TICAM1 Antibody (N-term)
Peptide Affinity Purified Rabbit Polyclonal Antibody (Pab)
|Application ||WB, E|
|Calculated MW||76422 Da|
|Antigen Region||115-143 aa|
|Other Names||TIR domain-containing adapter molecule 1, TICAM-1, Proline-rich, vinculin and TIR domain-containing protein B, Putative NF-kappa-B-activating protein 502H, Toll-interleukin-1 receptor domain-containing adapter protein inducing interferon beta, MyD88-3, TIR domain-containing adapter protein inducing IFN-beta, TICAM1, PRVTIRB, TRIF|
|Target/Specificity||This TICAM1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 115-143 amino acids from the N-terminal region of human TICAM1.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||TICAM1 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Involved in innate immunity against invading pathogens. Adapter used by TLR3 and TLR4 (through TICAM2) to mediate NF- kappa-B and interferon-regulatory factor (IRF) activation, and to induce apoptosis. Ligand binding to these receptors results in TRIF recruitment through its TIR domain. Distinct protein- interaction motifs allow recruitment of the effector proteins TBK1, TRAF6 and RIPK1, which in turn, lead to the activation of transcription factors IRF3 and IRF7, NF-kappa-B and FADD respectively.|
|Cellular Location||Cytoplasmic vesicle, autophagosome. Note=Colocalizes with UBQLN1 in the autophagosome.|
|Tissue Location||Ubiquitously expressed but with higher levels in liver.|
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Provided below are standard protocols that you may find useful for product applications.
Involved in innate immunity against invading pathogens. Adapter used by TLR3 and TLR4 (through TICAM2) to mediate NF-kappa-B and interferon-regulatory factor (IRF) activation, and to induce apoptosis. Ligand binding to these receptors results in TRIF recruitment through its TIR domain. Distinct protein-interaction motifs allow recruitment of the effector proteins TBK1, TRAF6 and RIPK1, which in turn, lead to the activation of transcription factors IRF3 and IRF7, NF-kappa-B and FADD respectively.
Bin L.-H., et al. J. Biol. Chem. 278:24526-24532(2003).
Yamamoto M., et al. J. Immunol. 169:6668-6672(2002).
Oshiumi H., et al. Nat. Immunol. 4:161-167(2003).
Nakajima T., et al. Immunogenetics 60:727-735(2008).
Matsuda A., et al. Oncogene 22:3307-3318(2003).
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