g-protein antagonist peptide

Substance P-related peptide that inhibits binding of G proteins to their receptors. Competitively and reversibly inhibits M2 muscarinic receptor activation of Gi or Go and inhibits Gs activation by β-adrenoceptors.

G-Protein antagonist peptide acetate is a truncated substance P-related peptide, competes with receptor for G protein binding. G-Protein antagonist peptide acetate inhibits the activation of Gi or Go by M2 muscarinic cholinergic receptor (M2 mAChR) or of Gs by beta-adrenergic receptor in the reconstituted phospholipid vesicles, assayed by receptor-promoted GTP hydrolysis

Protein Kinase C Peptide Substrate acetate targets specific cell spacers ina manner that is dependent on second messengers and specific adaptor proteins in response to extracellular signals that activate g protein-coupled receptors, tyrosine Kinase recept

RAGE antagonist peptide acetate is an advanced antagonist of glycation end products (RAGE). RAGE antagonist peptide acetate possesses anti-tumor and anti-inflammatory activities. RAGE antagonist peptide acetate prevents RAGE from binding with several of its most important ligands, including HMGB-1, S100P, and S100A4.

VSV-G Peptide acetate(103425-05-4 free base) is a 11 amino acid peptide derived from the Vesicular Stomatitis viral glycoprotein.

C5aR1 antagonist peptide, a biologically active linear peptide originating from the C-terminus of the chemokine complement fragment 5 anaphylatoxin (C5a), inhibits C5a binding and activity at human and rat C5a receptors. Overexpression of C5a is linked to various immunoinflammatory diseases, including arthritis, Alzheimer’s disease, cystic fibrosis, and systemic lupus erythematosus.

Antagonist G is an anticancer peptide and is also a broad spectrum neuropeptide growth factor antagonist.

Receptor for advanced glycation end products (RAGE) antagonist. Blocks S100P, S100A4 and HMGB-1 mediated RAGE activation in vitro and in vivo. Inhibits growth and metastasis of rat glioma tumors. Reduces cell growth and RAGE-mediated NF-κB activity in hum

Protein kinase inhibitor peptide matches the inhibitory domain of the heat-stable protein kinase inhibitor.

Ribosomal protein L3 peptide (202-222) is a peptide with the sequenceH2N-Met-Ser-His-Arg-Lys-Tyr-Glu-Ala-Pro-Arg-His-Gly-His-Leu-Gly-Phe-Leu-Pro-Arg-Lys-Arg-amide, MW=2573.

Protein Kinase C Peptide Substrate targets specific cell spacers ina manner that is dependent on second messengers and specific adaptor proteins in response to extracellular signals that activate g protein-coupled receptors, tyrosine Kinase receptors, or

Protein Kinase C (gamma) Peptide, a fragment of Protein Kinase Cγ, plays a role in dominant ataxia by inhibiting the nuclear import of aprataxin, which is associated with recessive ataxia [1].

Protein Kinase C (alpha) Peptide (TFA) is a PKC-α-associated peptide functioning as a lipid-dependent serine/threonine protein kinase. It plays a pivotal role in regulating several cellular functions such as survival, proliferation, differentiation, migration, and adhesion [1].

Protein Kinase C (19-35) Peptide, serving as the PKC pseudosubstrate inhibitor/region, potentially inhibits PKC activity by obstructing the substrate-binding site within its kinase domain, rendering the cytoplasmic form of PKC inactive [1] [2].

VSV-G is a vesicular stomatitis virus G (VSV-G) protein fragment. VSV-G protein is commonly used in biomedical research to pseudotype retroviral and lentiviral vectors, conveying the ability to transduce a broad range of mammalian cell types with genes of

Antagonist G TFA is a potent antagonist of vasopressin, with additional, weaker antagonistic effects on GRP and Bradykinin. This compound also promotes AP-1 transcription and enhances cellular sensitivity to chemotherapy [1] [2].

Using specific antisera raised against synthetic peptides, we find that three distinct GTP-binding protein alpha subunits remain bound to the plasma membrane even after activation with nonhydrolyzable GTP analog. Trypsin cleaves each alpha subunit at a si

Protein Kinase C (beta) Peptide, a fragment of Protein Kinase Cβ, is associated with hyperglycemia-induced decreases in endothelium-derived nitric oxide. Inhibiting Protein Kinase Cβ forestalls the impairment of endothelium-dependent vasodilation caused by acute hyperglycemia [1].

Kisspeptin-54 is a peptide ligand of the orphan G protein-coupled receptor GPR54 (Kis = 1.81 and 1.45 nM for rat and human receptors, respectively).1 It is a 54 amino acid peptide encoded by the metastasis suppressor gene KISS-1. Kisspeptin-54 induces calcium mobilization in CHO-K1 cells expressing rat and human receptors (EC50s = 1.39 and 5.47 nM, respectively). It also induces arachidonic acid release in CHO cells expressing rat and human GPR54 in a concentration-dependent manner. Kisspeptin-54 (10-1,000 nM) inhibits insulin secretion from isolated mouse pancreatic β-cells in the presence of 2.8 mM, but not 11.1 mM, glucose.2 Kisspeptin-54 (1-5 nmol, i.c.v.) increases serum levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in mice, an effect which is reversed by the gonadotropin releasing hormone (GNRH) antagonist acycline.3References1. Kotani, M., Detheux, M., Vandenbogaerde, A.L., et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J. Biol. Chem. 276(37), 34631-34636 (2001).2. Vikman, J., and Ahrén, B. Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets. Diabetes Obes. Metab. 11(Suppl 4), 197-201 (2009).3. Gottsch, M.L., Cunningham, M.J., Smith, J.T., et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology 145(9), 4073-4077 (2004). Kisspeptin-54 is a peptide ligand of the orphan G protein-coupled receptor GPR54 (Kis = 1.81 and 1.45 nM for rat and human receptors, respectively).1 It is a 54 amino acid peptide encoded by the metastasis suppressor gene KISS-1. Kisspeptin-54 induces calcium mobilization in CHO-K1 cells expressing rat and human receptors (EC50s = 1.39 and 5.47 nM, respectively). It also induces arachidonic acid release in CHO cells expressing rat and human GPR54 in a concentration-dependent manner. Kisspeptin-54 (10-1,000 nM) inhibits insulin secretion from isolated mouse pancreatic β-cells in the presence of 2.8 mM, but not 11.1 mM, glucose.2 Kisspeptin-54 (1-5 nmol, i.c.v.) increases serum levels of luteinizing hormone (LH) and follicular stimulating hormone (FSH) in mice, an effect which is reversed by the gonadotropin releasing hormone (GNRH) antagonist acycline.3 References1. Kotani, M., Detheux, M., Vandenbogaerde, A.L., et al. The metastasis suppressor gene KiSS-1 encodes kisspeptins, the natural ligands of the orphan G protein-coupled receptor GPR54. J. Biol. Chem. 276(37), 34631-34636 (2001).2. Vikman, J., and Ahrén, B. Inhibitory effect of kisspeptins on insulin secretion from isolated mouse islets. Diabetes Obes. Metab. 11(Suppl 4), 197-201 (2009).3. Gottsch, M.L., Cunningham, M.J., Smith, J.T., et al. A role for kisspeptins in the regulation of gonadotropin secretion in the mouse. Endocrinology 145(9), 4073-4077 (2004).

Proadrenomedullin N-terminal 12 peptide (PAMP-12), an endogenous fragment originating from the adrenal medulla and spanning amino acids 9-20 of human PAMP-20, plays a role in causing hypotension. It functions as an agonist for the MAS-related G protein-coupled receptor family member X2 (MRGPRX2), inhibiting forskolin-stimulated cAMP accumulation in CHO cells expressing human MRGPRX2 (EC50 = 57.2 nM) and selectively prompting calcium mobilization in these cells (EC50 = 41 nM), but not in cells expressing MRGPRX1, MRGPRX3, or MRGPRX4 at 1 µM. As an antagonist of nicotinic acetylcholine receptors (nAChRs), PAMP-12 obstructs carbachol-triggered catecholamine release and the influx of calcium and sodium (IC50s = 1.3, 0.39, and 0.87 µM, respectively) in primary bovine adrenal chromaffin cells, with no effect on histamine-induced responses (IC50s = >1 µM for all). Additionally, it decreases mean arterial blood pressure in normotensive rats at doses ranging from 10 to 50 nmol/kg.