Recombinant Mouse ApoE Protein (C-6His)

Name: Recombinant Mouse ApoE Protein (C-6His)
Brand: Beta LifeScience
SKU: BL-0941NP
Availability: InStock

BL-0941NP: Greater than 95% as determined by reducing SDS-PAGE. (QC verified)

Collections: High-quality recombinant proteins, Other recombinant proteins

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Product Overview

Description	Recombinant Mouse Apolipoprotein E is produced by our Mammalian expression system and the target gene encoding Glu19-Gln311 is expressed with a 6His tag at the C-terminus.
Accession	P08226
Synonym	Apolipoprotein E; Apo-E; APOE
Gene Background	Apolipoprotein E (Apo-E), is a member of the apolipoprotein A1/A4/E family. ApoE is a major protein component of serum LDL, VLDL, HDL, and chylomicrons. APOE may function in mediating the binding, internalization, and catabolism of lipoprotein particles. It can serve as a ligand for the LDL (apo B/E) receptor and for the specific apo-E receptor (chylomicron remnant) of hepatic tissues. APOE is usually secreted in plasma. Phosphorylation sites are present in the extracellular medium.
Molecular Mass	35 KDa
Apmol Mass	30-40 KDa, reducing conditions
Formulation	Lyophilized from a 0.2 μm filtered solution of 20mM PB, 150mM NaCl, pH 7.4.
Endotoxin	Less than 0.1 ng/µg (1 EU/µg) as determined by LAL test.
Purity	Greater than 95% as determined by reducing SDS-PAGE. (QC verified)
Biological Activity	Not tested
Reconstitution	Always centrifuge tubes before opening. Do not mix by vortex or pipetting. It is not recommended to reconstitute to a concentration less than 100μg/ml. Dissolve the lyophilized protein in distilled water. Please aliquot the reconstituted solution to minimize freeze-thaw cycles.
Storage	Lyophilized protein should be stored at ≤ -20°C, stable for one year after receipt. Reconstituted protein solution can be stored at 2-8°C for 2-7 days. Aliquots of reconstituted samples are stable at ≤ -20°C for 3 months.
Shipping	The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature listed below.
Usage	For Research Use Only

Target Details

Target Function	APOE is an apolipoprotein, a protein associating with lipid particles, that mainly functions in lipoprotein-mediated lipid transport between organs via the plasma and interstitial fluids. APOE is a core component of plasma lipoproteins and is involved in their production, conversion and clearance. Apoliproteins are amphipathic molecules that interact both with lipids of the lipoprotein particle core and the aqueous environment of the plasma. As such, APOE associates with chylomicrons, chylomicron remnants, very low density lipoproteins (VLDL) and intermediate density lipoproteins (IDL) but shows a preferential binding to high-density lipoproteins (HDL). It also binds a wide range of cellular receptors including the LDL receptor/LDLR and the very low-density lipoprotein receptor/VLDLR that mediate the cellular uptake of the APOE-containing lipoprotein particles. Finally, APOE has also a heparin-binding activity and binds heparan-sulfate proteoglycans on the surface of cells, a property that supports the capture and the receptor-mediated uptake of APOE-containing lipoproteins by cells.
Subcellular Location	Secreted. Secreted, extracellular space. Secreted, extracellular space, extracellular matrix.
Protein Families	Apolipoprotein A1/A4/E family
Database References	KEGG: mmu:11816 STRING: 10090.ENSMUSP00000003066 UniGene: Mm.305152

Gene Functions References

The ApoE Deletion Increases Both White Matter and Neuronal Injury After Subarachnoid Hemorrhage in Mice. PMID: 30225551
Using ex vivo and in vivo microscopy, we analyzed the interactive behavior of quantum dots with different surface functionalizations in atherosclerotic lesions of ApoE-deficient mice. PMID: 29334311
Aged ApoE-Knock Out mice exhibit severe osteoporosis compared to Wild Type mice. ApoE promotes osteoblastogenesis via ERK1/2 pathway. PMID: 29906458
These novel findings demonstrate that RAGE deficiency protects against aortic valve calcification in high cholesterol diet-fed ApoE(-/-) mice via inhibition of endoplasmic reticulum stress. PMID: 28024939
FGF21 alleviated atherosclerosis by ameliorating Fas-mediated apoptosis in apoE-/- mice. PMID: 30157856
The mice were crossed onto the athero-prone apoE(-/-) background to obtain Plpp3(f/f)apoE(-/-)Alb-Cre(+) and Plpp3(f/f)apoE(-/-)Alb-Cre(-) offspring, the latter of which were used as controls. The mice were fed chow or a Western diet for 32 or 12 weeks, respectively PMID: 28291223
results support that there are different vulnerabilities to postnatal CPF exposure according to the APOE polymorphism, which in turn affects the cholinergic system and defenses to oxidative stress PMID: 29729306
forskolin/rolipram incorporated into liposomes, designed to target inflamed endothelium, shows reduced atherosclerosis and CC formation in ApoE -/- mice PMID: 29066718
exposure to repeated social defeat promotes atherosclerosis by augmenting NETs formation within the plaque in socially defeated apoE(-/-) mice. PMID: 29673593
In vivo, the NHE6 knockout (NHE6(KO)) mouse model showed elevated Abeta in the brain, consistent with a causal effect. Increased nuclear translocation of histone deacetylase 4 (HDAC4) in ApoE4 astrocytes, compared with the nonpathogenic ApoE3 allele, suggested a mechanistic basis for transcriptional down-regulation of NHE6. PMID: 29946028
Platelet activation in ApoE and LDLR-deficient mice was not further increased by strenuous exercise, but was instead attenuated. PMID: 28067100
the ApoE KO and DKO mice cannot serve as mouse models for studying AD or pathological brain changes compatible with atherosclerosis. PMID: 29207114
High-fat and high-cholesterol diet induced atherosclerosis faster and more severe than normal diet in ApoE(-/-) mice35 PMID: 27698357
Exenatide enhances adiponectin production and the attenuates atherosclerotic plaque oxidative stress, inflammation, and proteolysis in ApoE(-/-) mice under chronic stress fed high fat diet. PMID: 28734203
Enhanced mitochondrial oxidative stress under hyperlipidemic conditions in aging induces plaque instability, in part by increasing smooth muscle cell apoptosis, necrotic core expansion, and matrix degradation in Sod2/ApoE knockout mice. PMID: 29079564
Danshensu Bingpian Zhi has antiatherosclerotic effects that involve the inhibition of inflammation, macrophage migration, leukocyte adhesion, and foam cell formation in ApoE-deficient mice. PMID: 28971954
Stimulation of nAChRalpha7 with GTS-21 reduced atherosclerosis, which was associated with dampened splenic myelopoiesis in ApoE knockout mice. PMID: 28858686
Subcutaneous injection of dendritic cells aggravates atherosclerosis in ApoE-knockout mice by activation of TLR4. PMID: 28849148
ApoE is essential to the development of cerebral malaria. The protection from ECM provided by the deletion of ApoE correlated with decreased sequestration of parasitized RBCs and T cells within the brain and was independent from the involvement of ApoE receptors and from the altered lipid metabolism present in the knock-out mice. PMID: 27647324
ApoAI modulates the cellular fate of Treg cells and thus influences the immune response during atherosclerosis. PMID: 29545616
SP-D deficiency reduces atherosclerosis in ApoE-knockout mice by decreasing the accumulation and proliferation of macrophages and by reducing IL-6 levels systemically. PMID: 28472244
brain APOE3 expression is associated with a potent inhibition of visceral white adipose tissue mitochondrial oxidative phosphorylation, leading to significantly reduced substrate oxidation, increased fat accumulation and obesity PMID: 29154926
The results of this study indicated that ApoE4 negatively impacts BDNF-5-HT2A signaling in the female brain. PMID: 28934977
The ApoE-/- mice were fed with western-type diet and HSP60 was administrated orally or subcutaneously for potential vaccine against atherosclerosis. ApoE-/- mice with oral HSP60 administration group showed a significant reduction in plaque size at the aortic root; accompanied by increased Myeloid derived suppressor cells (CD11b+Gr1+) in peripheral blood and spleen. PMID: 29107690
AIM2 overexpression and inhibition were studied in ApoE-/- mice that were fed a high-fat diet. The results showed that high fat diet increases the expression of AIM2. PMID: 29510138
Study observed that in the Apoe-deficient model of atherosclerosis, the female sex is a risk factor to develop more severe atherosclerotic lesions, although serum fat levels are not higher in females than in males. In contrast, female mice are protected from renal damage induced by the concomitant deficiency of Apoe and Itga8. PMID: 28572914
expression of CXCL16, TIMP-1, MMP-9, MMP-8, and LOX-1 is localized in the atherosclerotic lesions, which suggests their roles in the development of the lesions in ApoE-Knockout mice. PMID: 28247010
AMPK activation enhances the anti-atherogenic effects of high density lipoproteins in apoE(-/-) mice PMID: 28611100
GLP-1 receptor agonists suppress the progression of atherosclerosis by inhibiting vascular smooth muscle cell proliferation and enhancing AMP-activated protein kinase and cell cycle regulation in ApoE deficient mice. PMID: 28445811
results demonstrate that ApoE affects tau pathogenesis, neuroinflammation, and tau-mediated neurodegeneration independently of amyloid-beta pathology; ApoE4 exerts a 'toxic' gain of function whereas the absence of ApoE is protective PMID: 28959956
Data (including data from studies using knockout mice) suggest that CD59a, CD59b, and ApoE are involved in development of diabetes-induced atherosclerosis; here, deficiency of CD59a/CD59b (in ApoE deficient mice) accelerates development of atherosclerosis in mice with type 1 diabetes. (CD59a = CD59a antigen; CD59b = CD59b antigen; ApoE = apolipoprotein E) PMID: 27729184
Vitamin K2 can inhibit intimal calcification of aortic artery induced by high-fat diet in ApoE(-/-) mice via suppression of TLR2/4 expression. PMID: 28587577
the Chromogranin A-derived vasostatin-2 attenuates atherosclerosis in apoE(-/-) mice and, in addition to its anti-inflammatory property, also acts as an inhibitor in monocyte/macrophage recruitment. PMID: 27831589
Although the severity of adipose loss in female and male Seipin(-/-)apoE(-/-) mice were similar, hyperlipidemia, steatohepatitis and atherosclerosis were less severe in females than in males. PMID: 29428127
Report a disturbance in sphingolipid and glycerophospholipid metabolism during the progression of atherosclerotic dyslipidemia in ApoE knockout mice fed high fat diet. PMID: 28527370
Alzheimer disease susceptibility of APOE4 may originate in part from defective phagocytic capacity of astrocytes which accelerates the rate of accumulation of C1q coated senescent synapses, enhancing synaptic vulnerability to classical-complement-cascade mediated neurodegeneration. PMID: 27559087
Eight-week-old ApoE-/-mice were fed a western diet while being administered AnxA5 or control (M1234) for a total of 6 weeks. AnxA5 administration reduced plaque size in the aortic root as well as the aortic arch by 36% and 55% respectively PMID: 29267398
Study is the first showing the significance of APOE in attenuating early brain injury after subarachnoid hemorrhage through a blood-brain barrier modulation-dependent manner. PMID: 27463015
Tauroursodeoxycholic acid attenuates Ang II induced abdominal aortic aneurysm formation in ApoE(-/-) mice by inhibiting endoplasmic reticulum stress mediated apoptosis. PMID: 27889204
The combined data indicate that the K146N/R147W substitutions convert the full-length and the truncated apoE3[K146N/R147W] mutant into a dominant negative ligand that prevents receptor-mediated remnant clearance, exacerbates the dyslipidemia, and inhibits the biogenesis of HDL. PMID: 24776540
The ApoE4 brains showed increased expression of interleukin receptor-associated kinase-1and downregulated by miR146) that correlated inversely with miR146a levels. PMID: 27281274
Rutaecarpine was identified to be a candidate that protected ApoE(-/-) mice from developing atherosclerosis through preferentially promoting activities of ABCA1 and SR-BI within RCT. PMID: 24908654
224 male F2 mice were generated from the two Apoe (-/-) strains to perform quantitative trait locus (QTL) analysis of atherosclerosis. F2 mice were fed 5 weeks of Western diet and analyzed for atherosclerotic lesions in the aortic root PMID: 28116503
Low dose dietary nitrate improves endothelial dysfunction and plaque stability in the ApoE-deficient mouse fed a high fat diet. PMID: 27519268
Ovariectomy and ApoE deficiency showed interaction potentializing the insulin resistance, increasing triglycerides levels and altering angiotensin-converting enzyme (ACE)-2 and Mas receptor gene expressions. PMID: 28987631
AMPK activation reduces the formation of atheromata-inducing macrophages in ApoE(-/-)-deficient mice by inhibiting expression of Ccr2, thereby preventing the Ccr2-mediated migration of Ly6C(hi) monocytes from the bone marrow. PMID: 28235712
Deletion of apolipoprotein E in astrocytes ameliorates the spatial learning and memory deficits in Alzheimer's disease by inhibiting TGF-beta/Smad2/STAT3 signaling. PMID: 28366226
choroid plexus/CSF provides an additional source of apoE and the glymphatic fluid transporting system delivers it to brain via the periarterial space PMID: 27931262
Longxuetongluo capsule inhibits atherosclerosis progression in high-fat diet-induced ApoE(-/-) mice by improving endothelial dysfunction via MAPK/IKK/IkappaB/NF-kappaB signaling pathway. PMID: 27591127
Major orthopedic surgery in ApoE-/- mice triggers a systemic inflammatory response. Atherosclerotic plaque area is enlarged after surgery mainly due to an increase of the necrotic core. PMID: 27825629

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Proteins are sensitive to heat, and freeze-drying can preserve the activity of the majority of proteins. It improves protein stability, extends storage time, and reduces shipping costs. However, freeze-drying can also lead to the loss of the active portion of the protein and cause aggregation and denaturation issues. Nonetheless, these adverse effects can be minimized by incorporating protective agents such as stabilizers, additives, and excipients, and by carefully controlling various lyophilization conditions.

Commonly used protectant include saccharides, polyols, polymers, surfactants, some proteins and amino acids etc. We usually add 8% (mass ratio by volume) of trehalose and mannitol as lyoprotectant. Trehalose can significantly prevent the alter of the protein secondary structure, the extension and aggregation of proteins during freeze-drying process; mannitol is also a universal applied protectant and fillers, which can reduce the aggregation of certain proteins after lyophilization.

Our protein products do not contain carrier protein or other additives (such as bovine serum albumin (BSA), human serum albumin (HSA) and sucrose, etc., and when lyophilized with the solution with the lowest salt content, they often cannot form A white grid structure, but a small amount of protein is deposited in the tube during the freeze-drying process, forming a thin or invisible transparent protein layer.

Reminder: Before opening the tube cap, we recommend that you quickly centrifuge for 20-30 seconds in a small centrifuge, so that the protein attached to the tube cap or the tube wall can be aggregated at the bottom of the tube. Our quality control procedures ensure that each tube contains the correct amount of protein, and although sometimes you can't see the protein powder, the amount of protein in the tube is still very precise.

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