Apolipoprotein E Antibody [B14G10]

Catalog No.: F0975

Application: Reactivity: Human

Lane 1: Human liver, Lane 2: Human cerebellum, Lane 3: HepG2, Lane 4: Human serum

当該製品は品切れ状态で、ごメールアドレスを教えていただければ、在庫があると、メールで顧客様に伝えます。

代表番号: 045-509-1970|電子メール：sales@selleck.co.jp

使用情報

Dilution
WB1:1000 - 1:10000 IP1:20 IHC1:800 IF1:50 FCM1:20

Application
WB, IP, IHC, IF, FCM

Source
Rabbit Monoclonal Antibody

Reactivity
Human

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
36 kDa 34-37 kDa
^*なぜ予測分子量と実際の分子量が異なるのか？下記の原因により、実際の分子量が予測と異なる：タンパク質の翻訳後修飾（リン酸化/糖鎖付加），スプライシングバリアント，イソフォーム，相対的な電荷，ポリマー。

Datasheet & SDS

生物学的記述

Specificity
Apolipoprotein E Antibody [B14G10] detects endogenous levels of total Apolipoprotein E protein.

Clone
B14G10

Synonym(s)
Apolipoprotein E; Apo-E; APOE

Background
Apolipoprotein E (ApoE) is a glycoprotein produced predominantly by hepatocytes and astrocytes, essential for systemic and central nervous system lipid homeostasis. Circulating as three major isoforms, ApoE2, ApoE3, and ApoE4, which differ at residues Cys112 and Arg158, ApoE mediates receptor-dependent uptake, redistribution, and clearance of cholesterol-rich lipoproteins (HDL, VLDL, chylomicron remnants) throughout the body and brain. Lipid-free ApoE adopts a two-domain organization: an N-terminal receptor-binding domain (residues 1–191, forming a four-α-helix bundle with key motifs for LDL receptor family binding) and a C-terminal domain (residues 210–299) comprising amphipathic helices that mediate lipid association, joined by a flexible hinge. Upon lipidation, ApoE undergoes a conformational “domain unlocking,” exposing binding sites and stabilizing discoidal HDL-like particles. Lipidated ApoE directs lipoproteins to receptors such as LDLR, LRP1, CD36, and HSPGs, facilitating endocytosis, lysosomal lipolysis, cholesterol efflux, and esterification pathways critical for membrane repair, steroidogenesis, and neuronal health. In the brain, astrocyte-derived ApoE3 supports amyloid-β (Aβ) oligomerization and clearance via LRP1, and promotes synaptic plasticity through PI3K/Akt signaling. In contrast, the ApoE4 isoform’s structural instability impairs lipidation, enhances Aβ42 aggregation and seeding, increases neuroinflammation through TLR4/NF-κB activation, and disrupts tau phosphorylation and neurotrophic signaling, conferring a dramatically higher risk for Alzheimer’s disease, atherosclerosis, and neurodegeneration. ApoE2, conversely, enhances receptor binding and clearance, offering cardiovascular protection.

Background

Apolipoprotein E (ApoE) is a glycoprotein produced predominantly by hepatocytes and astrocytes, essential for systemic and central nervous system lipid homeostasis. Circulating as three major isoforms, ApoE2, ApoE3, and ApoE4, which differ at residues Cys112 and Arg158, ApoE mediates receptor-dependent uptake, redistribution, and clearance of cholesterol-rich lipoproteins (HDL, VLDL, chylomicron remnants) throughout the body and brain. Lipid-free ApoE adopts a two-domain organization: an N-terminal receptor-binding domain (residues 1–191, forming a four-α-helix bundle with key motifs for LDL receptor family binding) and a C-terminal domain (residues 210–299) comprising amphipathic helices that mediate lipid association, joined by a flexible hinge. Upon lipidation, ApoE undergoes a conformational “domain unlocking,” exposing binding sites and stabilizing discoidal HDL-like particles. Lipidated ApoE directs lipoproteins to receptors such as LDLR, LRP1, CD36, and HSPGs, facilitating endocytosis, lysosomal lipolysis, cholesterol efflux, and esterification pathways critical for membrane repair, steroidogenesis, and neuronal health. In the brain, astrocyte-derived ApoE3 supports amyloid-β (Aβ) oligomerization and clearance via LRP1, and promotes synaptic plasticity through PI3K/Akt signaling. In contrast, the ApoE4 isoform’s structural instability impairs lipidation, enhances Aβ42 aggregation and seeding, increases neuroinflammation through TLR4/NF-κB activation, and disrupts tau phosphorylation and neurotrophic signaling, conferring a dramatically higher risk for Alzheimer’s disease, atherosclerosis, and neurodegeneration. ApoE2, conversely, enhances receptor binding and clearance, offering cardiovascular protection.

References
[1] Huang Y, et al. Neurobiol Dis. 2014 Dec;72 Pt A:3-12. [2] Chen J, et al. Proc Natl Acad Sci U S A. 2011 Sep 6;108(36):14813-8.

PVDFメンブレン孔径参考表

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

技術サポート

ストックの作り方、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。

Handling Instructions

他に質問がある場合は、お気軽にお問い合わせください。

* 必須

* 大学・企業名 大学・企業名を記入してください

* 名前 名前を記入してください

* 電子メール 電子メール・アドレスを記入してください 有効なメールアドレスを入力してください

電話番号

* 内容 お問い合わせ内容をご入力ください

Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%