MABC985
Anti-TRAF4 Antibody, clone 5MLN-2H1
ascites fluid, clone 5MLN-2H1, from mouse
Synonym(s):
TNF receptor-associated factor 4, Cysteine-rich domain associated with RING and Traf domains protein 1, Metastatic lymph node gene 62 protein, MLN 62, RING finger protein 83
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About This Item
UNSPSC Code:
12352203
eCl@ss:
32160702
NACRES:
NA.41
Recommended Products
biological source
mouse
Quality Level
antibody form
ascites fluid
antibody product type
primary antibodies
clone
5MLN-2H1, monoclonal
species reactivity
mouse, human
species reactivity (predicted by homology)
rat (based on 100% sequence homology)
technique(s)
immunocytochemistry: suitable
immunohistochemistry: suitable
western blot: suitable
isotype
IgG1
NCBI accession no.
UniProt accession no.
shipped in
wet ice
target post-translational modification
unmodified
Gene Information
human ... TRAF4(9618)
Related Categories
General description
TNF receptor-associated factor 4 (TRAF4), also known as Cysteine-rich domain associated with RING and Traf domains protein 1 (CART1), Metastatic lymph node gene 62 protein (MLN 62), and RING finger protein 83 (RNF83), is an adapter protein and signal transducer that links members of the TNF family to different signaling pathways. As such TRAF4 plays a role in the activation of the NF-kappa- and JNK signaling as well as a player in apoptosis and cell survival pathways. In development, TRAF4 is necessary for proper skeleton development and lung development. TRAF4 is localized in the perinuclear region of the cell as well as other locations including cell junctions where it is associated with various cytoskeletal elements. TRAF4 is expressed in the epithelial cells of thymus, respiratory tract, salivary gland, and esophagus. TRAF4 expression is regulated via the ubiquitin proteasome system and is a polyubiquitin target protein.
Specificity
This antibody detects TRAF4 and is cited in publications as both clone 5MLN-2H1 and clone 2H1.
Immunogen
Linear peptide corresponding to Human TRAF4.
Application
Imunnohistochemistry Analysis: A representative lot of this antibody detected TRAF4 in multiple human cancer tissues (Camilleri-Broet. S., et al. (2007) Oncogene. 26:142-147).
Imunnohistochemistry Analysis: A representative lot of this antibody detected TRAF4 in Breast cancer tissue (Kedinger, V., et. al. (2008) PLoS ONE. 3(10):e3518).
Immunocytochemistry Analysis: A representative lot of this antibody detected TRAF4 in MCF-10A cells and tranfected HeLa cells (Kedinger, V., et. al. (2008) PLoS ONE. 3(10):e3518).
Imunnohistochemistry Analysis: A representative lot of this antibody detected TRAF4 in Breast cancer tissue (Kedinger, V., et. al. (2008) PLoS ONE. 3(10):e3518).
Immunocytochemistry Analysis: A representative lot of this antibody detected TRAF4 in MCF-10A cells and tranfected HeLa cells (Kedinger, V., et. al. (2008) PLoS ONE. 3(10):e3518).
Research Category
Apoptosis & Cancer
Apoptosis & Cancer
Research Sub Category
Tumor Markers
Tumor Markers
This Anti-TRAF4 Antibody, clone 5MLN-2H1 is validated for use in Western Blotting and Immunohistochemistry and Immunocytochemistry for the detection of TRAF4.
Quality
Evaluated by Western Blotting in HeLa cell lysate.
Western Blotting Analysis: A 1:1000 dilution of this antibody detected TRAF4 in 10 µg of HeLa cell lysate.
Western Blotting Analysis: A 1:1000 dilution of this antibody detected TRAF4 in 10 µg of HeLa cell lysate.
Target description
~53 kDa observed
Physical form
Mouse monoclonal IgG1 ascites without preservatives.
Unpurified
Storage and Stability
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.
Other Notes
Concentration: Please refer to lot specific datasheet.
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.
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wgk_germany
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Impaired neural tube closure, axial skeleton malformations, and tracheal ring disruption in TRAF4-deficient mice.
Regnier, CH; Masson, R; Kedinger, V; Textoris, J; Stoll, I; Chenard, MP; Dierich et al.
Proceedings of the National Academy of Sciences of the USA null
Tumor necrosis factor receptor-associated factor 4 is a dynamic tight junction-related shuttle protein involved in epithelium homeostasis.
Kedinger, V; Alpy, F; Baguet, A; Polette, M; Stoll, I; Chenard, MP; Tomasetto, C; Rio, MC
Testing null
TRAF4 overexpression is a common characteristic of human carcinomas.
Camilleri-Broet, S; Cremer, I; Marmey, B; Comperat, E; Viguie, F; Audouin, J; Rio et al.
Oncogene null
Xin Dong et al.
Cell death & disease, 14(2), 102-102 (2023-02-11)
The E3 ligase TNF receptor-associated factor 4 (TRAF4) is upregulated and closely associated with tumorigenesis and the progression of multiple human malignancies. However, its effect on radiosensitivity in colorectal cancer (CRC) has not been elucidated. The present study found that
Xinfang Yu et al.
Journal of hematology & oncology, 13(1), 40-40 (2020-05-03)
Aberrant activation of DNA damage response (DDR) is a major cause of chemoresistance in colorectal cancer (CRC). CHK1 is upregulated in CRC and contributes to therapeutic resistance. We investigated the upstream signaling pathways governing CHK1 activation in CRC. We identified
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