Apolipoprotein CI/Apo-CI Antibody [N16B24]

Catalog No.: F2820

Application: Reactivity: Human

Lane 1: Human plasma

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

使用情報

Dilution
WB1:1000 IP1:40 IHC1:800

Application
WB, IP, IHC

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
9 kDa 6.6 kDa, 88 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 CI/Apo-CI Antibody [N16B24] detects endogenous levels of total Apolipoprotein CI/Apo-CI protein.

Clone
N16B24

Synonym(s)
Apolipoprotein C-I; Apo-CI; ApoC-I; Apolipoprotein C1; APOC1

Background
Apolipoprotein CI (c), the smallest exchangeable apolipoprotein, is derived from an 83-residue precursor and is mainly expressed in the liver and macrophages. It circulates on HDL, VLDL, and chylomicrons, adopting a structure of two antiparallel α-helices connected by a flexible hinge with hydrophobic stacking interactions, and a lysine/arginine-rich C-terminal region that enables lipoprotein binding through electrostatic and amphipathic lipid interactions. ApoC-I strongly inhibits cholesteryl ester transfer protein (CETP) by increasing HDL electronegativity via its positively charged C-terminal helix, disrupting HDL-CETP complexes and thereby restricting neutral lipid transfer between HDL and triglyceride-rich lipoproteins (TRLs). ApoC-I competitively displaces apoE from β-VLDL, impairing receptor-mediated clearance via the LDL receptor-related protein (LRP), VLDL receptor, and LDL receptor, which leads to prolonged TRL circulation and triglyceride accumulation. These actions promote hypertriglyceridemia, foam cell formation, plaque inflammation, and the progression of atherosclerosis. Elevated ApoC-I levels are associated with increased risk of cardiovascular disease, enhanced Aβ aggregation and Alzheimer's disease, and macrovascular complications in type 1 diabetes due to CETP dysregulation and impaired reverse cholesterol transport.

Background

Apolipoprotein CI (c), the smallest exchangeable apolipoprotein, is derived from an 83-residue precursor and is mainly expressed in the liver and macrophages. It circulates on HDL, VLDL, and chylomicrons, adopting a structure of two antiparallel α-helices connected by a flexible hinge with hydrophobic stacking interactions, and a lysine/arginine-rich C-terminal region that enables lipoprotein binding through electrostatic and amphipathic lipid interactions. ApoC-I strongly inhibits cholesteryl ester transfer protein (CETP) by increasing HDL electronegativity via its positively charged C-terminal helix, disrupting HDL-CETP complexes and thereby restricting neutral lipid transfer between HDL and triglyceride-rich lipoproteins (TRLs). ApoC-I competitively displaces apoE from β-VLDL, impairing receptor-mediated clearance via the LDL receptor-related protein (LRP), VLDL receptor, and LDL receptor, which leads to prolonged TRL circulation and triglyceride accumulation. These actions promote hypertriglyceridemia, foam cell formation, plaque inflammation, and the progression of atherosclerosis. Elevated ApoC-I levels are associated with increased risk of cardiovascular disease, enhanced Aβ aggregation and Alzheimer's disease, and macrovascular complications in type 1 diabetes due to CETP dysregulation and impaired reverse cholesterol transport.

References
[1] Rouland A, et al. Cardiovasc Diabetol. 2022 Dec 5;21(1):272. [2] McPherson A, et al. J Lipid Res. 2019 Feb;60(2):400-411.

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

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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%