关于 "Cytoskeleton & Motor Proteins" 的结果157+ 个结果

C-Reactive Protein (CRP) 77-82 是 C-反应蛋白的 77-82 片段。C-Reactive Protein 可作为炎症的标记，是心血管风险的标志物，可能促进动脉粥样硬化形成。

Interphotoreceptor Retinoid Binding Protein Fragment (IRBP)，具有 20 个残基肽，也是主要的致病表位，存在于光受体间类视黄醇结合蛋白肽 (IRBP 161-180) 的第一个同源重复中, 可引起后葡萄膜炎 (EAU)。

Interphotoreceptor retinoid-binding protein(668-687) 是光受体视黄醇类结合蛋白的 668 到 687 氨基酸序列，可诱发葡萄膜炎。

H13R, a mutation in the metal-binding region of Abeta reduces its copper-mediated toxicity. The native rodent sequence containing an arginine at this position is more tolerant to metals than the human amyloid peptide.

The English (H6R) mutation of β-amyloid peptides accelerates fibrillation without increasing protofibril formation. Ono et al. showed that the English and Tottori mutations alter Abeta assembly at its earliest stages, monomer folding and oligomerization, and produce oligomers that are more toxic to cultured neuronal cells than are wild type oligomers. The exchange of His? by Arg influences the structure of the Cu(II) complex formed by Aβ peptides.

The Iowa (D23N) mutant of Aβ 40 considerably more rapidly assembles in solution to form fibrils than the WT Aβ sequence. These fibrils also show a different structure, which could be responsible for their increased toxicity.

The Tottori (D7N) mutation of β-amyloid peptides accelerates fibrillation without increasing protofibril formation. Ono et al. showed that the English and Tottori mutations alter Abeta assembly at its earliest stages, monomer folding and oligomerization, and produce oligomers that are more toxic to cultured neuronal cells than are wild type oligomers.

The G37D mutant does not show the aggregation behavior of WT Abeta42 nor its neurotoxicity.

Cys-Aβ1-40 can be easily and selectively modified, labeled, coupled to carriers e.g. by maleimide chemistry without affecting the sequences involved in fibril formation. The free mercapto moiety of the peptide adheres to gold surfaces.

Aβ40 S26C has been used for generating the covalently linked Aβ40 homodimer. Dimerization can be easily reverted by reducing the soluble dimer with thiols as β-mercaptoethanol. Aβ40 S26C is perfectly suited for labeling with fluorescent tags

A prion peptide

Myelin Basic Protein(87-99) TFA 是一种致脑肽，可诱导碱性蛋白特异性 T 细胞增殖。Myelin Basic Protein(87-99) TFA 在外周血单核细胞中引起 Th1 极化，与多发性硬化症 (MS) 有关。

2:PN:US20040072744SEQID:2claimedprotein是一种合成多肽，可用于唐氏综合症和精神分裂症的研究。

髓鞘碱性蛋白 (68-82)，豚鼠是髓鞘碱性蛋白 (MBP) 的片段。

HIV-1 tat Protein (47-57) is a potent cell penetrating peptides.

Interphotoreceptor Retinoid Binding Protein Fragment (IRBP) TFA，具有 20 个残基肽，也是主要的致病表位，存在于光受体间类视黄醇结合蛋白肽 (IRBP 161-180) 的第一个同源重复中, 可引起后葡萄膜炎 (EAU)。

This all-D peptide contains two retro-inverso peptide klvff motifs of KLVFF (H-3682) corresponding to amino acids 16 to 20 of amyloid β-protein. The tandem dimer retro-inverso peptide showed about a 100-fold higher binding affinity (Kd = 1.3 . 10?² µM) for amyloid β-protein (1-40) fibrils than KLVFF (Kd = 1.1 ± 0.3 µM). It was also found to be more effective in preventing ordered fibril formation than the parent peptide KLVFF as judged by its increased ability to inhibit thioflavin T binding to β-sheet structures.

一种MBP拮抗剂

A CaMKII inhibitor

The Osaka mutation was the first deletion-type mutation to be identified in APP and Aβ. The Aβ E22delta mutant is more resistant to degradation by two major Aβ-degrading enzymes, neprilysin and insulin-degrading enzyme. Synthetic mutant Aβ showed unusual aggregation properties with enhanced oligomerization but no fibrillization. It also inhibited hippocampal long-term potentiation more efficiently than wild-type Aβ. A transgenic mouse model containing APP with the E693delta mutation has been developed. APP(OSK)-Tg mice exhibit intraneuronal Aβ E22delta oligomers and memory impairment as early as eight months of age.

Transgenic mice expressing the vasculotropic Dutch/Iowa (E693Q/D694N) mutant human Aβ precursor protein in brain (Tg-SwDI) accumulate abundant cerebral microvascular fibrillar amyloid deposits and exhibit robust neuroinflammation. In vitro, the doubly mutated Aβ peptides showed an increased propensity to fibrillation and pathogenicity compared to the Dutch and Iowa single mutants.

Oxidation of Met35 attenuates the formation of Aβ40 oligomers.

(Met(O)³?)-Amyloid β-protein (1-42) (H-5888), in contrast to Aβ 1-42 (H-1368), has been shown to be non-toxic to 9-11 day-old rat embryonic hippocampal neuronal cultures and not to produce any protein oxidation. It has also been demonstrated that fibril formation is not affected by Met(O)³?. For the Nle analog see H-7308.

Sulfoxide of Aβ 25-35.