癌症的基本特征包括细胞增殖、血管生成、迁移、凋亡逃避机制和细胞永生等。找到癌症发生过程中这些通路的关键标记物和对应的抗体用于检测至关重要。
为您推荐一个泛素化位点预测神器——泛素化分析工具，可以为您的蛋白的泛素化位点作出预测和评分。
细胞自噬受体图形绘图工具为你的蛋白的细胞受体结合位点作出预测和评分，识别结合到自噬通路中的蛋白是非常重要的，便于让我们理解自噬在正常生理、病理过程中的作用，如发育、细胞分化、神经退化性疾病、压力条件下、感染和癌症。
TICAM1 Antibody (N-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
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Application 
| WB, E |
|---|---|
| Primary Accession | Q8IUC6 |
| Reactivity | Human, Mouse |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 76422 Da |
| Antigen Region | 115-143 aa |
| Gene ID | 148022 |
|---|---|
| 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. |
| Dilution | WB~~1:1000 E~~Use at an assay dependent concentration. |
| 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. |
| Name | TICAM1 |
|---|---|
| Synonyms | PRVTIRB, TRIF |
| Function | Involved in innate immunity against invading pathogens. Adapter used by TLR3, TLR4 (through TICAM2) and TLR5 to mediate NF- kappa-B and interferon-regulatory factor (IRF) activation, and to induce apoptosis (PubMed:12471095, PubMed:12539043, PubMed:14739303, PubMed:28747347, PubMed:35215908). Ligand binding to these receptors results in TRIF recruitment through its TIR domain (PubMed:12471095, PubMed:12539043, PubMed:14739303). 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 (PubMed:12471095, PubMed:12539043, PubMed:14739303). Phosphorylation by TBK1 on the pLxIS motif leads to recruitment and subsequent activation of the transcription factor IRF3 to induce expression of type I interferon and exert a potent immunity against invading pathogens (PubMed:25636800). Component of a multi- helicase-TICAM1 complex that acts as a cytoplasmic sensor of viral double-stranded RNA (dsRNA) and plays a role in the activation of a cascade of antiviral responses including the induction of pro- inflammatory cytokines (By similarity). |
| Cellular Location | Cytoplasmic vesicle, autophagosome. Cytoplasm, cytosol {ECO:0000250|UniProtKB:Q80UF7}. Mitochondrion {ECO:0000250|UniProtKB:Q80UF7}. Note=Colocalizes with UBQLN1 in the autophagosome (PubMed:21695056). Colocalizes in the cytosol with DDX1, DDX21 and DHX36. Colocalizes in the mitochondria with DDX1 and poly(I:C) RNA ligand. The multi-helicase-TICAM1 complex may translocate to the mitochondria upon poly(I:C) RNA ligand stimulation (By similarity). {ECO:0000250|UniProtKB:Q80UF7, ECO:0000269|PubMed:21695056} |
| Tissue Location | Ubiquitously expressed but with higher levels in liver. |
For Research Use Only. Not For Use In Diagnostic Procedures.
Provided below are standard protocols that you may find useful for product applications.
BACKGROUND
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.
REFERENCES
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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