产品名称
Anti-JAM-A Antibody, clone BV11, clone BV11, from rat
biological source
rat
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
BV11, monoclonal
species reactivity
mouse
technique(s)
flow cytometry: suitable
immunocytochemistry: suitable
immunoprecipitation (IP): suitable
isotype
IgG2bκ
NCBI accession no.
UniProt accession no.
shipped in
dry ice
target post-translational modification
unmodified
Quality Level
Gene Information
mouse ... F11R(16456)
Physical form
Protein G Purified
Purified rat monocolonal IgG2bκ in buffer containing PBS and no preservatives.
Format: Purified
Analysis Note
Control
bEnd.3 cells
bEnd.3 cells
Evaluated by Flow Cytometry in bEnd.3 cells.
Flow Cytometry Analysis: A 1:1,000 dilution of this antibody detected JAM-A in bEnd.3 cells.
Flow Cytometry Analysis: A 1:1,000 dilution of this antibody detected JAM-A in bEnd.3 cells.
Application
Detect JAM-A using this Anti-JAM-A Antibody, clone BV11 validated for use in FC, IC & IP.
Immunoprecipitation Analysis: A representative lot was used by an independent laboratory in cell extracts from Mouse H5V and PDV cells, and in COS cultures transfected with full length cDNA of mouse JAM-A (Martin-Padura, I., et al. (1998). J Cell Biol. 142(1):117-127).
Immunocytochemistry Analysis: A representative lot was used by an independent laboratory in cultured epithelial cells, cremaster muscles, and Schwann Cells (Martin-Padura, I., et al. (1998). J Cell Biol. 142(1):117-127).
Immunocytochemistry Analysis: A representative lot was used by an independent laboratory in cultured epithelial cells, cremaster muscles, and Schwann Cells (Martin-Padura, I., et al. (1998). J Cell Biol. 142(1):117-127).
Research Category
Cell Structure
Cell Structure
Research Sub Category
Adhesion (CAMs)
Adhesion (CAMs)
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
General description
32 kDa calculated
Junctional adhesion molecule A (JAM-A) is found in endothelial and epithelial tight junctions and is involved in the inflammatory enlistment of mononuclear cells containing LFA-1. JAM-A is linked to atherogenesis, platelet activation, transmigration of leukocytes and angiogenesis. JAM-A is also found to be important in the development of many different organ systems, and is mostly expressed in the epithelial parts and the embryonic vasculature. JAM-A is indicated to play a role in epithelial permeability, inflammation and proliferation in the intestine, aiding in homeostasis.
Immunogen
H5V murine heart capillary endothelial cells.
Preparation Note
Stable for 1 year at -20°C from date of receipt.
Handling Recommendations: Upon receipt and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.
Handling Recommendations: Upon receipt and prior to removing the cap, centrifuge the vial and gently mix the solution. Aliquot into microcentrifuge tubes and store at -20°C. Avoid repeated freeze/thaw cycles, which may damage IgG and affect product performance.
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存储类别
12 - Non Combustible Liquids
wgk
WGK 2
flash_point_f
Not applicable
flash_point_c
Not applicable
Caio S Bonilha et al.
Immunology letters, 235, 32-40 (2021-05-18)
The junctional adhesion molecule-A (JAM-A) is an adhesion molecule present in the surface of several cell types, such as endothelial cells and leukocytes as well as Dendritic Cells (DC). Given the potential relevance of JAM-A in diverse pathological conditions such
Catriona T Prendergast et al.
JCI insight, 7(7) (2022-02-23)
Mechanisms governing entry and exit of immune cells into and out of inflamed joints remain poorly understood. We sought herein to identify the key molecular pathways regulating such migration. Using murine models of inflammation in conjunction with mice expressing a
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