所有图片(1)
About This Item
经验公式（希尔记法）:
C45H81N13O14S
CAS号:
分子量:
1060.27
MDL號碼:
分類程式碼代碼:
51111800
PubChem物質ID:
NACRES:
NA.32
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品質等級
化驗
≥95% (HPLC)
形狀
powder
UniProt登錄號
儲存溫度
−20°C
SMILES 字串
CCC(C)C(NC(=O)CNC(=O)C(CC(C)C)NC(=O)C(N)CCSC)C(=O)NC(C(C)CC)C(=O)NC(C)C(=O)NCC(=O)NC(CCCCN)C(=O)NC(CC(N)=O)C(=O)NC(CO)C(=O)NCC(O)=O
InChI
1S/C45H81N13O14S/c1-9-24(5)36(57-34(62)20-50-40(67)29(17-23(3)4)54-39(66)27(47)14-16-73-8)45(72)58-37(25(6)10-2)44(71)52-26(7)38(65)49-19-33(61)53-28(13-11-12-15-46)42(69)55-30(18-32(48)60)43(70)56-31(22-59)41(68)51-21-35(63)64/h23-31,36-37,59H,9-22,46-47H2,1-8H3,(H2,48,60)(H,49,65)(H,50,67)(H,51,68)(H,52,71)(H,53,61)(H,54,66)(H,55,69)(H,56,70)(H,57,62)(H,58,72)(H,63,64)
InChI 密鑰
IDGOADDOQWKZOX-UHFFFAOYSA-N
基因資訊
human ... APP(351)
Amino Acid Sequence
Met-Leu-Gly-Ile-Ile-Ala-Gly-Lys-Asn-Ser-Gly
一般說明
β淀粉样前体蛋白(APP)属于Ⅰ型跨膜蛋白。APP广泛表达，主要存在于突触与神经元中。APP基因位于人染色体 21q21.3。
應用
β淀粉样蛋白片段35-25可作为对照肽，用于Aβ诱导的细胞凋亡，研究铁调素过表达对小鼠β淀粉样蛋白诱导的大脑损伤的影响。
生化／生理作用
β淀粉样前体蛋白(APP)经水解形成β淀粉样蛋白(Aβ)，沉积为阿尔茨海默病的主要生物标志物——大脑淀粉样斑块。APP参与神经发生、突触形成、轴突运输、神经元迁移和神经突生长。还参与线粒体相关内质网膜(MAM)活动、抗菌保护作用、胆固醇和铁稳态过程。β淀粉样蛋白片段35-25是失活对照。
其他說明
片段 25-35的N—C反向序列
儲存類別代碼
11 - Combustible Solids
水污染物質分類（WGK）
WGK 3
閃點（°F）
Not applicable
閃點（°C）
Not applicable
個人防護裝備
Eyeshields, Gloves, type N95 (US)
其他客户在看
Jasmine Chebli et al.
Scientific reports, 11(1), 19115-19115 (2021-09-29)
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Anatoliy I Yashin et al.
Mechanisms of ageing and development, 196, 111477-111477 (2021-04-03)
Emerging evidence from experimental and clinical research suggests that stress-related genes may play key roles in AD development. The fact that genome-wide association studies were not able to detect a contribution of such genes to AD indicates the possibility that
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Elvis Cuevas et al.
Metabolic brain disease, 34(5), 1365-1374 (2019-07-04)
The amyloid β-peptide (Aβ) is transported across the blood-brain barrier (BBB) by binding with the receptor for advanced glycation end products (RAGE). Previously, we demonstrated that the Aβ fraction 25-35 (Aβ25-35) increases RAGE expression in the rat hippocampus, likely contributing
Xinwei Zhang et al.
Cell death discovery, 6(1), 113-113 (2020-12-11)
Progressive iron accumulation in the brain and iron-induced oxidative stress are considered to be one of the initial causes of Alzheimer's disease (AD), and modulation of brain iron level shows promise for its treatment. Hepcidin expressed by astrocytes has been
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