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Gastrin and Gastrin Sequences
Browse products name by alphabetical order:
|Cat. #||Product Name||Price|
|G03002||Leptin (93-105), human||Inquiry|
|G03019||Leptin (22-56), human.||Inquiry|
|G03004||Leptin (116-130), mouse.||Inquiry|
|G03001||GRP (18-27) (human, porcine, canine)||Inquiry|
|G03009||Gastrin-Releasing Peptide (1-17)||Inquiry|
|G03014||Gastrin-1, human, sulfated (Gastrin II)||Inquiry|
|G03021||Gastrin Tetrapeptide, Gastrin (14-17), human||Inquiry|
|G03015||Gastrin Releasing Peptide, porcine||Inquiry|
|G03016||Gastrin Releasing Peptide, human||Inquiry|
Gastrins are peptide hormones secreted by G cells from the gastric antrum and duodenal mucosa. They were discovered and named in 1906 by British scholar Edkins. Post-translational processing of gastrin is a typical process of processing a prohormone into a prohormone, which is processed into a biologically active body with different functions, wherein amidated gastrin is the main product. Gastrin is a class of gastrointestinal hormones that normally promote gastric acid secretion and gastrointestinal mucosal growth by binding to corresponding receptors. Exogenous gastrin can cause the development of various tumors (including gastric cancer, intestinal cancer, pancreatic cancer, esophageal cancer, etc.) by autocrine, paracrine or endocrine methods. Gastrin has now become a target for the treatment of related tumors.
Mechanism of action
Normally, the amidoxime gastrin exerts an effect of promoting gastric acid secretion and gastric mucosal cell growth by endocrine means. The main by enterochromaffin-like cells (enterochromaffin-like cells, ECL) on CCK-B receptor (cholecystokinin B receptors, CCKBR), promoting gene expression (particularly histamine synthesis and storage related gene) and histamine secretion, and then histamine stimulates parietal cells to secrete gastric acid. Gastrin also binds to CCK-B receptors on parietal cells and promotes gastric acid secretion by causing changes in Ca2+ concentrations in parietal cells. Gastrin regulates cell growth, differentiation, and apoptosis by activating various signaling pathways, including ERK 1/2, JNK, p38-MAPK signaling pathway, and JAK2-STAT3 signaling pathway. Gastrin participates in tumor formation by activating these signaling pathways.
Application of Gastrin and Gastrin Sequences
At present, anti-gastrin has become an effective means for treating related tumors, and specific methods thereof include secretion inhibition, receptor antagonism and anti-gastrin antibody method. The main receptor for gastrin binding is CCK-R. CCK-R antagonists mainly include specific CCK-AR antagonists, specific CCK-BR antagonists, and non-specific CCK-R antagonists. Its anti-tumor effect has been confirmed in both in vitro and in vivo experiments and clinical trials. Anti-gastrin antibody methods include passive immunization and active immunization, and passive immunization includes anti-gastrin 17 polyclonal or monoclonal antibody.
1. Smith, J. P, Fonkoua, L. K, & Moody, T. W. (2016). The role of gastrin and cck receptors in pancreatic cancer and other malignancies. International Journal of Biological Sciences, 12(3), 283-291.
2. Hayakawa, Y., Chang, W., Jin, G., & Wang, T. C. (2016). Gastrin and upper gi cancers. Current Opinion in Pharmacology, 31, 31-37.