MIP 3a Human
Description
Functional Roles in Immune Response
MIP-3α mediates immune cell recruitment and antimicrobial defense:
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Chemotaxis: Attracts memory T cells, dendritic cells, and natural killer cells via CCR6 .
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Antimicrobial Activity: The C-terminal α-helix peptide (residues 51–70) exhibits bactericidal effects against E. coli and S. aureus .
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Antiviral Activity: Neutralizes vaccinia virus (VV) and reduces replication in keratinocytes .
Key Disease Associations:
Research Applications and Methodologies
MIP-3α is utilized in both basic and translational studies:
Recombinant Production:
| Parameter | Specification | Source |
|---|---|---|
| Expression System | E. coli (His-tagged) | |
| Purity | ≥95% (SDS-PAGE) | |
| Biological Activity | Chemotaxis at 1–10 ng/mL (Jurkat cells) |
Detection Methods:
| Assay | Application | Source |
|---|---|---|
| Quantikine ELISA | Serum/plasma MIP-3α quantification | |
| Chemotaxis Assay | Functional activity assessment |
Key Research Findings
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Antimicrobial Peptide: The C-terminal α-helix (residues 51–70) forms an amphipathic structure critical for microbial membrane disruption .
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Antiviral Defense: Neutralization of MIP-3α in keratinocytes increases VV replication, highlighting its role in innate immunity .
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HIV-1 Pathogenesis: Elevated serum MIP-3α correlates with immune activation markers (e.g., CD38+ CD8+ T cells) and disease progression .
Product Specs
Q&A
Basic Questions
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What is the role of MIP-3α in human physiology?
MIP-3α is a C-C chemokine expressed by various cell types, including keratinocytes and renal proximal tubule cells. It plays a critical role in immune responses by attracting memory T lymphocytes and dendritic cells via CCR6 receptor activation. Its functions include antimicrobial activity and involvement in inflammation and fibrosis, particularly in conditions like diabetic nephropathy and atopic dermatitis . -
How is MIP-3α expression regulated under pathological conditions?
MIP-3α expression is influenced by factors such as high glucose levels and transforming growth factor-beta 1 (TGF-β1). For example, in diabetic nephropathy, high glucose induces MIP-3α expression through a TGF-β1-dependent mechanism. This regulation can be studied using real-time RT-PCR, ELISA, and immunohistochemistry techniques . -
What experimental models are used to study MIP-3α?
Research on MIP-3α often employs in vitro models like HK-2 human proximal tubular cells and in vivo models such as transgenic diabetic rats (mRen-2). These models allow for investigation of gene silencing, protein expression, and immune cell recruitment under controlled conditions . -
What methods are used to quantify MIP-3α levels in research?
Common methods include:
Advanced Research Questions
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How does MIP-3α contribute to the pathogenesis of diabetic nephropathy?
In diabetic nephropathy, hyperglycemia triggers the upregulation of MIP-3α via TGF-β1 signaling. This leads to increased recruitment of immune cells like T lymphocytes, exacerbating inflammation and fibrosis in renal tissues. Experimental data show significant fold changes in mRNA and protein levels under high glucose conditions compared to controls . -
What structural features of MIP-3α influence its receptor binding specificity?
Structural studies using X-ray crystallography have revealed key motifs that determine the binding specificity of MIP-3α to CCR6 receptors. Differences in crystallographic space groups (I4 vs P61) highlight subtle variations that may affect receptor activation mechanisms . -
How does MIP-3α deficiency impact immune responses against viral infections?
Research indicates that reduced levels of MIP-3α impair innate immunity against viruses like vaccinia virus (VV). This deficiency compromises the skin's ability to mount effective antiviral responses, as evidenced by lower plaque reduction rates in standard viral assays . -
What are the challenges in interpreting contradictory data regarding MIP-3α expression?
Contradictions often arise from differences in experimental setups, such as variations in cell types, glucose concentrations, or assay sensitivity. To address these discrepancies, researchers should standardize protocols and use robust statistical methods to validate findings across multiple studies .
Methodological Insights
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How can small interfering RNA (siRNA) technology be applied to study MIP-3α?
siRNA can be used to silence the TGF-β1 gene in cell models like HK-2 cells, enabling researchers to observe downstream effects on MIP-3α expression. This approach helps elucidate signaling pathways and identify therapeutic targets for diseases involving chemokine dysregulation . -
How does experimental design ensure reliability in studying chemokine dynamics?
Reliable experimental design includes: -
What are emerging trends in interdisciplinary research involving MIP-3α?
Interdisciplinary approaches integrate computational modeling with empirical studies to predict chemokine interactions and their systemic effects. Additionally, collaborations between immunology, structural biology, and bioinformatics are advancing the understanding of chemokine-mediated diseases .
Data Table Example
| Condition | MIP-3α mRNA Fold Change | Protein Level (pg/ml) | Statistical Significance |
|---|---|---|---|
| Normal Glucose (5 mM) | 1.0 | 50 ± 5 | Reference |
| High Glucose (30 mM) | 2.4 ± 0.12 | 120 ± 10 | |
| Osmotic Control | 1.2 ± 0.08 | 60 ± 6 |
Product Science Overview
Human recombinant CCL20 is a protein consisting of 70 amino acids with a molecular weight of approximately 8 kDa . It contains four highly conserved cysteine residues, which are characteristic of CC chemokines . The protein is typically produced in an E. coli expression system and purified to a high degree of purity (>98%) for research purposes .
CCL20 signals through the G protein-coupled receptor CCR6 . It acts as a chemoattractant, primarily attracting lymphocytes and dendritic cells to sites of inflammation . This chemokine is particularly important in mucosal immunity, where it helps to recruit immune cells to the mucosal surfaces of the gut, lungs, and skin .
