InVivoMAb human IgG2 isotype control

Catalog #BE0301
Product Citations:
1

$164.00 - $4,280.00

Choose an Option...
  • 100 mg - $4,280.00
  • 50 mg - $3,024.00
  • 25 mg - $2,009.00
  • 5 mg - $600.00
  • 1 mg - $164.00
  • Custom Amount (Quotes Only)
In stock
Only %1 left

Product Details

The human IgG2 isotype control antibody is purified from human myeloma serum and is of unknown specificity. This antibody is suitable for use as a non-targeting isotype control in various in vitro and in vivo studies. It can also be used as a negative control in various diagnostic applications such as ELISA, Western blot, immunofluorescence, immunohistochemistry, immunoprecipitation, and flow cytometry. For research use only.

Specifications

Isotype Human IgG2, Ī»
Recommended Dilution Buffer InVivoPure pH 7.0 Dilution Buffer
Conjugation This product is unconjugated. Conjugation is available via our Antibody Conjugation Services.
Formulation PBS, pH 7.0
Contains no stabilizers or preservatives
Endotoxin <2EU/mg (<0.002EU/Ī¼g)
Determined by LAL gel clotting assay
Purity >95%
Determined by SDS-PAGE
Sterility 0.2 Āµm filtration
Production Purified from human myeloma serum
Purification Protein A
RRID AB_2715459
Molecular Weight 150 kDa
Human Pathogen Test Results Hepatitis B Surface Antigen: Negative
Human Immunodeficiency Virus 1 antibodies: Negative
Human Immunodeficiency Virus 2 antibodies: Negative
Hepatitis C Virus antibodies: Negative
* These tests cannot guarantee the absence of infective agents
Storage The antibody solution should be stored at the stock concentration at 4Ā°C. Do not freeze.

Additional Formats

    • In Vitro
    • ,
    • Homo sapiens (Human)
    Identification of specific Tie2 cleavage sites and therapeutic modulation in experimental sepsis.

    In eLife on 24 August 2020 by Idowu, T. O., Etzrodt, V., et al.

    PubMed

    Endothelial Tie2 signaling plays a pivotal role in vascular barrier maintenance at baseline and after injury. We previously demonstrated that a sharp drop in Tie2 expression observed across various murine models of critical illnesses is associated with increased vascular permeability and mortality. Matrix metalloprotease (MMP)-14-mediated Tie2 ectodomain shedding has recently been recognized as a possible mechanism for Tie2 downregulation in sepsis. Here, we identified the exact MMP14-mediated Tie2 ectodomain cleavage sites and could show that pharmacological MMP14 blockade in experimental murine sepsis exerts barrier protective and anti-inflammatory effects predominantly through the attenuation of Tie2 cleavage to improve survival both in a pre-treatment and rescue approach. Overall, we show that protecting Tie2 shedding might offer a new therapeutic opportunity for the treatment of septic vascular leakage. Ā© 2020, Idowu et al.

Related Products