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D-SAL和NAP:两种共享SIP结构域的肽。

D-SAL and NAP: Two Peptides Sharing a SIP Domain.

作者信息

Gozes Illana, Sragovich Shlomo, Schirer Yulie, Idan-Feldman Anat

机构信息

The Lily and Avraham Gildor Chair for the Investigation of Growth Factors, The Dr. Diana and Zelman Elton (Elbaum) Laboratory for Neuroendocrinology, Department of Human Molecular Genetics and Biochemistry, Sackler Faculty of Medicine, Sagol School of Neuroscience and The Adams Super Center for Brain Studies, Tel Aviv University, Tel Aviv, 69978, Israel.

出版信息

J Mol Neurosci. 2016 Jun;59(2):220-31. doi: 10.1007/s12031-015-0701-8.

Abstract

NAPVSIPQ (NAP) and all D-amino acid SALLRSIPA (D-SAL) are neuroprotective peptides derived from activity-dependent neuroprotective protein (ADNP) and activity-dependent neurotrophic factor (ADNF), respectively. Both proteins were shown to protect against cognitive impairment, using different animal models and to increase neuronal survival following exposure to neurotoxins. NAP was extensively tested and found to increase microtubule stability, protect axonal transport, and inhibit apoptosis. Here, we aimed to further evaluate and correlate effects at the behavioral level, in a rat model of diabetes. Diabetes is primarily a metabolic disorder which presents secondary neurological manifestations. Diabetes induces peripheral nervous system damage which is translated into impaired sensory perception and is termed diabetic neuropathy. Diabetes-related central nervous system damage causes cognitive decline. The behavioral study aimed to evaluate the effect of NAP and D-SAL on peripheral neuropathy and cognitive decline. Peripheral neuropathy was tested by measuring the response to a thermal stimulus, and cognitive ability was measured by a social memory test and a spatial memory test using long- and short-term dependent tasks and a reference memory task. Results indicated an immediate sensory neuropathy in the diabetic model, which was prevented by both peptides and a later neuropathic phase, prevented only by NAP treatment. Cognitive tests revealed impaired performance in both social and spatial memory tests in the diabetes model. Each of the peptides improved different aspects of cognitive behavior, with NAP being more potent than D-SAL. Mechanistically, both NAP and SAL contain a SIP (SxIP) domain that has been shown to interact with microtubule end-binding proteins (EBs). Specifically, we have previously shown a direct interaction of NAP with EB1 and EB3; we have further shown an interaction of the NAP-derived 4 amino acid SKIP peptide with EB3, stimulating axonal transport. Interestingly, the all D-amino acid peptide, D-SKIP, only partially mimicked SKIP activity. Our current results implicate D-SAL activity with potentially reduced potency compared to NAP, partially mimicking the SKIP/D-SKIP results and placing the SIP (SxIP) motif as a central focus for microtubule-based neuroprotection.

摘要

NAPVSIPQ(NAP)和所有D - 氨基酸SALLRSIPA(D - SAL)分别是源自活性依赖神经保护蛋白(ADNP)和活性依赖神经营养因子(ADNF)的神经保护肽。使用不同的动物模型均已表明这两种蛋白可预防认知障碍,并在暴露于神经毒素后提高神经元存活率。NAP经过广泛测试,发现其可增加微管稳定性、保护轴突运输并抑制细胞凋亡。在此,我们旨在进一步评估并关联在糖尿病大鼠模型行为水平上的效应。糖尿病主要是一种代谢紊乱疾病,会出现继发性神经学表现。糖尿病会导致外周神经系统损伤,进而转化为感觉知觉受损,称为糖尿病性神经病变。糖尿病相关的中枢神经系统损伤会导致认知能力下降。该行为学研究旨在评估NAP和D - SAL对周围神经病变和认知能力下降的影响。通过测量对热刺激的反应来测试周围神经病变,通过使用长期和短期依赖任务以及参考记忆任务的社会记忆测试和空间记忆测试来测量认知能力。结果表明糖尿病模型中存在即时性感觉神经病变,两种肽均可预防该病变,而后期神经病变阶段仅NAP治疗可预防。认知测试显示糖尿病模型在社会和空间记忆测试中的表现均受损。每种肽均改善了认知行为的不同方面,其中NAP比D - SAL更有效。从机制上讲,NAP和SAL均含有一个已被证明可与微管末端结合蛋白(EBs)相互作用的SIP(SxIP)结构域。具体而言,我们之前已表明NAP与EB1和EB3存在直接相互作用;我们进一步表明源自NAP的4氨基酸SKIP肽与EB3相互作用,刺激轴突运输。有趣的是,全D - 氨基酸肽D - SKIP仅部分模拟了SKIP活性。我们目前的结果表明,与NAP相比,D - SAL的活性可能降低,部分模拟了SKIP/D - SKIP的结果,并将SIP(SxIP)基序作为基于微管的神经保护的核心关注点。

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