is characterized by a marked increase of intraocular pressure at birth or early childhood, large ocular globes (buphthalmos), and corneal edema.
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TMPY-06836 | NR3C1 Protein, Human, Recombinant (His) | Human | E. coli | ||
NR3C1 (Nuclear Receptor Subfamily 3 Group C Member 1) is a Protein Coding gene. This gene encodes glucocorticoid receptor, which can function both as a transcription factor that binds to glucocorticoid response elements in the promoters of glucocorticoid responsive genes to activate their transcription, and as a regulator of other transcription factors. NR3C1 is a transcriptional regulator of many drug-metabolizing enzymes and anti-inflammatory molecules. NR3C1 polymorphisms associate with obesity, muscle strength, and cortisol sensitivity. Glucocorticoid receptor gene polymorphism (NR3C1 646 C>G) may play an important role in the development of severe bronchial asthma and resistance to glucocorticoids (GCs). Disturbances in the structure and function of the glucocorticoid receptor (GR) alter the glucocorticoid regulation of the corticotropin-releasing hormone, which leads to nonspecific activation of numerous receptors in the brain and alters the metabolism.
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TMPJ-00110 | GITR/TNFRSF18 Protein, Mouse, Recombinant (hFc & His) | Mouse | Human Cells | ||
Tumor necrosis factor receptor superfamily member 18(Gitr) contains 3 TNFR-Cys repeats and it have four isforms.IsformA、isformB and isformC is single-pass type I membrane protein and isformD is a secreted protein. The protein is the receptor for TNFSF18.It seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. It mediated NF-kappa-B activation via the TRAF2/NIK pathway.It binds to TRAF1, TRAF2, and TRAF3, but not TRAF5 and TRAF6 and binds through its C-terminus to SIVA1/SIVA.It preferentially expressed in activated T lymphocytes and up-regulated in peripherical mononuclear cells after antigen stimulation/lymphocyte activation.
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TMPJ-00432 | GITR Ligand/TNFSF18 Protein, Cynomolgus, Recombinant (His) | Cynomolgus | Human Cells | ||
TNFSF18 is a single-pass type II membrane protein. It is expressed at high levels in the small intestine, ovary, testis, kidney and endothelial cells. TNFSF18 cytokine binds to TNFRSF18/AITR/GITR. It regulates T-cell responses, and functions as costimulator and lower the threshold for T-cell activation and T-cell proliferation. It is Important for interactions between activated T-lymphocytes and endothelial cells and Promotes leukocyte adhesion to endothelial cells. TNFSF18 mediates activation of NF-kappa-B. As Triggers increased phosphorylation of STAT1 and up-regulates expression of VCAM1 and ICAM1. It also regulates migration of monocytes from the splenic reservoir to sites of inflammation.
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TMPJ-01319 | TINAGL1 Protein, Human, Recombinant (His) | Human | Human Cells | ||
TINAGL1 is a secreted protein and contains one SMB (somatomedin-B) domain. TINAGL1 is expressed in aorta, lymph nodes, heart, bone marrow, placenta, lung, kidney, skeletal muscle, pancreas, thyroid, adrenal gland and so on. TINAGL1 may be implicated in the adrenocortical zonation and in mechanisms for repressing the CYP11B1 gene expression in adrenocortical cells.
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TMPH-00844 | HSD11B2 Protein, Human, Recombinant (His) | Human | Yeast | ||
Catalyzes the conversion of cortisol to the inactive metabolite cortisone. Modulates intracellular glucocorticoid levels, thus protecting the nonselective mineralocorticoid receptor from occupation by glucocorticoids.
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TMPY-01117 | MRAP Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
MRAP (Melanocortin 2 Receptor Accessory Protein) is a Protein Coding gene. This gene encodes a melanocortin receptor-interacting protein. It belongs to the MRAP family. MRAP, which contains a single transmembrane domain, has a unique structure, an antiparallel homodimer. MRAP is a single transmembrane domain accessory protein and a critical component of the hypothamo pituitary-adrenal axis. MRAP is highly expressed in the adrenal gland and is essential for adrenocorticotropin hormone (ACTH) receptor expression and function. In adrenal cells, MRAP is essential for adrenocorticotropic hormone (ACTH)-induced activation of the cAMP/protein kinase A (PKA) pathway by melanocortin 2 receptor (MC2R), leading to glucocorticoid production and secretion. Diseases associated with MRAP include Glucocorticoid Deficiency 2 and Glucocorticoid Deficiency 1.
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TMPK-01064 | GITR Ligand/TNFSF18 Protein, Mouse, Recombinant (hFc) | Mouse | HEK293 | ||
Glucocorticoid-induced TNFR-related protein (TNFRSF18, GITR, CD357), expressed by T cells, and its ligand (TNFSF18, GITRL), expressed by myeloid populations, provide co-stimulatory signals that boost T cell activity. Due to the important role that GITR plays in regulating immune functions, agonistic stimulation of GITR is a promising therapeutic concept.
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TMPK-00053 | GITR Ligand/TNFSF18 Protein, Human, Recombinant (His & Flag) | Human | HEK293 | ||
Glucocorticoid-induced TNFR-related protein (TNFRSF18, GITR, CD357), expressed by T cells, and its ligand (TNFSF18, GITRL), expressed by myeloid populations, provide co-stimulatory signals that boost T cell activity. Due to the important role that GITR plays in regulating immune functions, agonistic stimulation of GITR is a promising therapeutic concept.
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TMPK-00054 | GITR Ligand/TNFSF18 Protein (Primary Amine Labeling), Human, Recombinant (His & Flag), Biotinylated | Human | HEK293 | ||
Glucocorticoid-induced TNFR-related protein (TNFRSF18, GITR, CD357), expressed by T cells, and its ligand (TNFSF18, GITRL), expressed by myeloid populations, provide co-stimulatory signals that boost T cell activity. Due to the important role that GITR plays in regulating immune functions, agonistic stimulation of GITR is a promising therapeutic concept.
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TMPK-01086 | GITR/TNFRSF18 Protein, Mouse, Recombinant (aa 22-153, His) | Mouse | HEK293 | ||
GITR (glucocorticoid-induced tumor necrosis factor receptor), also known as AITR and TNFRSF18, is a 40 kDa transmembrane glycoprotein that functions in immune regulation.GIRT is a receptor for TNFSF18. Seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. Mediated NF-kappa-B activation via the TRAF2/NIK pathway.
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TMPK-00133 | GITR/TNFRSF18 Protein, Human, Recombinant (aa 26-161, His) | Human | HEK293 | ||
GITR (glucocorticoid-induced tumor necrosis factor receptor), also known as AITR and TNFRSF18, is a 40 kDa transmembrane glycoprotein that functions in immune regulation.GIRT is a receptor for TNFSF18. Seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. Mediated NF-kappa-B activation via the TRAF2/NIK pathway.
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TMPY-06327 | Calreticulin Protein, Human, Recombinant | Human | HEK293 | ||
Calreticulin is a multifunctional protein. It acts as a main Ca(2+)-binding (storage) protein in the lumen of the endoplasmic reticulum. Calreticulin binds Ca2+ ions (a second messenger in signal transduction), rendering it inactive. The Ca2+ is bound with low affinity, but high capacity, and can be released on a signal. Located in storage compartments associated with the endoplasmic reticulum, calreticulin also binds to misfolded proteins and prevents them from being exported from the endoplasmic reticulum to the golgi apparatus. The amino terminus of calreticulin interacts with the DNA-binding domain of the glucocorticoid receptor and prevents the receptor from binding to its specific glucocorticoid response element. Calreticulin reduces the binding of androgen receptor to its hormone-responsive DNA element and inhibits androgen receptor and retinoic acid receptor transcriptional activities in vivo, as well as retinoic acid-induced neuronal differentiation. Therefore, calreticulin acts as a significant modulator of the regulation of gene transcription by nuclear hormone receptors.
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TMPK-01260 | GITR/TNFRSF18 Protein, Cynomolgus, Recombinant (aa 20-156, His) | Cynomolgus | HEK293 | ||
GITR (glucocorticoid-induced tumor necrosis factor receptor), also known as AITR and TNFRSF18, is a 40 kDa transmembrane glycoprotein that functions in immune regulation.GIRT is a receptor for TNFSF18. Seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. Mediated NF-kappa-B activation via the TRAF2/NIK pathway.
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TMPK-00132 | GITR/TNFRSF18 Protein, Human, Recombinant (aa 26-161, His & Avi), Biotinylated | Human | HEK293 | ||
GITR (glucocorticoid-induced tumor necrosis factor receptor), also known as AITR and TNFRSF18, is a 40 kDa transmembrane glycoprotein that functions in immune regulation.GIRT is a receptor for TNFSF18. Seems to be involved in interactions between activated T-lymphocytes and endothelial cells and in the regulation of T-cell receptor-mediated cell death. Mediated NF-kappa-B activation via the TRAF2/NIK pathway.
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TMPY-03259 | Calreticulin Protein, Human, Recombinant (His) | Human | HEK293 | ||
Calreticulin is a multifunctional protein. It acts as a main Ca(2+)-binding (storage) protein in the lumen of the endoplasmic reticulum. Calreticulin binds Ca2+ ions (a second messenger in signal transduction), rendering it inactive. The Ca2+ is bound with low affinity, but high capacity, and can be released on a signal. Located in storage compartments associated with the endoplasmic reticulum, calreticulin also binds to misfolded proteins and prevents them from being exported from the endoplasmic reticulum to the golgi apparatus. The amino terminus of calreticulin interacts with the DNA-binding domain of the glucocorticoid receptor and prevents the receptor from binding to its specific glucocorticoid response element. Calreticulin reduces the binding of androgen receptor to its hormone-responsive DNA element and inhibits androgen receptor and retinoic acid receptor transcriptional activities in vivo, as well as retinoic acid-induced neuronal differentiation. Therefore, calreticulin acts as a significant modulator of the regulation of gene transcription by nuclear hormone receptors.
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TMPY-03258 | Calreticulin Protein, Human, Recombinant (hFc) | Human | HEK293 | ||
Calreticulin is a multifunctional protein. It acts as a main Ca(2+)-binding (storage) protein in the lumen of the endoplasmic reticulum. Calreticulin binds Ca2+ ions (a second messenger in signal transduction), rendering it inactive. The Ca2+ is bound with low affinity, but high capacity, and can be released on a signal. Located in storage compartments associated with the endoplasmic reticulum, calreticulin also binds to misfolded proteins and prevents them from being exported from the endoplasmic reticulum to the golgi apparatus. The amino terminus of calreticulin interacts with the DNA-binding domain of the glucocorticoid receptor and prevents the receptor from binding to its specific glucocorticoid response element. Calreticulin reduces the binding of androgen receptor to its hormone-responsive DNA element and inhibits androgen receptor and retinoic acid receptor transcriptional activities in vivo, as well as retinoic acid-induced neuronal differentiation. Therefore, calreticulin acts as a significant modulator of the regulation of gene transcription by nuclear hormone receptors.
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TMPY-01383 | PRMT6 Protein, Human, Recombinant (His & Flag) | Human | HEK293 | ||
Protein arginine N-methyltransferase 6, also known as Histone-arginine N-methyltransferase PRMT6, PRMT6, and HRMT1L6, is a member of the protein arginine N-methyltransferase family and PRMT6 subfamily. PRMT6 is highly expressed in kidney and testes. PRMT6 is known to catalyze the generation of asymmetric dimethylarginine in polypeptides. It has been implicated in human immunodeficiency virus pathogenesis, DNA repair, and transcriptional regulation. PRMT6 is known to methylate histone H3 Arg-2 (H3R2), and this negatively regulates the lysine methylation of H3K4 resulting in gene repression. PRMT6 plays a key role in coupling process by functioning as a transcriptional coactivator that can regulate alternative splicing. PRMT6 coactivates the progesterone, glucocorticoid and oestrogen receptors in luciferase reporter assays in a hormone-dependent manner. Small interfering RNA (siRNA) oligonucleotide duplex knockdown of PRMT6 disrupts oestrogen-stimulated transcription of endogenous GREB1 and progesterone receptor in MCF-7 breast cancer cells. Neutralizing the activity of PRMT6 could inhibit tumor progression and may be of cancer therapeutic significance.
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TMPY-02041 | Cortisol Binding Globulin Protein, Human, Recombinant (His) | Human | HEK293 | ||
Corticosteroid-binding globulin (CBG), also known as SerpinA6, is a non-inhibitory member of the serine proteinase inhibitor (serpin) superfamily. It is the high-affinity transport protein for glucocorticoids in vertebrate blood. CBG is specifically cleaved by this protease at a precise site close to its carboxy-terminus. This induces a conformation change and disrupts the binding between glucocorticoids and CBG, and promotes a significant and local release of glucocorticoids (over 90% of them are bound to CBG in human plasma). In this context, CBG directs glucocorticoids to sites of inflammation, and plays in consequence a crucial role in efficient glucocorticoid action in physiology. The SerpinA6 protein is mainly secreted by the liver. This negative acute phase protein regulates free cortisol levels in the blood and distributes cortisol to its target tissues. SerpinA6 deficiency is an extremely rare hereditary disorder characterized by reduced corticosteroid-binding capacity with normal or low plasma corticosteroid-binding globulin concentration, and normal or low basal cortisol levels associated with hypo-/hypertension and muscle fatigue. There are three heritable, human CBG gene mutations that can reduce CBG-cortisol binding affinity and/or reduce circulating CBG levels.
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TMPY-06702 | Cortisol Binding Globulin Protein, Mouse, Recombinant (His & Avi), Biotinylated | Mouse | HEK293 | ||
Corticosteroid-binding globulin (CBG), also known as SerpinA6, is a non-inhibitory member of the serine proteinase inhibitor (serpin) superfamily. It is the high-affinity transport protein for glucocorticoids in vertebrate blood. CBG is specifically cleaved by this protease at a precise site close to its carboxy-terminus. This induces a conformation change and disrupts the binding between glucocorticoids and CBG, and promotes a significant and local release of glucocorticoids (over 90% of them are bound to CBG in human plasma). In this context, CBG directs glucocorticoids to sites of inflammation, and plays in consequence a crucial role in efficient glucocorticoid action in physiology. The SerpinA6 protein is mainly secreted by the liver. This negative acute phase protein regulates free cortisol levels in the blood and distributes cortisol to its target tissues. SerpinA6 deficiency is an extremely rare hereditary disorder characterized by reduced corticosteroid-binding capacity with normal or low plasma corticosteroid-binding globulin concentration, and normal or low basal cortisol levels associated with hypo-/hypertension and muscle fatigue. There are three heritable, human CBG gene mutations that can reduce CBG-cortisol binding affinity and/or reduce circulating CBG levels.
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TMPY-02107 | Cortisol Binding Globulin Protein, Mouse, Recombinant (His) | Mouse | HEK293 | ||
Corticosteroid-binding globulin (CBG), also known as SerpinA6, is a non-inhibitory member of the serine proteinase inhibitor (serpin) superfamily. It is the high-affinity transport protein for glucocorticoids in vertebrate blood. CBG is specifically cleaved by this protease at a precise site close to its carboxy-terminus. This induces a conformation change and disrupts the binding between glucocorticoids and CBG, and promotes a significant and local release of glucocorticoids (over 90% of them are bound to CBG in human plasma). In this context, CBG directs glucocorticoids to sites of inflammation, and plays in consequence a crucial role in efficient glucocorticoid action in physiology. The SerpinA6 protein is mainly secreted by the liver. This negative acute phase protein regulates free cortisol levels in the blood and distributes cortisol to its target tissues. SerpinA6 deficiency is an extremely rare hereditary disorder characterized by reduced corticosteroid-binding capacity with normal or low plasma corticosteroid-binding globulin concentration, and normal or low basal cortisol levels associated with hypo-/hypertension and muscle fatigue. There are three heritable, human CBG gene mutations that can reduce CBG-cortisol binding affinity and/or reduce circulating CBG levels.
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TMPY-05329 | Cortisol Binding Globulin Protein, Human, Recombinant (His & Avi), Biotinylated | Human | HEK293 | ||
Corticosteroid-binding globulin (CBG), also known as SerpinA6, is a non-inhibitory member of the serine proteinase inhibitor (serpin) superfamily. It is the high-affinity transport protein for glucocorticoids in vertebrate blood. CBG is specifically cleaved by this protease at a precise site close to its carboxy-terminus. This induces a conformation change and disrupts the binding between glucocorticoids and CBG, and promotes a significant and local release of glucocorticoids (over 90% of them are bound to CBG in human plasma). In this context, CBG directs glucocorticoids to sites of inflammation, and plays in consequence a crucial role in efficient glucocorticoid action in physiology. The SerpinA6 protein is mainly secreted by the liver. This negative acute phase protein regulates free cortisol levels in the blood and distributes cortisol to its target tissues. SerpinA6 deficiency is an extremely rare hereditary disorder characterized by reduced corticosteroid-binding capacity with normal or low plasma corticosteroid-binding globulin concentration, and normal or low basal cortisol levels associated with hypo-/hypertension and muscle fatigue. There are three heritable, human CBG gene mutations that can reduce CBG-cortisol binding affinity and/or reduce circulating CBG levels.
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