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Merck

A4559

Sigma-Aldrich

Amyloid β-Protein Fragment 25-35

≥97% (HPLC)

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About This Item

Fórmula empírica (notación de Hill):
C45H81N13O14S
Número de CAS:
Peso molecular:
1060.27
MDL number:
UNSPSC Code:
12352202
PubChem Substance ID:
NACRES:
NA.32

Quality Level

assay

≥97% (HPLC)

form

powder

composition

Protein Content, ≥80%

UniProt accession no.

storage temp.

−20°C

SMILES string

CCC(C)C(NC(=O)C(NC(=O)C(C)NC(=O)CNC(=O)C(CCCCN)NC(=O)C(CC(N)=O)NC(=O)C(CO)NC(=O)CN)C(C)CC)C(=O)NCC(=O)NC(CC(C)C)C(=O)NC(CCSC)C(O)=O

InChI

1S/C45H81N13O14S/c1-9-24(5)36(43(69)50-21-35(63)52-29(17-23(3)4)40(66)55-28(45(71)72)14-16-73-8)58-44(70)37(25(6)10-2)57-38(64)26(7)51-34(62)20-49-39(65)27(13-11-12-15-46)54-41(67)30(18-32(48)60)56-42(68)31(22-59)53-33(61)19-47/h23-31,36-37,59H,9-22,46-47H2,1-8H3,(H2,48,60)(H,49,65)(H,50,69)(H,51,62)(H,52,63)(H,53,61)(H,54,67)(H,55,66)(H,56,68)(H,57,64)(H,58,70)(H,71,72)

InChI key

WIHBNMPFWRHGDF-UHFFFAOYSA-N

Gene Information

human ... APP(351)

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Amino Acid Sequence

Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met

General description

Amyloid β-Protein Fragment 25-35 (Aβ25-35) is derived from the amyloid-β protein.amyloid-β protein, which is mapped to human chromosome 21q21. Aβ25-35 lacks the N-terminal domain and the metal binding site and is majorly generated by proteolytic cleavage of Aβ(1−40) peptides. It has a β-sheet and β-turn structure.

Application

Amyloid β-Protein Fragment 25-35 has been used:
  • to induce neurotoxicity in cortical cultures
  • to induce Alzheimer′s disease in rat model
  • to induce apoptosis in mesenchymal stem cells (MSCs)

Biochem/physiol Actions

Amyloid β-Protein Fragment 25-35 (Aβ25-35) is involved in the pathogenesis of Alzheimer′s disease. Inhibitors of this transition may serve as a potential agent in managing Alzheimer′s disease. It is present in the subiculum and entorhinal cortex neurons of Alzheimer′s brain samples and inclusion-body myositis (IBM) muscle. It binds to receptors present in microglia and is capable of lipid membrane insertion. The functional domain sequence of Aβ comprising of sequence GSNKGAIIGLM elicits neurotrophic and neurotoxic effects. Aβ25-35 exhibits rapid aggregation and displays age dependant neurotoxicity.

Other Notes

Lyophilized from 0.1% TFA in H2O

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)


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Visite la Librería de documentos

Rapid aggregation and assembly in aqueous solution of Abeta (25-35) peptide
Millucci L, et al.
Journal of Biosciences, 34(2), 293-303 (2009)
Wen Zhou et al.
Frontiers in aging neuroscience, 13, 629891-629891 (2021-03-13)
The pathogenesis of Alzheimer's disease (AD) involves activation of many NLRP3 inflammatory bodies, which may be related to amyloid β peptide and aggregation of misfolded proteins. Autophagy is an important regulator of inflammatory bodies. However, autophagy shows dynamic changes in
Jiale Wang et al.
Evidence-based complementary and alternative medicine : eCAM, 2022, 6091671-6091671 (2022-03-29)
Jiedu-Yizhi formula (JDYZF) is prescribed for the treatment of Alzheimer's disease (AD) and was created by Jixue Ren, a master of traditional Chinese medicine, based on the "marrow deficiency and toxin damage" theory. In our clinic, this formula has been
RKIP-Mediated NF-kappaB Signaling is involved in ELF-MF-mediated improvement in AD rat
Zuo H, et al.
International Journal of Molecular Sciences, 15(14), 1658-1658 (2018)
Farnaz Nikbakht et al.
Basic and clinical neuroscience, 10(6), 557-566 (2020-06-02)
Cognitive dysfunction is the most common problem of patients with Alzheimer Disease (AD). The pathological mechanism of cognitive impairment in AD may contribute to neuronal loss, synaptic dysfunction, and alteration in neurotransmitters receptors. Mitochondrial synapses dysfunction due to the accumulation

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