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A4559

Sigma-Aldrich

Amyloid β-Protein Fragment 25-35

≥97% (HPLC)

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250 μG
100,00 €
1 MG
279,00 €

About This Item

Formula empirica (notazione di Hill):
C45H81N13O14S
Numero CAS:
Peso molecolare:
1060.27
Numero MDL:
Codice UNSPSC:
12352202
ID PubChem:
NACRES:
NA.32

100,00 €


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Livello qualitativo

Saggio

≥97% (HPLC)

Stato

powder

Composizione

Protein Content, ≥80%

N° accesso UniProt

Temperatura di conservazione

−20°C

Stringa SMILE

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)
WIHBNMPFWRHGDF-UHFFFAOYSA-N

Informazioni sul gene

human ... APP(351)

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Amino Acid Sequence

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

Descrizione generale

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.[1] Aβ25-35 lacks the N-terminal domain and the metal binding site and is majorly generated by proteolytic cleavage of Aβ(1−40) peptides.[1] It has a β-sheet and β-turn structure.[2]

Applicazioni

Amyloid β-Protein Fragment 25-35 has been used:
  • to induce neurotoxicity in cortical cultures[3]
  • to induce Alzheimer′s disease in rat model[4]
  • to induce apoptosis in mesenchymal stem cells (MSCs)[5]

Azioni biochim/fisiol

Amyloid β-Protein Fragment 25-35 (Aβ25-35) is involved in the pathogenesis of Alzheimer′s disease.[6] Inhibitors of this transition may serve as a potential agent in managing Alzheimer′s disease.[2] 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.[7]

Altre note

Lyophilized from 0.1% TFA in H2O

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Punto d’infiammabilità (°F)

Not applicable

Punto d’infiammabilità (°C)

Not applicable

Dispositivi di protezione individuale

Eyeshields, Gloves, type N95 (US)


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Rapid aggregation and assembly in aqueous solution of Abeta (25-35) peptide
Millucci L, et al.
Journal of Biosciences, 34(2), 293-303 (2009)
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
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
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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