| Description | (Ser8)-GLP-1 (7-36) amide, human is a glucagon-like peptide 1 amide derived from glucagonogen, a cleavage product of the GLP-1 (1-36) amide peptide. (Ser8)-GLP-1 (7-36) amide, human is an entero-insulinotropic hormone that causes glucose-dependent release of insulin from pancreatic β-cells and (Ser8)-GLP-1 (7-36) amide, human is a glucagon-like peptide 1 amide derived from glucagonogen, a cleavage product of the GLP-1 (1-36) amide peptide. (Ser8)-GLP-1 (7-36) amide, human is an entero-insulinotropic hormone that causes glucose-dependent release of insulin from pancreatic β-cells and affects gastrointestinal motility and secretion... Read More | Inquire | Amino Acid Sequence Asn-Ser-Lys-Met-Ala-His-S?er-Ser-Ser-Cys-Phe-Gly-Gl?n-Lys-Ile-Asp-Arg-Ile-Gly?-Ala-Val-Ser-Arg-Leu-Gly-?Cys-Asp-Gly-Leu-Arg-Leu-P?he | Biochemical Test:SDS-PAGE (purity > 80%); Western blot with patient sample.Calculated Isoelectric Point:pH 5.68 | PTD-p65-P1 Peptide TFA is a potent, selective nuclear transcription factor NF-κB inhibitor and derives from the p65 subunit of NF-κB amino acid residues 271-282, which selectively inhibits NF-κB activation induced by various inflammatory stimulation, downAppearance:SolidIC50& PTD-p65-P1 Peptide TFA is a potent, selective nuclear transcription factor NF-κB inhibitor and derives from the p65 subunit of NF-κB amino acid residues 271-282, which selectively inhibits NF-κB activation induced by various inflammatory stimulation, downAppearance:SolidIC50& Target:NF-kappaBIn Vitro:PTD-p65-P1 Peptide TFA (10-150 µM; 0-60 min; KBM-5 cells) inhibits TNF-induced NF-κB activation in a dose-dependent manner and suppresses TNF-induced NF-κB activation by 25% at 100 µM and completely at 150 µM. PTD-p65-P1 Peptide TFA (150 µM; 0-60 minBiological Activity:PTD-p65-P1 Peptide TFA is a potent, selective nuclear transcription factor NF-κB inhibitor and derives from the p65 subunit of NF-κB amino acid residues 271-282, which selectively inhibits NF-κB activation induced by various inflammatory stimulation, down... Read More |