Search results for: 'Peptide'

Cat.No. 产品名称 Information

GA20722 Amyloid β-Protein (1-14) The N-terminal Aβ fragments Aβ1-14, Aβ1-15 (H-6368), and Aβ1-16 (H-2958) are elevated in cell media and in CSF in response to γ-secretase inhibitor treatment. The presence of these small peptides is consistent with a catabolic amyloid precursor protein cleavage pathway by β- followed by α-secretase. It has been shown that Aβ1-14, Aβ1-15, and Aβ1-16 increase dose-dependently in response to γ-secretase inhibitor treatment while Aβ1-42 levels are unchanged.

GA20718 Amyloid β/A4 Protein Precursor₇₇₀ (667-676)

Β-基质分泌酶Ⅲ

The peptide substrate APP (667-676), SEVKMDAEFR, corresponds to the wild-type amyloid precursor protein (APP) β-secretase cleavage site. SEVKMDAEFR has been used for assaying β-secretase activity.

GA20534 Acetyl-Amyloid β-Protein (15-20) amide Incubation of Ac-QKLVFF-NH? with the amyloid β-protein (1-40) inhibited polymerization of the amyloid β-protein (1-40) into amyloid fibrils. The peptide is thought to block the polymerization sites.

GA20283 (Pyr³)-Amyloid β-Protein (3-40) The pyroglutamate-modified amyloid-β peptides derived from Aβ40 (H-7422) and Aβ42 (H-4796) have gained considerable attention as potential key participants in the pathology of Alzheimer's disease (AD) due to their abundance in AD brain, high aggregation propensity, stability, and cellular toxicity. Aβ40 and 42 can be N-terminally truncated by action of cathepsin B. The cyclization of Glu³ is catalyzed by glutaminyl cyclase. Hence, inhibition of these enzymes could be a therapeutic approach to AD.

GA20282 (Pyr¹¹)-Amyloid β-Protein (11-40) pEVHHQKLVFFAEDVGSNKGAIIGLMVGGVV, the N-terminally truncated isoform of the amyloid β-protein (Aβ) beginning with a pyroglutamate (Pyr) residue at position 11 was used in experiments studying the generality of fibrillogenesis-related helix formation. Comparing the fibrillogenesis kinetics of many of the most important clinically relevant amyloid β-protein alloforms it could be observed that among these peptides (Pyr¹¹)-amyloid β-protein (11-40) exhibited the greatest retardation of fibrillization rate.

GA20259 (Nle³⁵)-Amyloid β-Protein (1-40) The reactive thioether of Met³? is crucial for the activity of Aβ 1-40 and Aβ 1-42. Due to the replacement of Met by inert Nle, M35Nle Aβ 1-40 was no longer toxic to cultured hippocampal neurons and had little effect on the level of protein carbonyl residues. The Nle peptide showed the same propensity to aggregate, whereas sulfoxide formation hindered the required conformational transition from random coil to β-sheet.

GA20200 (Gly²²)-Amyloid β-Protein (1-42) The arctic mutant of amyloid β peptide 1-42, in which Glu²² is substituted by Gly, is distinctly more amyloidogenic than the wild-type Aβ 1-42.

GA20197 (Gly²¹)-Amyloid β-Protein (1-40) Contrary to β-amyloid peptides mutated at position 22 (Dutch, Italian, Arctic mutants) the Flemish mutation (A21G) shows a decreased tendency to aggregate and a reduced neurotoxicity. In the studies of Betts and Tsubuki, A21G was degraded significantly more slowly by neprilysin than the wild-type Aβ 1-40 and the E22 mutants. The relative resistance to proteolytic degradation may account for the pathogenicity of the Aβ mutant.

GA20184 (Gln²²,Asn²³)-Amyloid β-Protein (1-40) 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.

GA20050 (Cys⁰)-Amyloid β-Protein (1-40) 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.

GA20042 (Asn⁷)-Amyloid β-Protein (1-40) 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.

GA20041 (Asn⁶⁷⁰,Sta⁶⁷¹,Val⁶⁷²)-Amyloid β/A4 Protein Precursor₇₇₀ (662-675) Amyloid precursor protein (APP) β-secretase from human brain cleaves full-length APP at the amino terminus of the amyloid β-protein (Aβ) sequence, thus leading to the generation and extracellular release of β-cleaved soluble APP and a corresponding cell-associated carboxy-terminal fragment. The subsequent cleavage of the C-terminal fragment by γ-secretase(s) leads to the formation of Aβ. This new peptide represents a potent substrate analog inhibitor of APP β-secretase with IC?? = 30 nM.

GA20040 (Asn⁶⁷⁰,Leu⁶⁷¹)-Amyloid β/A4 Protein Precursor₇₇₀ (667-676)

Β-基质分泌酶Ⅱ

This peptide substrate corresponds to the 'Swedish' Lys-Met/Asn-Leu (K670N/M671L) mutation of the amyloid precursor protein (APP) β-secretase cleavage site. It has been used for assaying β-secretase activity.

GA20039 (Asn⁶⁷⁰,Leu⁶⁷¹)-Amyloid β/A4 Protein Precursor₇₇₀ (667-675) SEVNLDAEF corresponds to the mutant junctional sequence of the amyloid precursor protein (APP) found in a Swedish family with early-onset Alzheimer's disease, therefore referred to as the 'Swedish' mutation (K670N/M671L). The peptide has been used for assaying cleavage at leucine-aspartate by cathepsin G and chymotrypsin, whereas neither cathepsin B, D nor L generated any products.

GA20029 (Arg¹³)-Amyloid β-Protein (1-40) 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.

GP10097 Amyloid β-Protein (1-15)

H2N-Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-Val-His-His-Gln-OH

淀粉样蛋白 β-蛋白 (1-15) 是 β-淀粉样蛋白肽的片段。

GP10083 Beta-Amyloid (1-11)

H2N-Asp-Ala-Glu-Phe-Arg-His-Asp-Ser-Gly-Tyr-Glu-OH

Beta-Amyloid (1-11) 是 Amyloid-&#946 的片段；肽，可用于神经系统疾病的研究。

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