多肽課題組

課題組網(wǎng)址：https://www.mls.ls.tum.de/pbch/home/

我們的研究旨在了解蛋白質(zhì)和多肽的生物分子相互作用通過肽化學介導生物學和疾病相關的過程，并開發(fā)新的分子和工具來控制或可視化這些過程。

我們特別有興趣理解介導淀粉樣蛋白錯誤折疊和相關細胞變性的蛋白質(zhì)相互作用，以及設計基于肽的分子和化學方法來抑制這些過程。我們還有興趣表征動脈粥樣硬化中的促炎性趨化因子相互作用，并設計肽來調(diào)節(jié)這些相互作用并控制它們的作用。我們正在使用蛋白質(zhì)（肽）化學設計和合成策略以及廣泛的生化和生物物理方法。

當前的研究活動目的是：

了解蛋白質(zhì)錯誤折疊和淀粉樣蛋白自組裝潛在的細胞變性和蛋白質(zhì)聚集疾病的發(fā)病機理，阿爾茨海默氏?。ˋD）和II型糖尿病（T2D）。
設計基于肽的分子以干擾或可視化淀粉樣蛋白自組裝為AD和T2D中的治療鉛或非侵入性淀粉樣蛋白診斷。 
表征了促炎的非典型趨化因子MIF與其受體的相互作用，并設計了構(gòu)象約束的肽，以干預這些相互作用，作為動脈粥樣硬化的治療鉛。

Our research aims at understanding biomolecular interactions of proteins and polypeptides mediating biological and disease-associated processes via peptide chemistry and at developing novel molecules and tools to control or visualize these processes.

We are especially interested in understanding protein interactions mediating amyloid protein misfolding and related cell degeneration and in devising peptide-based molecules and chemical approaches to suppress these processes. We are also interested in characterizing proinflammatory chemokine interactions in atherosclerosis and in designing peptides to modulate these interactions and control their effects. We are using protein(peptide) chemical design and synthesis strategies and a broad range of biochemical and biophysical methods.

Current research activities aim at:

understanding protein misfolding and amyloid self-assembly underlying cell degeneration and pathogenesis of the protein aggregation diseases Alzheimer`s disease (AD) and type II diabetes (T2D).
devising peptide-based molecules to interfere with or visualize amyloid self-assembly as therapeutic leads or non-invasive amyloid diagnostics in AD and T2D. 
characterizing interactions of the proinflammatory atypical chemokine MIF with its receptors and designing conformationally constrained peptides to intervene with these interactions as therapeutic leads for atherosclerosis.