ApoE Antibody (YA1516)(PBS only)
(Synonyms: APOE; Apolipoprotein E; Apo-E)ApoE Antibody (YA1516)(PBS only) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to ApoE.
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-P, ICC/IF, IP
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Reactivity :
Human, Mouse
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Formulation:
Supplied in 10 mM PBS, pH 7.4.
Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
IP
IP: Immunoprecipitation
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|---|---|---|---|---|
| Dilution Ratio | 1:1000-1:2000 | 1:100-1:200 | 1:50-1:200 | 1:50 |
Product Details
ApoE Antibody (YA1516)(PBS only) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to ApoE.
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Host Rabbit
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Clonality Monoclonal,Recombinant
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Species ReactivityHuman, Mouse
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Observed Molecular WeightObserved band size: 36 kDaNote: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
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Calculated Molecular Weight Predicted band size: 36 kDa
A synthesized peptide derived from human Apolipoprotein E aa300-317.
Affinity Chromatography
Unmodified
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in 10 mM PBS, pH 7.4.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Shipping
Shipping with blue ice.
Background
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Function
Apolipoprotein E (ApoE) is a key regulator of lipoprotein metabolism that mediates the hepatic clearance of diet-derived chylomicron remnants and liver-derived very-low-density lipoprotein (VLDL) remnants through interactions with members of the low-density lipoprotein receptor family[1][2]. ApoE deficiency disrupts this clearance pathway, resulting in marked hypercholesterolemia, accumulation of remnant lipoproteins, and enhanced susceptibility to atherosclerotic lesion formation[1][3][4]. Mechanistically, ApoE regulates cholesterol homeostasis and influences macrophage biology, linking lipid metabolism to vascular inflammation and atherogenesis[2][5]. In disease models, Apoe−/− mice develop spontaneous atherosclerosis even when maintained on a low-cholesterol diet and therefore represent one of the most widely used experimental systems for investigating cardiovascular disease mechanisms and therapeutic interventions[3][4][6]. Atherosclerotic lesions in these mice progress in a manner that reproduces many pathological features of human disease, making the model highly valuable for studies of plaque development and progression[6][2]. Compared with related human APOE isoforms, ApoE deficiency represents a complete loss-of-function state rather than an isoform-specific alteration, providing a robust platform for dissecting the physiological roles of ApoE in lipoprotein transport, monocyte/macrophage biology, and atherosclerosis[2][5]. For experimental applications, the Apoe−/− model is extensively used to evaluate genetic, nutritional, and pharmacological factors that modify atherosclerotic burden and vascular inflammation[6][2].
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Subcellular Localization
Secreted; Cell membrane; Single-pass membrane protein
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Isoforms & Post-Translational Modification
P01871 has 2 isomers: P01871-2: 51924 Da (predicted); P01871-1: 49440 Da (predicted).
N-glycosylated; important for IgM secretion and its localization at the plasma membrane. The interaction with FCMR is glycan-independent -
Subunit
The basic structural unit of both sIgM and mIgM molecules consists of two identical heavy chains and two identical light chains; disulfide-linked. N-terminal variable regions of the heavy and light chains form the antigen binding sites, whereas the C-terminal constant regions of the heavy chains interact with immune receptors to mediate effector functions
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SwissProt ID
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Synonyms
APOE; Apolipoprotein E; Apo-E
Documentation
References
[1]. Pendse AA, et al. Apolipoprotein E knock-out and knock-in mice: atherosclerosis, metabolic syndrome, and beyond. J Lipid Res. 2009 Apr;50 Suppl(Suppl):S178-82. [Content Brief]
[3]. Buzello M, et al. The apolipoprotein e knockout mouse: a model documenting accelerated atherogenesis in uremia. J Am Soc Nephrol. 2003 Feb;14(2):311-6. [Content Brief]
[4]. Lo Sasso G, et al. The Apoe(-/-) mouse model: a suitable model to study cardiovascular and respiratory diseases in the context of cigarette smoke exposure and harm reduction. J Transl Med. 2016 May 20;14(1):146. [Content Brief]
[6]. Meir KS, et al. Atherosclerosis in the apolipoprotein-E-deficient mouse: a decade of progress. Arterioscler Thromb Vasc Biol. 2004 Jun;24(6):1006-14. [Content Brief]
[7]. Getz GS, et al. ApoE knockout and knockin mice: the history of their contribution to the understanding of atherogenesis. J Lipid Res. 2016 May;57(5):758-66. [Content Brief]