c-peptide

Proinsulin C-Peptide (31-63), porcine, is a peptide derived from the cleavage of porcine proinsulin, covering amino acid residues 31 to 63.

C-Peptide 2, rat, a 31-amino-acid peptide, serves as a constituent in proinsulin. It possesses the ability to hinder glucose-triggered insulin secretion.

C-Peptide 2, rat acetate is a proinsulin component of inhibiting glucose-induced insulin secretion, consisting of acetate and a polypeptide composed of 31 amino acid residues [1] [2].

C-Peptide 1 (rat), a β-catenin GSK-3β activator and regulator of the Wnt β-catenin signaling pathway, is utilized in cancer research [1].

Pegylated synthetic human C-peptide exhibits similar bioactivity to natural C-peptides (non-polyethylene glycolated) and demonstrates an extended plasma half-life, making it suitable for research in diabetic peripheral neuropathy [1].

C-Peptide, dog, is a component of proinsulin released from pancreatic beta cells into the blood alongside insulin. It plays a crucial role in the biosynthesis of insulin but has long been considered biologically inert.

Proinsulin C-peptide (human) is a 31-amino acid peptide that links the Proinsulin A and B chains, ensuring their proper folding, biological activity, and regulation of cellular functions.

Proinsulin C-peptide human acetate (Proinsulin C-peptide human acetate (33017-11-7 Free base)) is a polypeptide of 31 amino acid residues that links the A and B chains of proinsulin to ensure proper folding, has biological activity and regulates cellular functions.

Human proinsulin, the single-chain peptide precursor of insulin, consists of the insulin A and B chains connected by the 31 amino acid C-peptide. Cleavage of proinsulin by proteolytic enzymes produces insulin and free C-peptide.

Relaxin C-peptide, as a synthetic 14-amino acid peptide found in human decidua & placenta, can represent a partial sequence of human relaxin connecting peptide.

C-Type Natriuretic Peptide (CNP) (1-22), human, is the 1-22 fragment of the parent C-Type Natriuretic Peptide.

C-Type Natriuretic Peptide (CNP) (1-22), human acetate is an agonist of natriuretic peptide receptor B (NPR-B), an endothelial-derived relaxant and growth inhibitory factor. C-Type Natriuretic Peptide (CNP) (1-22), human acetate inhibits cAMP synthesis stimulated by histamine and 5-HT or directly by Forskolin.

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

C-MYC PEPTIDE EPITOPE TFA, the product of the c-myc proto-oncogene, is a helix-loop-helix leucine zipper phosphoprotein that regulates gene transcription in cell proliferation, cell differentiation and apoptosis. This peptide is a human c-myc epitope.

C-Type Natriuretic Peptide (CNP) (1-22), human (TFA), is a 22 amino acid fragment of CNP that functions as an agonist for the natriuretic peptide receptor B (NPR-B). It can inhibit cAMP synthesis induced by histamine, 5-HT, or Forskolin, while exhibiting strong endothelial-derived relaxation properties and acting as a growth inhibitor.

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 (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 (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].

Protein Kinase C (19-35) Peptide, acting as a PKC pseudosubstrate inhibitor region, can potentially inhibit PKC activity by blocking the substrate-binding site within the kinase domain, thereby inactivating the cytoplasmic form of PKC [1] [2].

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

c-Myc Peptide Trifluoroacetate is a synthetic peptide corresponding to the C-terminal amino acids (410-419) of human c-myc protein. c-Myc Peptide Trifluoroacetate participates in regulation of growth-related gene transcription.

CNP, a member of the natriuretic peptide family, was first identified in porcine brain and later found in other mammals as well as non-mammals. Processing of the CNP precursor gives rise to CNP-22 and its N-terminally elongated form, CNP-53. The CNPs shar

Thymus peptide C, a hormonal drug derived from the thymus glands of young calves, acts as a substitute for the physiological functions of the thymus.

Peptide comprising residues 33 - 57 of the JNK binding (δ) domain of human c-Jun. Disrupts JNK/c-Jun interaction leading to inhibition of serum-induced c-Jun phosphorylation, up-regulation of p21cip/waf and modulation of inflammatory gene expression. Spec