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  3. SARM1 (D2M5I) Rabbit mAb (BSA and Azide Free)
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Recombinant: Superior lot-to-lot consistency, continuous supply, and animal-free manufacturing.

SARM1 (D2M5I) Rabbit mAb (BSA and Azide Free) #32629

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  • WB

    Product Specifications

    REACTIVITY H
    SENSITIVITY Endogenous
    MW (kDa) 73
    Source/Isotype Rabbit IgG
    Application Key:
    • WB-Western Blotting 
    Species Cross-Reactivity Key:
    • H-Human 

    Product Information

    Product Usage Information

    This product is the carrier free version of product #13022. All data were generated using the same antibody clone in the standard formulation which contains BSA and glycerol.

    This formulation is ideal for use with technologies requiring specialized or custom antibody labeling, including fluorophores, metals, lanthanides, and oligonucleotides. It is not recommended for ChIP, ChIP-seq, CUT&RUN or CUT&Tag assays. If you require a carrier free formulation for chromatin profiling, please contact us. Optimal dilutions/concentrations should be determined by the end user.

    BSA and Azide Free antibodies are quality control tested by size exclusion chromatography (SEC) to determine antibody integrity.

    Formulation

    Supplied in 1X PBS (10 mM Na2HPO4, 3 mM KCl, 2 mM KH2PO4, and 140 mM NaCl (pH 7.8)). BSA and Azide Free.

    For standard formulation of this product see product #13022

    Storage

    Store at -20°C. This product will freeze at -20°C so it is recommended to aliquot into single-use vials to avoid multiple freeze/thaw cycles. A slight precipitate may be present and can be dissolved by gently vortexing. This will not interfere with antibody performance.

    Specificity / Sensitivity

    SARM1 (D2M5I) Rabbit mAb recognizes endogenous levels of total human SARM1 protein and transfected levels of total mouse SARM1 protein.

    Species Reactivity:

    Human

    Source / Purification

    Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro324 of human SARM1 protein.

    Background

    Members of the Toll-like receptor (TLR) family, named for the closely related Toll receptor in Drosophila, play a pivotal role in innate immune responses (1-4). TLRs recognize conserved motifs found in various pathogens and mediate defense responses (5-7). Triggering of the TLR pathway leads to the activation of NF-κB and subsequent regulation of immune and inflammatory genes (4). The TLRs and members of the IL-1 receptor family share a conserved stretch of approximately 200 amino acids known as the Toll/Interleukin-1 receptor (TIR) domain (1). Upon activation, TLRs associate with a number of cytoplasmic adapter proteins containing TIR domains, including myeloid differentiation factor 88 (MyD88), MyD88-adapter-like/TIR-associated protein (MAL/TIRAP), TIR domain-containing adapter-inducing IFN-β (TRIF), and Toll-receptor-associated molecule (TRAM) (8-10). This association leads to the recruitment and activation of IRAK1 and IRAK4, which form a complex with TRAF6 to activate TAK1 and IKK (8,11-14). Activation of IKK leads to the degradation of IκB, which normally maintains NF-κB in an inactive state by sequestering it in the cytoplasm.
    Sterile alpha and TIR motif-containing protein 1 (SARM1) is a TIR domain-containing adaptor protein that contains two sterile alpha motif (SAM) domains (15). SARM1 is the only known TIR domain-containing adaptor that does not activate NF-κB, but instead negatively regulates toll-like receptor signaling (16). Research studies suggest that SARM1 inhibits signaling by TLR3 and TLR4 through direct interaction with the TIR domain-containing adapter TRIF, which is required for TLR3 and MyD88-independent TLR4 signaling (16-18). Additional research indicates that SARM1 can mediate injury-induced axon death, neuronal cell death in response to infection with the encephalitis-causing La Crosse virus, and T cell death following an immune response to infection (19-21).
    1. Akira, S. (2003) J Biol Chem 278, 38105-8.
    2. Beutler, B. (2004) Nature 430, 257-63.
    3. Dunne, A. and O'Neill, L.A. (2003) Sci STKE 2003, re3.
    4. Medzhitov, R. et al. (1997) Nature 388, 394-7.
    5. Schwandner, R. et al. (1999) J Biol Chem 274, 17406-9.
    6. Takeuchi, O. et al. (1999) Immunity 11, 443-51.
    7. Alexopoulou, L. et al. (2001) Nature 413, 732-8.
    8. Zhang, F.X. et al. (1999) J Biol Chem 274, 7611-4.
    9. Horng, T. et al. (2001) Nat Immunol 2, 835-41.
    10. Oshiumi, H. et al. (2003) Nat Immunol 4, 161-7.
    11. Muzio, M. et al. (1997) Science 278, 1612-5.
    12. Wesche, H. et al. (1997) Immunity 7, 837-47.
    13. Suzuki, N. et al. (2002) Nature 416, 750-6.
    14. Irie, T. et al. (2000) FEBS Lett 467, 160-4.
    15. Mink, M. et al. (2001) Genomics 74, 234-44.
    16. Carty, M. et al. (2006) Nat Immunol 7, 1074-81.
    17. Yamamoto, M. et al. (2002) J Immunol 169, 6668-72.
    18. Yamamoto, M. et al. (2003) Science 301, 640-3.
    19. Osterloh, J.M. et al. (2012) Science 337, 481-4.
    20. Mukherjee, P. et al. (2013) Immunity 38, 705-16.
    21. Panneerselvam, P. et al. (2013) Cell Death Differ 20, 478-89.

    Database Links

    UniProt ID: Q6SZW1


    Entrez-Gene Id: 23098


    Limited Uses

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    For Research Use Only. Not for Use in Diagnostic Procedures.
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