IREG3 Antibody

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Product Specs

Buffer
**Preservative:** 0.03% Proclin 300
**Constituents:** 50% Glycerol, 0.01M PBS, pH 7.4
Form
Liquid
Lead Time
Made-to-order (14-16 weeks)
Synonyms
IREG3 antibody; FPN3 antibody; MAR1 antibody; RTS3 antibody; At5g26820 antibody; F2P16.6 antibody; Solute carrier family 40 member 3 antibody; chloroplastic antibody; Ferroportin-3 antibody; Iron-regulated transporter 3 antibody; AtIREG3 antibody; Protein MULTIPLE ANTIBIOTIC RESISTANCE 1 antibody
Target Names
IREG3
Uniprot No.

Target Background

Function
IREG3 is a probable plastid transporter that may play a role in iron chelation, storage, or sequestration under conditions of limited iron availability. In the presence of exogenous antibiotics, IREG3 may allow the opportunistic entry of multiple aminoglycoside antibiotics into the chloroplast.
Gene References Into Functions
  1. Research has identified and characterized a transporter gene in Arabidopsis thaliana, designated MAR1, which appears to regulate antibiotic entry into the chloroplast. PMID: 20592808
  2. MAR1 is a plastid transporter likely involved in cellular iron homeostasis and facilitates the opportunistic entry of multiple antibiotics into the chloroplast. [MAR1] PMID: 19675150
Database Links

KEGG: ath:AT5G26820

STRING: 3702.AT5G26820.1

UniGene: At.27285

Protein Families
Ferroportin (FP) (TC 2.A.100) family, SLC40A subfamily
Subcellular Location
Membrane; Multi-pass membrane protein. Plastid, chloroplast envelope.
Tissue Specificity
Widely expressed.

Q&A

The following FAQs address key research considerations for IgG3 antibodies (note: presumed query intent refers to IgG3 based on search result analysis; no relevant data found for "IREG3"):

Advanced Research Challenges

How to resolve contradictory data on IgG3's therapeutic potential?

Address these variables in study design:

Conflict SourceResolution StrategyExample Studies
Antigen densityStandardize coating concentrations Fig. S6
Allotype variationUse homozygous donor cells Table 2
Protease susceptibilityAdd serum stability time-courses In vitro half-life

Can IgG3's short serum half-life be engineered for therapeutics?

Recent approaches show promise:

StrategyOutcomeEvidence Source
Hinge domain truncation↑ Serum stability (t<sub>1/2</sub> +72hr)
C1-C3S mutation↑ TRIM21-mediated neutralization Fig. 3g-h
Fc-engineered variants↑ FcRn binding affinity SPR data

Implementation note: Combine surface plasmon resonance (FcRn binding) with viral microneutralization assays for iterative optimization .

How does IgG3 mediate cross-protection against antigenic drift?

Mechanistic insights from influenza studies:

FeatureEffect on Drifted VariantsExperimental Validation
Hinge flexibilityEnables bivalent low-affinity binding ELISA/FRET assays
Fab-Fc distanceFacilitates inter-spike bridgingCryo-EM of IgG3-spike complexes

Technical consideration: Use Biolayer Interferometry with variant RBDs to quantify avidity effects .

Critical Research Gaps

  • Standardized assays for IgG3-specific effector functions (current methods optimized for IgG1)

  • Allotype-dependent therapeutic response profiles

  • Synergy between IgG3 and mucosal IgA responses

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