Render Target: STATIC
Render Timestamp: 2024-12-20T12:00:22.562Z
Commit: f2d32940205a64f990b886d724ccee2c9935daff
XML generation date: 2024-09-30 01:59:32.758
Product last modified at: 2024-09-30T08:00:14.602Z
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PDP - Template Name: Monoclonal Antibody
PDP - Template ID: *******c5e4b77
R Recombinant
Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

MBL (E2F7B) Rabbit mAb #99395

Filter:
  • WB

    Supporting Data

    REACTIVITY H M
    SENSITIVITY Endogenous
    MW (kDa) 30
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 
    • M-Mouse 

    Product Information

    Product Usage Information

    Application Dilution
    Western Blotting 1:1000

    Storage

    Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/mL BSA, 50% glycerol, and less than 0.02% sodium azide. Store at –20°C. Do not aliquot the antibody.

    Protocol

    Specificity / Sensitivity

    MBL (E2F7B) Rabbit mAb recognizes endogenous levels of total MBL protein.

    Species Reactivity:

    Human, Mouse

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gln194 of human MBL protein.

    Background

    Mannose-binding lectin (MBL) is a member of the collectin family of proteins and plays a key role in innate immunity via activation of the lectin complement pathway (1). MBL is produced in the liver and circulates in the serum in complexes with MBL-associated serine proteases (MASPS) (1,2). MBL acts as a pattern recognition receptor and binds carbohydrates on the surface of various microorganisms as well as on dying host cells (3,4). In humans, only one MBL protein form is found in the serum, but in rodents, two MBL forms have been characterized, MBL-A and MBL-C (5). Polymorphisms in the MBL gene, MBL-2, are associated with predisposition to myocardial infarction, pathogenesis of pulmonary tuberculosis (PTB), and three single point mutations in exon 1 are responsible for the most common human immunodeficiencies leading to increased susceptibility to infectious disease (6-8).
    For Research Use Only. Not For Use In Diagnostic Procedures.
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