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Merck

A4559

Amyloid β-Protein Fragment 25-35

≥97% (HPLC)

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제품정보 (DICE 배송 시 비용 별도)

실험식(Hill 표기법):
C45H81N13O14S
CAS 번호:
Molecular Weight:
1060.27
NACRES:
NA.32
PubChem Substance ID:
UNSPSC Code:
12352202
MDL number:
Form:
powder
Assay:
≥97% (HPLC)
기술 서비스
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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)

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 key

WIHBNMPFWRHGDF-UHFFFAOYSA-N

assay

≥97% (HPLC)

form

powder

composition

Protein Content, ≥80%

UniProt accession no.

storage temp.

−20°C

Quality Level

Gene Information

human ... APP(351)

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

저장 등급

11 - Combustible Solids

wgk

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)


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문서 라이브러리에서 최근에 구매한 제품에 대한 문서를 찾아보세요.

문서 라이브러리 방문

Conformations and biological activities of amyloid beta peptide 25-35
Millucci L, et al.
Current Protein and Peptide Science, 11(1), 54-67 (2010)
MicroRNA Let-7f-5p Promotes Bone Marrow Mesenchymal Stem Cells Survival by Targeting Caspase-3 in Alzheimer Disease Model
Han L, et al.
Frontiers in Neuroscience, 12 (2018)
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
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)
Leticia R Dare et al.
Frontiers in behavioral neuroscience, 14, 152-152 (2020-09-26)
Alzheimer's disease (AD) is the leading cause of dementia in the world, accounting for 50-75% of cases. Currently, there is limited treatment for AD. The current pharmacological therapy minimizes symptom progression but does not reverse brain damage. Studies focused on

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