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LL-37, human 是一种由37 个氨基酸残基组成的两亲性组织蛋白酶衍生的抗菌肽，具有广泛的抗菌活性。它有助于保护角膜免受感染，对于伤口愈合有着良好的促进作用，同时对多种革兰氏阳性和革兰氏阴性病原体具有抗菌和抗生物膜活性。

LL-37, human is a 37-residue, amphipathic, cathelicidin-derived antimicrobial peptide, which exhibits a broad spectrum of antimicrobial activity. LL-37, human could help protect the cornea from infection and modulates wound healing.

LL-37是一种具有血管生成活性的抗菌肽。它对应于人组织蛋白酶抗菌蛋白hCAP18/LL-37的C末端序列（134-170），并通过蛋白水解过程从hCAP18/LL-37细胞外释放。hCAP18/LL-37是先天免疫系统的效应器，在白细胞和上皮细胞中表达，与炎症和损伤相关上调。可以证明hCAP18/LL-37在一系列乳腺癌中的过表达。LL-37被认为部分通过甲酰肽受体样1（FPRL1）刺激上皮细胞增殖，因为用百日咳毒素阻断受体会使LL-37的增殖作用降低约50%。

LL-37 is an antimicrobial peptide with angiogenic activity. It corresponds to the C-terminal sequence (134-170) of the human cathelicidin antimicrobial protein hCAP18/LL-37 and is extracellularly released from hCAP18/LL-37 by proteolytic processing. hCAP18/LL-37 is an effector of the innate immune system and is expressed in leukocytes and epithelial cells where it is upregulated in association with inflammation and injury. An overexpression of hCAP18/LL-37 in a series of breast carcinomas could be demonstrated. LL-37 has been suggested to stimulate epithelial cell proliferation partially through formyl peptide receptor-like 1 (FPRL1) since blocking the receptor with pertussis toxin decreased the proliferative effect of LL-37 by approximately 50 %.

Peptide H-VKDLATVYVDVLK-OH is a Research Peptide with significant interest within the field academic and medical research. Recent citations using H-VKDLATVYVDVLK-OH include the following: Lysine glycation of apolipoprotein AI impairs its anti-inflammatory function in type 2 diabetes mellitus D Liu, L Ji, M Zhao, Y Wang, Y Guo, L Li - Journal of Molecular and , 2018 - Elsevierhttps://www.sciencedirect.com/science/article/pii/S002228281830734X

LL-37 is a 37 amino acid peptide that is produced by neutrophils and other leukocytes. This peptide has been shown to have anti-inflammatory properties, which may be due to its ability to bind and activate the G protein coupled receptor (GPCR) formyl peptide receptor-like 1 (FPRL1), leading to inhibition of the production of inflammatory mediators such as IL-8. LL-37 also binds to ion channels, which may lead to membrane depolarization, thereby blocking calcium influx into the cell. LL-37 has been shown to inhibit the activation of T cells by inhibiting T cell receptor signaling and reducing cytokine production.\nLL-37 also has a high affinity for antibody binding sites on B cells and macrophages and can bind with high specificity to IgE on mast cells, leading to inhibition of mast cell degranulation. The binding of LL-37 with these receptors leads to reduced inflammation in tissues, which may

LL-37 is a potent antimicrobial peptide that has been shown to be effective against cancer cells and is currently being investigated as a potential antineoplastic agent. LL-37 binds to the leukocyte receptor, which leads to chemotaxis, increased expression of p53 and apoptosis. LL-37 also induces apoptotic cell death in epithelial tissues, both in vitro and in vivo. This peptide has been shown to induce death in cancer cells, as well as cell death in other types of cells.