Search results for: PKA (Protein Kinase A) Activity Assay kit
#26798992 2016/04/11 Save this To Up
PAC1R agonist maxadilan enhances hADSC viability and neural differentiation potential.Pituitary adenylate cyclase-activating polypeptide (PACAP) is a structurally endogenous peptide with many biological roles. However, little is known about its presence or effects in human adipose-derived stem cells (hADSCs). In this study, the expression of PACAP type I receptor (PAC1R) was first confirmed in hADSCs. Maxadilan, a specific agonist of PAC1R, could increase hADSC proliferation as determined by Cell Counting Kit-8 and cell cycle analysis and promote migration as shown in wound-healing assays. Maxadilan also showed anti-apoptotic activity in hADSCs against serum withdrawal-induced apoptosis based on Annexin V/propidium iodide analysis and mitochondrial membrane potential assays. The anti-apoptotic effects of maxadilan correlated with the down-regulation of Cleaved Caspase 3 and Caspase 9 as well as up-regulation of Bcl-2. The chemical neural differentiation potential could be enhanced by maxadilan as indicated through quantitative PCR, Western blot and cell morphology analysis. Moreover, cytokine neural redifferentiation of hADSCs treated with maxadilan acquired stronger neuron-like functions with higher voltage-dependent tetrodotoxin-sensitive sodium currents, higher outward potassium currents and partial electrical impulses as determined using whole-cell patch clamp recordings. Maxadilan up-regulated the Wnt/β-catenin signalling pathway associated with dimer-dependent activity of PAC1R, promoting cell viability that was inhibited by XAV939, and it also activated the protein kinase A (PKA) signalling pathway associated with ligand-dependent activity of PAC1R, enhancing cell viability and neural differentiation potential that was inhibited by H-89. In summary, these results demonstrated that PAC1R is present in hADSCs, and maxadilan could enhance hADSC viability and neural differentiation potential in neural differentiation medium.
2248 related Products with: PAC1R agonist maxadilan enhances hADSC viability and neural differentiation potential.Epidermal Growth Factor ( Epidermal Growth Factor ( Growth Differentiation Fa Growth Differentiation Fa Human Growth and Differen Human Growth and Differen Human Growth and Differen Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge TGR5 Receptor Agonist
#26279440 2015/08/17 Save this To Up
The Neuroprotective Effect of Liraglutide is Mediated by Glucagon-Like Peptide 1 Receptor-Mediated Activation of cAMP/PKA/CREB Pathway.Glucagon-like peptide-1 (GLP-1)-based drugs are being used to achieve better glucose control in patients with type 2 diabetes, and GLP-1 mimetics such as liraglutide have shown therapeutic potential in preventing diabetes-related microvascular and macrovascular complications as well as comorbidities such as neurodegenerative disorders. In the present study, we investigated the effects of liraglutide on primary rat cortical astrocytes treated with advanced glycation end-products (AGEs).
2585 related Products with: The Neuroprotective Effect of Liraglutide is Mediated by Glucagon-Like Peptide 1 Receptor-Mediated Activation of cAMP/PKA/CREB Pathway.Glucagon like peptide 1 r interleukin 17 receptor C Natriuretic peptides B ( CREB Phospho-Specific Arr IGF-1R Signaling Phospho- T-Cell Receptor Signaling Rabbit Anti-Leptin recept Rabbit Anti-Leptin recept Rabbit Anti-Leptin recept Rabbit Anti-Leptin recept Rabbit Anti-Leptin recept Rabbit Anti-Leptin recept
#25579542 2015/01/12 Save this To Up
Carvedilol suppresses migration and invasion of malignant breast cells by inactivating Src involving cAMP/PKA and PKCδ signaling pathway.Carvedilol (CAR) can inhibit cell growth and induce cell apoptosis in breast cancer in vitro. But it is still not known whether CAR affects the migration and invasion of breast cancer cells.
1453 related Products with: Carvedilol suppresses migration and invasion of malignant breast cells by inactivating Src involving cAMP/PKA and PKCδ signaling pathway.AP-1 Reporter – HEK293 Wnt Signaling Pathway TCF Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Hh Signaling Pathway Anta Androgen Receptor (Ab 650 SRE Reporter - HEK293 Cel JAK pathway ISRE reporter Nrf antioxidant pathway A AZD-3514 Mechanisms: Andr
#24977411 2014/12/22 Save this To Up
Synthetic (+)-antroquinonol exhibits dual actions against insulin resistance by triggering AMP kinase and inhibiting dipeptidyl peptidase IV activities.The fungal product (+)-antroquinonol activates AMP kinase (AMPK) activity in cancer cell lines. The present study was conducted to examine whether chemically synthesized (+)-antroquinonol exhibited beneficial metabolic effects in insulin-resistant states by activating AMPK and inhibiting dipeptidyl peptidase IV (DPP IV) activity.
2762 related Products with: Synthetic (+)-antroquinonol exhibits dual actions against insulin resistance by triggering AMP kinase and inhibiting dipeptidyl peptidase IV activities.Dipeptidyl Peptidase IV, ELISA Human , Dipeptidyl Insulin 1 (Rat), syntheti Dipeptidyl-peptidase 3 an Amplite™ Universal Fluo to DPP-8 (Dipeptidyl Pep to DPP-9 (Dipeptidyl Pep Anti-DPP-10 (Dipeptidyl AMPKâ„¢1 (dn) AMPKâ„¢2 (dn) AMPKâ„¢2 (constitutiv Glycerol kinase
#24694916 2014/04/03 Save this To Up
[Regulation of aquaporin 3 protein expression in amnion epithelial cells through cAMP-PKA signal pathway].To investigate the expression of aquaporins-3 (AQP3) in amniotic epithelial cells regulated by cyclic adenosine monophosphate-protein kinase A (cAMP-PKA) signal pathway and to explore the mechanisms of its expression.
1886 related Products with: [Regulation of aquaporin 3 protein expression in amnion epithelial cells through cAMP-PKA signal pathway].DNA (cytosine 5) methyltr GLP 2 ELISA Kit, Rat Prog Proteinase Inhibitor 6 (P AP-1 Reporter – HEK293 Wnt Signaling Pathway TCF Signal transduction antib AKT PKB Signaling Phospho AMPK Signaling Phospho-Sp ErbB Her Signaling Phosph ERK Signaling Phospho-Spe GPCR Signaling to MAPK ER IGF-1R Signaling Phospho-
#23341462 2013/03/11 Save this To Up
Forskolin-inducible cAMP pathway negatively regulates T-cell proliferation by uncoupling the interleukin-2 receptor complex.Cytokine-mediated regulation of T-cell activity involves a complex interplay between key signal transduction pathways. Determining how these signaling pathways cross-talk is essential to understanding T-cell function and dysfunction. In this work, we provide evidence that cross-talk exists between at least two signaling pathways: the Jak3/Stat5 and cAMP-mediated cascades. The adenylate cyclase activator forskolin (Fsk) significantly increased intracellular cAMP levels and reduced proliferation of the human T-cells via inhibition of cell cycle regulatory genes but did not induce apoptosis. To determine this inhibitory mechanism, effects of Fsk on IL-2 signaling was investigated. Fsk treatment of MT-2 and Kit 225 T-cells inhibited IL-2-induced Stat5a/b tyrosine and serine phosphorylation, nuclear translocation, and DNA binding activity. Fsk treatment also uncoupled IL-2 induced association of the IL-2Rβ and γc chain, consequently blocking Jak3 activation. Interestingly, phosphoamino acid analysis revealed that Fsk-treated cells resulted in elevated serine phosphorylation of Jak3 but not Stat5, suggesting that Fsk can negatively regulate Jak3 activity possibly mediated through PKA. Indeed, in vitro kinase assays and small molecule inhibition studies indicated that PKA can directly serine phosphorylate and functionally inactivate Jak3. Taken together, these findings suggest that Fsk activation of adenylate cyclase and PKA can negatively regulate IL-2 signaling at multiple levels that include IL-2R complex formation and Jak3/Stat5 activation.
2737 related Products with: Forskolin-inducible cAMP pathway negatively regulates T-cell proliferation by uncoupling the interleukin-2 receptor complex.Mouse Anti-Human Interleu MTT Cell Proliferation As IGF-1R Signaling Phospho- Insulin Receptor Phospho- T-Cell Receptor Signaling Human soluble interleukin Human Killer cell immunog Quick Cell Proliferation Quick Cell Proliferation Rat monoclonal anti mouse Alamar Blue™, REDOX ind CytoX Violet Cell Proli
#22447140 2012/07/13 Save this To Up
Effect of triptolide on estradiol release from cultured rat granulosa cells.Triptolide, a major active component of Tripterygium wilfordii Hook F (TWHF), is known to have multiple pharmacological activities. However, studies have also shown that triptolide is highly toxic to the reproductive system by disrupting normal androgen and estrogen signaling. In the present study, we investigated the effect of triptolide (5, 10, or 20 nM for 24 h) on estradiol production by rat granulosa cells. Triptolide inhibited basal and human chorionic gonadotropin (HCG)- or 8-bromo-cAMP-stimulated estradiol production as revealed by RIA assay. Furthermore, the HCG-evoked increase in cellular cAMP content was also inhibited by triptolide, indicating that disruption of the cAMP/PKA signaling pathway may mediate the deleterious effects of triptolide on steroid hormone regulation. In addition, (3)H(2)O tests showed that aromatase activity was significantly inhibited by triptolide in granulosa cells. Western blot and quantitative real-time PCR (qRT-PCR) assays further revealed that triptolide decreased protein and mRNA expression of aromatase in granulosa cells. Moreover, mRNA expression of luteinizing hormone receptor (LHR) was induced by triptolide also using qRT-PCR method. In contrast, cell viability tests using Cell Counting Kit-8 (CCK-8) and 3-(4,5-dimethyl-thiazol-2-yl)-2,5- diphenyl-tetrazolium bromide (MTT) method indicated that triptolide did not cause measurable cell death at doses that suppressed steroidogenesis. The reproductive toxicity of triptolide may be mainly caused by disruption of cAMP/PKA-mediated expression of estrogen synthesis enzymes, leading to reduced estradiol synthesis and reproductive dysfunction.
2165 related Products with: Effect of triptolide on estradiol release from cultured rat granulosa cells.Rat Estradiol(E2)ELISA Ki GLP 1 ELISA Kit, Rat Gluc GLP 2 ELISA Kit, Rat Prog C Peptide ELISA Kit, Rat Glucagon ELISA KIT, Rat G Leptin ELISA Kit, Rat Lep Rat Mesenchymal Cells Rat Anti-Mouse Dendritic Rat Anti-Human Endothelia Mouse Anti-Rat Granulocyt Mouse Anti-Rat Reticulum Mouse Anti-Rat Reticulum
#20889222 2010/11/29 Save this To Up
Exendin-4 protects murine pancreatic β-cells from dexamethasone-induced apoptosis through PKA and PI-3K signaling.To explore the effect and mechanism of exendin-4 on dexamethasone-induced apoptosis in pancreatic β-cells.
1933 related Products with: Exendin-4 protects murine pancreatic β-cells from dexamethasone-induced apoptosis through PKA and PI-3K signaling.Anti C Reactive Protein A Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Recombinant Human PKAkt1 Recombinant Human PKAkt1 Cell Meter™ Annexin V B Cell Meter™ Annexin V B Cell Meter™ Annexin V B Cell Meter™ Phosphatidy Cell Meter™ Phosphatidy Glucagon ELISA KIT, Rat G AP-1 Reporter – HEK293
#19144957 2009/04/29 Save this To Up
Participation of the human sperm proteasome in the capacitation process and its regulation by protein kinase A and tyrosine kinase.The proteasome is a multicatalytic cellular complex present in human sperm that plays a significant role during several steps of mammalian fertilization. Here, we present evidence that the proteasome is involved in human sperm capacitation. Aliquots of highly motile sperm were incubated with proteasome inhibitors MG132 or epoxomicin. The percentage of capacitated sperm, the chymotrypsin-like activity of the proteasome, cAMP content, and the pattern of protein phosphorylation were assayed by using the chlortetracycline hydrochloride assay, a fluorogenic substrate, the cAMP enzyme immunoassay kit, and Western blot analysis, respectively. Our results indicate that treatment of sperm with proteasome inhibitors blocks the capacitation process, does not alter cAMP concentration, and changes the pattern of protein phosphorylation. To elucidate how proteasome activity is regulated during capacitation, sperm were incubated with: 1) tyrosine kinase (TK) inhibitors (genistein or herbimycin A); 2) protein kinase (PK) A inhibitors or activators (H89 and Rp-cAMPS, and 8-Br-cAMP, respectively); or 3) PKC inhibitors (tamoxifen or staurosporin) at different capacitation times. The chymotrypsin-like activity and degree of phosphorylation of the proteasome were then assayed. The results indicate that sperm treatment with TK and PKA inhibitors significantly decreases the chymotrypsin-like activity of the proteasome during capacitation. Immunoprecipitation and Western blot results suggest that the proteasome is phosphorylated during capacitation in a TK- and PKA-dependent pathway. In conclusion, we suggest that the sperm proteasome participates in the capacitation process, and that its activity is modulated by PKs.
1931 related Products with: Participation of the human sperm proteasome in the capacitation process and its regulation by protein kinase A and tyrosine kinase.Tyrosine Kinase Adaptors Goat Anti-Human Casein Ki Goat Anti-Human CKB Brain Rabbit Anti-Human Ribosom Rabbit Anti-Human S-phase Recombinant Human Androge Human Macrophage Inflamma Human Macrophage Inflamma Mouse Anti-Human Phosphot Rabbit Anti-Human Androge Rabbit Anti-Human Androge Aurora Kinase B Inhibitor
Voortstraat 49, 1910 Kampenhout BELGIUM
Tel 0032 16 58 90 45 Fax 0032 16 50 90 45
9, rue Lagrange, 75005 Paris
Tel 01 43 25 01 50 Fax 01 43 25 01 60
52062 Aachen Deutschland
Tel 0241 40 08 90 86 Fax 0241 55 91 05 36
Howard Frank Turnberry House
1404-1410 High Road
Whetstone London N20 9BH
Tel 020 3393 8531 Fax 020 8445 9411
Schweiz Züri +41435006251
Česká republika Praha +420246019719
Ireland Dublin +35316526556
Norge Oslo +4721031366
Finland Helsset +358942419041
Sverige Stockholm +46852503438
Ελλάς Αθήνα +302111768494
Magyarország Budapest +3619980547
GENTAUR Poland Sp. z o.o.
ul. Grunwaldzka 88/A m.2
81-771 Sopot, Poland
Tel 058 710 33 44
Fax 058 710 33 48
GENTAUR Nederland BV
5521 DG Eersel Nederland
Tel 0208-080893 Fax 0497-517897
Piazza Giacomo Matteotti, 6, 24122 Bergamo
Tel 02 36 00 65 93 Fax 02 36 00 65 94
53 Iskar Str. 1191 Kokalyane, Sofia