目录号 | 产品详情 | 靶点 | |
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T72886 | |||
Akt1&PKA-IN-2 ((R)-29) 是一种具有周期蛋白依赖性激酶 2 (CDK2) 选择性的酰胺类 PKB/AKT 抑制剂。Akt1&PKA-IN-2 抑制 AKT1、PKAa 和 CDK2a,IC50值分别为 0.007 µM、0.01 µM 和 0.69 µM。 | |||
T72885 | |||
Akt1&PKA-IN-1 是一种有效的Akt/PKA 双重抑制剂,对 PKAa、Akt 和CDK2的IC50值分别为 0.03、0.11 μM 和 9.8 μM。Akt1&PKA-IN-1 对细胞周期蛋白依赖性激酶 2 (CDK2) 具有选择性。 | |||
T2482 | ROCK SGK Akt PKA S6 Kinase | ||
AT13148 是一种 ATP 竞争性 AGC 激酶口服抑制剂,能够抑制 Akt1/Akt2/Akt3、p70S6K、PKA 和 ROCKI/ROCKII 的活性,IC50值分别为 38/402/50、8、3 和 6 nM/4 nM。 | |||
T14069 | CaMK Casein Kinase PKA PKC | ||
A-3 hydrochloride 是一种细胞可渗透的、可逆的、ATP 竞争性非选择性拮抗剂。它抑制 PKA 、酪蛋白激酶 II 和肌球蛋白轻链激酶,Ki 值分别为4.3 µM、5.1 µM 和7.4 µM。它还抑制 PKC 和酪蛋白激酶 I 的活性,Ki 分别为 47 µM 和 80 µM。 | |||
TP1351 | PKA | ||
Kemptide 是一种 cAMP 依赖性蛋白激酶的特异性底物,是一种合成的七肽。 | |||
T6250 | PKA S6 Kinase Autophagy | ||
H-89 dihydrochloride (5-Isoquinolinesulfonamide) 是一种选择性 cAMP 依赖性蛋白激酶A(PKA) 抑制剂,IC50值为 48 nM。也可轻微抑制 PKG、PKC 和酪蛋白激酶活性。 | |||
T6747 | PKA | ||
8-Bromo-cAMP sodium salt (8-Br-Camp sodium salt) 是一种环 AMP 依赖性蛋白激酶 (PKA) 激活剂,是一种环 AMP 类似物。 | |||
T2851 | EGFR PKA PKC Parasite Autophagy | ||
Daphnetin (7,8-Dihydroxycoumarin) 是从 Genus Daphne 中分离得到的香豆素衍生物,有抗氧化、抗炎、抗疟疾和解热作用,可用于凝血功能障碍、类风湿性关节炎等疾病的相关研究。 | |||
T76381 | |||
H1-7 (histone H1 phosphorylation site),PKASubstrate 是一种合成多肽,可作为PKA 底物。 | |||
T6680 | Apoptosis PKA Antibacterial Antibiotic Src PKC Antifungal | ||
Staurosporine (AM-2282) 是一种蛋白激酶抑制剂,对 PKC、PKA、c-Fgr、Phosphorylase kinase 和 TAOK2 均有抑制活性 (IC50=6/15/2/3/3000 nM),具有 ATP 竞争性和非选择性。Staurosporine 也可以诱导凋亡。 |
目录号 | 产品名/同用名 | 种属 | 表达系统 | ||
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TMPK-00677 | PKA/PRKACA Protein, Canine, Recombinant (His) | Canine | E. coli | ||
The cAMP-dependent protein kinase PKA is a well-characterized member of the serine-threonine protein AGC kinase family and is the effector kinase of cAMP signaling. As such, PKA is involved in the control of a wide variety of cellular processes including metabolism, cell growth, gene expression and apoptosis. cAMP-dependent PKA signaling pathways play important roles during infection and virulence of various pathogens. Since fluxes in cAMP are involved in multiple intracellular functions, a variety of different pathological infectious processes can be affected by PKA signaling pathways.
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TMPY-05207 | PRKAR1A Protein, Mouse, Recombinant (His) | Mouse | Baculovirus-Insect Cells | ||
PRKAR1A, also known as PRKAR1 and PKR1, is one of the regulatory subunits of cAMP-dependent protein kinase A (PKA). PKA can be activated by cAMP. cAMP is a signaling molecule important for a variety of cellular functions. cAMP exerts its effects by activating PKA, which transduces the signal throughphosphorylation of different target proteins. The inactive holoenzyme of PKA is a tetramer composed of two regulatory and two catalytic subunits. cAMP causes the dissociation of the inactive holoenzyme into a dimer of regulatory subunits bound to four cAMP and two free monomeric catalytic subunits. Four different regulatory subunits and three catalytic subunits of PKA have been identified in humans. PRKAR1A was found to be a tissue-specific extinguisher that down-regulates the expression of seven liver genes in hepatoma x fibroblast hybrids Three alternatively spliced transcript variants encoding the same protein have been observed.
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TMPY-03656 | PRKAR1A Protein, Human, Recombinant (His) | Human | HEK293 | ||
PRKAR1A, also known as PRKAR1 and PKR1, is one of the regulatory subunits of cAMP-dependent protein kinase A (PKA). PKA can be activated by cAMP. cAMP is a signaling molecule important for a variety of cellular functions. cAMP exerts its effects by activating PKA, which transduces the signal throughphosphorylation of different target proteins. The inactive holoenzyme of PKA is a tetramer composed of two regulatory and two catalytic subunits. cAMP causes the dissociation of the inactive holoenzyme into a dimer of regulatory subunits bound to four cAMP and two free monomeric catalytic subunits. Four different regulatory subunits and three catalytic subunits of PKA have been identified in humans. PRKAR1A was found to be a tissue-specific extinguisher that down-regulates the expression of seven liver genes in hepatoma x fibroblast hybrids Three alternatively spliced transcript variants encoding the same protein have been observed.
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TMPJ-01309 | PKI-Beta Protein, Human, Recombinant (His) | Human | E. coli | ||
cAMP-Dependent Protein Kinase Inhibitor β (PKI-β) is a member of the PKI family. As a member of the cAMP-dependent protein kinase inhibitor family,It has been shown that PKI-β is an extremely potent competitive inhibitor of cAMP-dependent protein kinase activity; this protein interacts with the catalytic subunit of the enzyme after the cAMP-induced dissociation of its regulatory chains. It may play a role in the protein kinase A (PKA) pathway by interacting with the catalytic subunit of PKA, and overexpression of this gene may play a role in prostate cancer.
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TMPH-00269 | GPR52 Protein, Bovine, Recombinant (His & KSI) | Bovine | E. coli | ||
G- protein coupled receptor activated by antipsychotics reserpine leading to an increase in intracellular cAMP and its internalization. May play a role in locomotor activity through modulation of dopamine, NMDA and ADORA2A-induced locomotor activity. These behavioral changes are accompanied by modulation of the dopamine receptor signaling pathway in striatum. Modulates HTT level via cAMP-dependent but PKA independent mechanisms throught activation of RAB39B that translocates HTT to the endoplasmic reticulum, thus avoiding proteasome degradation.
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TMPJ-00528 | PPP1R1A Protein, Human, Recombinant (His) | Human | E. coli | ||
Protein Phosphatase 1 Regulatory Subunit 1A (PPP1R1A) is an inhibitor of protein-phosphatase 1. PPP1R1A is a cellular regulator of eIF2 alpha phosphorylation. In hormonal control of glycogen metabolism, IPP-1 protein plays important function. Hormones can elevate intracellular cAMP level and elevate IPP-1 activity. PPP1R1A activation caused cAMP increase , cAMP control over proteins that are not directly phosphorylated by PKA following a rise in intracellular calcium. IPP-1 is inactivated by calcineurin (PP2B). Multiple domains in IPP-1 target cellular PP1 complexes.
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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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TMPH-00028 | Adeno-associated virus 2 (isolate Srivastava/1982) Rep78 Protein (His & MBP) | AAV-2 | E. coli | ||
Plays an essential role in the initiation of viral DNA synthesis. Binds specifically to an inverted terminal repeat element (ITR) on the 3' and 5' ends of the viral DNA, where it cleaves a site specifically to generate a priming site for initiation of the synthesis of a complementary strand. Plays also a role as transcriptional regulator, DNA helicase and as key factors in site-specific integration of the viral genome. Regulates host PKA activity by interacting with host PRKX as a mechanism of interfering with helper virus propagation and promoting its own replication. Inhibits the host cell cycle G1/S, S and G2/M transitions. These arrests may provide essential cellular factors for viral DNA replication.
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TMPH-01092 | CHGA Protein, Human, Recombinant (His) | Human | Yeast | ||
Strongly inhibits glucose induced insulin release from the pancreas.; Inhibits catecholamine release from chromaffin cells and noradrenergic neurons by acting as a non-competitive nicotinic cholinergic antagonist. Displays antibacterial activity against Gram-positive bacteria S.aureus and M.luteus, and Gram-negative bacteria E.coli and P.aeruginosa. Can induce mast cell migration, degranulation and production of cytokines and chemokines. Acts as a potent scavenger of free radicals in vitro. May play a role in the regulation of cardiac function and blood pressure.; Regulates granule biogenesis in endocrine cells by up-regulating the transcription of protease nexin 1 (SERPINE2) via a cAMP-PKA-SP1 pathway. This leads to inhibition of granule protein degradation in the Golgi complex which in turn promotes granule formation.
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TMPH-02910 | Somatostatin Protein, Mouse, Recombinant (His & KSI) | Mouse | E. coli | ||
Inhibits the secretion of pituitary hormones, including that of growth hormone/somatotropin (GH1), PRL, ACTH, luteinizing hormone (LH) and TSH. Also impairs ghrelin- and GnRH-stimulated secretion of GH1 and LH; the inhibition of ghrelin-stimulated secretion of GH1 can be further increased by neuronostatin.; May enhance low-glucose-induced glucagon release by pancreatic alpha cells. This effect may be mediated by binding to GPR107 and PKA activation. May regulate cardiac contractile function. May compromise cardiomyocyte viability. In the central nervous system, may impair memory retention and may affect hippocampal excitability. May also have anxiolytic and anorexigenic effects. May play a role in arterial pressure regulation. May inhibit basal, but not ghrelin- or GnRH-stimulated secretion of GH1 or LH, but does not affect the release of other pituitary hormones, including PRL, ACTH, FSH or TSH. Potentiates inhibitory action of somatostatin on ghrelin-stimulated secretion of GH1, but not that on GnRH-stimulated secretion of LH.
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TMPJ-00886 | ATF1 Protein, Human, Recombinant (His) | Human | E. coli | ||
Cyclic AMP-dependent transcription factor ATF-1(ATF1) which contains 1 bZIP (basic-leucine zipper) domain and 1 KID (kinase-inducible) domain, belongs to the bZIP family. It influences cellular physiologic processes by regulating the expression of downstream target genes, which are related to growth, survival, and other cellular activities. ATF1 binds the cAMP response element (CRE) (consensus: 5'-GTGACGT[AC][AG]-3'), a sequence present in many viral and cellular promoters. It also binds to the Tax-responsive element (TRE) of HTLV-I. ATF1 mediates PKA-induced stimulation of CRE-reporter genes, represses the expression of FTH1 and other antioxidant detoxification genes, triggers cell proliferation and transformation. ATF1 is phosphorylated at serine 63 in its kinase-inducible domain by serine/threonine kinases, cAMP-dependent protein kinase A, calmodulin-dependent protein kinase I/II, mitogen- and stress-activated protein kinase and CDK3. Its phosphorylation enhances its transactivation and transcriptional activities, and enhances cell transformation.
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TMPH-01857 | PIK3CG Protein, Human, Recombinant (His & Myc) | Human | E. coli | ||
Phosphoinositide-3-kinase (PI3K) that phosphorylates PtdIns(4,5)P2 (Phosphatidylinositol 4,5-bisphosphate) to generate phosphatidylinositol 3,4,5-trisphosphate (PIP3). PIP3 plays a key role by recruiting PH domain-containing proteins to the membrane, including AKT1 and PDPK1, activating signaling cascades involved in cell growth, survival, proliferation, motility and morphology. Links G-protein coupled receptor activation to PIP3 production. Involved in immune, inflammatory and allergic responses. Modulates leukocyte chemotaxis to inflammatory sites and in response to chemoattractant agents. May control leukocyte polarization and migration by regulating the spatial accumulation of PIP3 and by regulating the organization of F-actin formation and integrin-based adhesion at the leading edge. Controls motility of dendritic cells. Together with PIK3CD is involved in natural killer (NK) cell development and migration towards the sites of inflammation. Participates in T-lymphocyte migration. Regulates T-lymphocyte proliferation and cytokine production. Together with PIK3CD participates in T-lymphocyte development. Required for B-lymphocyte development and signaling. Together with PIK3CD participates in neutrophil respiratory burst. Together with PIK3CD is involved in neutrophil chemotaxis and extravasation. Together with PIK3CB promotes platelet aggregation and thrombosis. Regulates alpha-IIb/beta-3 integrins (ITGA2B/ ITGB3) adhesive function in platelets downstream of P2Y12 through a lipid kinase activity-independent mechanism. May have also a lipid kinase activity-dependent function in platelet aggregation. Involved in endothelial progenitor cell migration. Negative regulator of cardiac contractility. Modulates cardiac contractility by anchoring protein kinase A (PKA) and PDE3B activation, reducing cAMP levels. Regulates cardiac contractility also by promoting beta-adrenergic receptor internalization by binding to GRK2 and by non-muscle tropomyosin phosphorylation. Also has serine/threonine protein kinase activity: both lipid and protein kinase activities are required for beta-adrenergic receptor endocytosis. May also have a scaffolding role in modulating cardiac contractility. Contributes to cardiac hypertrophy under pathological stress. Through simultaneous binding of PDE3B to RAPGEF3 and PIK3R6 is assembled in a signaling complex in which the PI3K gamma complex is activated by RAPGEF3 and which is involved in angiogenesis.
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TMPH-03256 | CNR1 Protein, Rat, Recombinant (His) | Rat | in vitro E. coli expression system | ||
G-protein coupled receptor for cannabinoids, including endocannabinoids (eCBs), such as N-arachidonoylethanolamide (also called anandamide or AEA) and 2-arachidonoylglycerol (2-AG). Mediates many cannabinoid-induced effects, acting, among others, on food intake, memory loss, gastrointestinal motility, catalepsy, ambulatory activity, anxiety, chronic pain. Signaling typically involves reduction in cyclic AMP. In the hypothalamus, may have a dual effect on mitochondrial respiration depending upon the agonist dose and possibly upon the cell type. Increases respiration at low doses, while decreases respiration at high doses. At high doses, CNR1 signal transduction involves G-protein alpha-i protein activation and subsequent inhibition of mitochondrial soluble adenylate cyclase, decrease in cyclic AMP concentration, inhibition of protein kinase A (PKA)-dependent phosphorylation of specific subunits of the mitochondrial electron transport system, including NDUFS2. In the hypothalamus, inhibits leptin-induced reactive oxygen species (ROS) formation and mediates cannabinoid-induced increase in SREBF1 and FASN gene expression. In response to cannabinoids, drives the release of orexigenic beta-endorphin, but not that of melanocyte-stimulating hormone alpha/alpha-MSH, from hypothalamic POMC neurons, hence promoting food intake. In the hippocampus, regulates cellular respiration and energy production in response to cannabinoids. Involved in cannabinoid-dependent depolarization-induced suppression of inhibition (DSI), a process in which depolarization of CA1 postsynaptic pyramidal neurons mobilizes eCBs, which retrogradely activate presynaptic CB1 receptors, transiently decreasing GABAergic inhibitory neurotransmission. Also reduces excitatory synaptic transmission. In superior cervical ganglions and cerebral vascular smooth muscle cells, inhibits voltage-gated Ca(2+) channels in a constitutive, as well as agonist-dependent manner. Induces leptin production in adipocytes and reduces LRP2-mediated leptin clearance in the kidney, hence participating in hyperleptinemia. In adipose tissue, CNR1 signaling leads to increased expression of SREBF1, ACACA and FASN genes. In the liver, activation by endocannabinoids leads to increased de novo lipogenesis and reduced fatty acid catabolism, associated with increased expression of SREBF1/SREBP-1, GCK, ACACA, ACACB and FASN genes. May also affect de novo cholesterol synthesis and HDL-cholesteryl ether uptake. Peripherally modulates energy metabolism. In high carbohydrate diet-induced obesity, may decrease the expression of mitochondrial dihydrolipoyl dehydrogenase/DLD in striated muscles, as well as that of selected glucose/ pyruvate metabolic enzymes, hence affecting energy expenditure through mitochondrial metabolism. In response to cannabinoid anandamide, elicits a proinflammatory response in macrophages, which involves NLRP3 inflammasome activation and IL1B and IL18 secretion. In macrophages infiltrating pancreatic islets, this process may participate in the progression of type-2 diabetes and associated loss of pancreatic beta-cells.
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TMPH-01035 | CNR1 Protein-VLP, Human, Recombinant (His) | Human | HEK293 | ||
G-protein coupled receptor for endogenous cannabinoids (eCBs), including N-arachidonoylethanolamide (also called anandamide or AEA) and 2-arachidonoylglycerol (2-AG), as well as phytocannabinoids, such as delta(9)-tetrahydrocannabinol (THC). Mediates many cannabinoid-induced effects, acting, among others, on food intake, memory loss, gastrointestinal motility, catalepsy, ambulatory activity, anxiety, chronic pain. Signaling typically involves reduction in cyclic AMP. In the hypothalamus, may have a dual effect on mitochondrial respiration depending upon the agonist dose and possibly upon the cell type. Increases respiration at low doses, while decreases respiration at high doses. At high doses, CNR1 signal transduction involves G-protein alpha-i protein activation and subsequent inhibition of mitochondrial soluble adenylate cyclase, decrease in cyclic AMP concentration, inhibition of protein kinase A (PKA)-dependent phosphorylation of specific subunits of the mitochondrial electron transport system, including NDUFS2. In the hypothalamus, inhibits leptin-induced reactive oxygen species (ROS) formation and mediates cannabinoid-induced increase in SREBF1 and FASN gene expression. In response to cannabinoids, drives the release of orexigenic beta-endorphin, but not that of melanocyte-stimulating hormone alpha/alpha-MSH, from hypothalamic POMC neurons, hence promoting food intake. In the hippocampus, regulates cellular respiration and energy production in response to cannabinoids. Involved in cannabinoid-dependent depolarization-induced suppression of inhibition (DSI), a process in which depolarization of CA1 postsynaptic pyramidal neurons mobilizes eCBs, which retrogradely activate presynaptic CB1 receptors, transiently decreasing GABAergic inhibitory neurotransmission. Also reduces excitatory synaptic transmission. In superior cervical ganglions and cerebral vascular smooth muscle cells, inhibits voltage-gated Ca(2+) channels in a constitutive, as well as agonist-dependent manner. In cerebral vascular smooth muscle cells, cannabinoid-induced inhibition of voltage-gated Ca(2+) channels leads to vasodilation and decreased vascular tone. Induces leptin production in adipocytes and reduces LRP2-mediated leptin clearance in the kidney, hence participating in hyperleptinemia. In adipose tissue, CNR1 signaling leads to increased expression of SREBF1, ACACA and FASN genes. In the liver, activation by endocannabinoids leads to increased de novo lipogenesis and reduced fatty acid catabolism, associated with increased expression of SREBF1/SREBP-1, GCK, ACACA, ACACB and FASN genes. May also affect de novo cholesterol synthesis and HDL-cholesteryl ether uptake. Peripherally modulates energy metabolism. In high carbohydrate diet-induced obesity, may decrease the expression of mitochondrial dihydrolipoyl dehydrogenase/DLD in striated muscles, as well as that of selected glucose/ pyruvate metabolic enzymes, hence affecting energy expenditure through mitochondrial metabolism. In response to cannabinoid anandamide, elicits a proinflammatory response in macrophages, which involves NLRP3 inflammasome activation and IL1B and IL18 secretion. In macrophages infiltrating pancreatic islets, this process may participate in the progression of type-2 diabetes and associated loss of pancreatic beta-cells.; Binds both 2-AG and anandamide.; Only binds 2-AG with high affinity. Contrary to its effect on isoform 1, 2-AG behaves as an inverse agonist on isoform 2 in assays measuring GTP binding to membranes.; Only binds 2-AG with high affinity. Contrary to its effect on isoform 1, 2-AG behaves as an inverse agonist on isoform 3 in assays measuring GTP binding to membranes.
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