Recombinant Mouse Apolipoprotein E (Apoe)

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Code CSB-YP001936MO
Size $306
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  • (Tris-Glycine gel) Discontinuous SDS-PAGE (reduced) with 5% enrichment gel and 15% separation gel.

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Product Details

Purity
Greater than 90% as determined by SDS-PAGE.
Target Names
Apoe
Uniprot No.
Research Area
Others
Alternative Names
ApoeApolipoprotein E; Apo-E
Species
Mus musculus (Mouse)
Source
Yeast
Expression Region
19-311aa
Target Protein Sequence
EGEPEVTDQLEWQSNQPWEQALNRFWDYLRWVQTLSDQVQEELQSSQVTQELTALMEDTMTEVKAYKKELEEQLGPVAEETRARLGKEVQAAQARLGADMEDLRNRLGQYRNEVHTMLGQSTEEIRARLSTHLRKMRKRLMRDAEDLQKRLAVYKAGAREGAERGVSAIRERLGPLVEQGRQRTANLGAGAAQPLRDRAQAFGDRIRGRLEEVGNQARDRLEEVREHMEEVRSKMEEQTQQIRLQAEIFQARLKGWFEPIVEDMHRQWANLMEKIQASVATNPIITPVAQENQ
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Mol. Weight
36.0kDa
Protein Length
Full Length of Mature Protein
Tag Info
N-terminal 6xHis-tagged
Form
Liquid or Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer
If the delivery form is liquid, the default storage buffer is Tris/PBS-based buffer, 5%-50% glycerol.
Note: If you have any special requirement for the glycerol content, please remark when you place the order.
If the delivery form is lyophilized powder, the buffer before lyophilization is Tris/PBS-based buffer, 6% Trehalose, pH 8.0.
Reconstitution
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20°C/-80°C. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
3-7 business days
Notes
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Datasheet & COA
Please contact us to get it.
Description

The production of this Recombinant Mouse Apoe protein required the insertion of a DNA fragment (Apoe, 19-311aa) into a plasmid vector and the transferral of this vector into Yeast cells (the step of transformation). The cells were then cultured and induced to express the Apoe protein. This recombinant protein was fused with N-terminal 6xHis tag. Its purity is 90%+ determined by SDS-PAGE.

Apoe is a gene providing an instruction of making a protein named apolipoprotein E (Apo-E) in mus musculus (mouse). This gene has many orthologs in multiple mammals, such as human, norway rat, pig, cattle, etc. Apo-E protein belongs to a family of fat-binding proteins called apolipoproteins, which combines with fats (lipids) in the body to form molecules called lipoproteins. Increasing studies has demonstrated that apoE-deficient mice exhibit neuronal abnormalities similar to those in Alzheimer's disease and enhanced sensitivity to stroke-associated injuries.

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Target Background

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.
Gene References into Functions
  1. The ApoE Deletion Increases Both White Matter and Neuronal Injury After Subarachnoid Hemorrhage in Mice. PMID: 30225551
  2. 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
  3. Aged ApoE-Knock Out mice exhibit severe osteoporosis compared to Wild Type mice. ApoE promotes osteoblastogenesis via ERK1/2 pathway. PMID: 29906458
  4. 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
  5. FGF21 alleviated atherosclerosis by ameliorating Fas-mediated apoptosis in apoE-/- mice. PMID: 30157856
  6. 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
  7. 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
  8. forskolin/rolipram incorporated into liposomes, designed to target inflamed endothelium, shows reduced atherosclerosis and CC formation in ApoE -/- mice PMID: 29066718
  9. exposure to repeated social defeat promotes atherosclerosis by augmenting NETs formation within the plaque in socially defeated apoE(-/-) mice. PMID: 29673593
  10. 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
  11. Platelet activation in ApoE and LDLR-deficient mice was not further increased by strenuous exercise, but was instead attenuated. PMID: 28067100
  12. the ApoE KO and DKO mice cannot serve as mouse models for studying AD or pathological brain changes compatible with atherosclerosis. PMID: 29207114
  13. High-fat and high-cholesterol diet induced atherosclerosis faster and more severe than normal diet in ApoE(-/-) mice35 PMID: 27698357
  14. 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
  15. 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
  16. 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
  17. Stimulation of nAChRalpha7 with GTS-21 reduced atherosclerosis, which was associated with dampened splenic myelopoiesis in ApoE knockout mice. PMID: 28858686
  18. Subcutaneous injection of dendritic cells aggravates atherosclerosis in ApoE-knockout mice by activation of TLR4. PMID: 28849148
  19. 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
  20. ApoAI modulates the cellular fate of Treg cells and thus influences the immune response during atherosclerosis. PMID: 29545616
  21. 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
  22. 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
  23. The results of this study indicated that ApoE4 negatively impacts BDNF-5-HT2A signaling in the female brain. PMID: 28934977
  24. 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
  25. 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
  26. 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
  27. 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
  28. AMPK activation enhances the anti-atherogenic effects of high density lipoproteins in apoE(-/-) mice PMID: 28611100
  29. 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
  30. 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
  31. 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
  32. 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
  33. 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
  34. 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
  35. Report a disturbance in sphingolipid and glycerophospholipid metabolism during the progression of atherosclerotic dyslipidemia in ApoE knockout mice fed high fat diet. PMID: 28527370
  36. 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
  37. 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
  38. 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
  39. Tauroursodeoxycholic acid attenuates Ang II induced abdominal aortic aneurysm formation in ApoE(-/-) mice by inhibiting endoplasmic reticulum stress mediated apoptosis. PMID: 27889204
  40. 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
  41. The ApoE4 brains showed increased expression of interleukin receptor-associated kinase-1and downregulated by miR146) that correlated inversely with miR146a levels. PMID: 27281274
  42. 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
  43. 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
  44. Low dose dietary nitrate improves endothelial dysfunction and plaque stability in the ApoE-deficient mouse fed a high fat diet. PMID: 27519268
  45. 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
  46. 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
  47. 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
  48. 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
  49. 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
  50. 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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Subcellular Location
Secreted. Secreted, extracellular space. Secreted, extracellular space, extracellular matrix.
Protein Families
Apolipoprotein A1/A4/E family
Database Links
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