AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE
AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE атрибут
Температура кипения: |
1517.3±65.0 °C(Predicted) |
плотность: |
1.248±0.06 g/cm3(Predicted) |
RTECS: |
BU7435200 |
температура хранения: |
-20°C |
растворимость: |
нерастворим в EtOH; нерастворим в H2O; ≥106 мг/мл в ДМСО |
форма: |
Лиофилизированный. |
пка: |
3.24±0.10(Predicted) |
цвет: |
Lyophilized White |
Растворимость в воде: |
Растворим в воде. |
Последовательность: |
H-Gly-Ser-Asn-Lys-Gly-Ala-Ile-Ile-Gly-Leu-Met-OH |
ИнЧИКей: |
WIHBNMPFWRHGDF-SLVFWPMISA-N |
Заявления о рисках и безопасности
WGK Германия |
3 |
кода HS |
2930909899 |
AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE химические свойства, назначение, производство
Использование
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)
Общее описание
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.
Биохимия/физиол Действия
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.
AMYLOID BETA-PROTEIN (HUMAN, 25-35) TRIFLUOROACETATE препаратная продукция и сырье
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