Recombinant Mouse Apolipoprotein C-I (Apoc1)

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Description

Introduction to Recombinant Mouse Apolipoprotein C-I (Apoc1)

Recombinant Mouse Apolipoprotein C-I (Apoc1) is a synthetic version of the endogenous protein, engineered for research purposes. Native Apoc1 is a 6.6 kDa apolipoprotein involved in lipid metabolism, primarily associated with VLDL and HDL particles. The recombinant form retains core functional domains but often includes modifications such as N-terminal His/GST tags and utilizes expression systems like E. coli or cell-free platforms to enhance yield and solubility .

Primary Roles in Lipid Metabolism

FunctionMechanismSupportive Evidence
Lipoprotein receptor inhibitionBlocks LDLR, LRP, and VLDLR binding via competitive displacement of apoE Transgenic mouse studies
LPL inhibitionDirectly impairs LPL-mediated triglyceride hydrolysis (60% efficiency vs. apoC-III) In vitro lipolysis assays
CETP inhibitionN-terminal domain (aa 1–38) inhibits cholesteryl ester transfer Synthetic peptide studies
Free fatty acid bindingReduces intracellular esterification; modulates lipid flux Radiolabeled fatty acid assays

Key Experimental Insights

Model/ExperimentOutcomeImplications
APOC1 transgenic mice12–55× elevation in plasma triglycerides (VLDL-rich) Hypertriglyceridemia mechanism
ApoC1 knockout miceNormal lipids on chow; hypercholesterolemia on high-fat diets Conditional metabolic role
In vitro lipolysis assaysApoc1 inhibits VLDL-TG hydrolysis by 60% (vs. apoC-III) Direct LPL inhibition
Hepatic clearance studies2× prolonged plasma half-life of VLDL-TG mimetics Delayed lipoprotein catabolism

Pathophysiological Roles

  1. Hypertriglyceridemia:

    • Overexpression causes VLDL retention due to impaired LPL activity and delayed hepatic uptake .

    • Synergy with apoE deficiency amplifies lipid accumulation (55× TG elevation in ApoE−/− APOC1 mice) .

  2. Cardiovascular Risk:

    • Inhibits CETP, potentially altering HDL-LDL cholesterol balance .

    • Associates with atherosclerosis and metabolic syndrome in human studies .

  3. Metabolic Regulation:

    • Binds free fatty acids, reducing adipocyte uptake and esterification .

    • Modulates LCAT activity, influencing HDL cholesterol esterification .

Product Specs

Buffer
For liquid delivery forms, the protein is stored in a Tris/PBS-based buffer containing 5%-50% glycerol. Note: Specify your desired glycerol concentration in order comments if different from the default.
Form
Available in liquid or lyophilized powder format. Note: We prioritize shipping the available format; however, please specify your preferred format in the order comments for custom preparation.
Lead Time
3-7 business days
Notes
Avoid repeated freeze-thaw cycles. Store working aliquots at 4°C for up to one week.
Reconstitution
Centrifuge the vial briefly before opening to collect the contents. Reconstitute the protein in sterile deionized water to a concentration of 0.1-1.0 mg/mL. We recommend adding 5-50% glycerol (final concentration) and aliquoting for long-term storage at -20°C/-80°C. Our default glycerol concentration is 50%.
Shelf Life
Shelf life depends on storage conditions, buffer composition, temperature, and protein stability. Generally, liquid formulations have a 6-month shelf life at -20°C/-80°C, while lyophilized formulations have a 12-month shelf life at -20°C/-80°C.
Storage Condition
Upon receipt, store at -20°C/-80°C. Aliquot for multiple uses. Avoid repeated freeze-thaw cycles.
Tag Info
N-terminal 10xHis-tagged
Synonyms
Apoc1; Apolipoprotein C-I; Apo-CI; ApoC-I; Apolipoprotein C1
Datasheet & Coa
Please contact us to get it.
Expression Region
27-88aa
Mol. Weight
12.5 kDa
Protein Length
Full Length of Mature Protein
Purity
Greater than 90% as determined by SDS-PAGE.
Research Area
Cardiovascular
Source
in vitro E.coli expression system
Species
Mus musculus (Mouse)
Target Names
Target Protein Sequence
APDLSGTLESIPDKLKEFGNTLEDKARAAIEHIKQKEILTKTRAWFSEAFGKVKEKLKTTFS
Note: The complete sequence including tag sequence, target protein sequence and linker sequence could be provided upon request.
Uniprot No.

Target Background

Function
Recombinant Mouse Apolipoprotein C-I (ApoC1) is an inhibitor of lipoprotein binding to the low-density lipoprotein (LDL) receptor, LDL receptor-related protein, and very-low-density lipoprotein (VLDL) receptor. It associates with high-density lipoproteins (HDL) and triacylglycerol-rich lipoproteins in plasma, comprising approximately 10% of VLDL protein and 2% of HDL protein. ApoC1 directly interferes with fatty acid uptake and is the major plasma inhibitor of cholesteryl ester transfer protein (CETP). It modulates the interaction of APOE with beta-migrating VLDL and inhibits beta-VLDL binding to the LDL receptor-related protein. Furthermore, ApoC1 binds free fatty acids, reducing their intracellular esterification.
Gene References Into Functions
Key Research Findings on ApoC1:
  1. APOC1 expression induces glomerulosclerosis, potentially by increasing the cytokine response in macrophages. (PMID: 27976371)
  2. Apolipoprotein C-I was significantly increased in obese mice plasma. (PMID: 22404376)
  3. ApoC-I deficiency results in impaired memory functions, suggesting a critical, bell-shaped dose-dependent role in brain function. (PMID: 21157034)
  4. ApoC-I's stimulatory effect on the lipopolysaccharide (LPS) response resembles that of LPS-binding protein (LBP) and depends on CD14/Toll-like receptor 4 signaling. (PMID: 20335569)
  5. Regulates gene cluster expression in macrophages. (PMID: 12032151)
  6. Potently inhibits CETP in vivo. (PMID: 12070157)
  7. Lipoprotein remnant apoC-I content may serve as an early marker for coronary artery disease risk. (PMID: 12231568)
  8. TR4 regulates apolipoprotein E, C-I, and C-II gene expression. (PMID: 12954636)
  9. ApoC-I potently inhibits LPL-mediated triglyceride lipolysis. (PMID: 15576844)
  10. Liver-specific ApoC-I expression causes hypertriglyceridemia. (PMID: 16478678)
  11. Endogenous ApoC-I increases hyperlipidemia by stimulating VLDL production and inhibiting LPL. (PMID: 16537968)
  12. ApoC-I knockout mice show increased hepatic cholesteryl esters, triglycerides, and biliary cholesterol. (PMID: 17053273)
  13. Systemic ApoC-I increases atherosclerosis, likely via hyperlipidemia. (PMID: 17320883)
  14. ApoC-I binds free fatty acids, reducing blood FFA uptake. (PMID: 17339654)
  15. ApoC-I is involved in LPS-induced atherosclerosis via increased inflammatory response. (PMID: 17967778)
  16. ApoC-I inhibits scavenger receptor BI-mediated HDL cholesterol uptake and influences HDL plasma levels and size. (PMID: 18992221)
Database Links
Protein Families
Apolipoprotein C1 family
Subcellular Location
Secreted.
Tissue Specificity
Adult and fetal liver.

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