TICAM1 Antibody - #DF6289

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Product: TICAM1 Antibody
Catalog: DF6289
Description: Rabbit polyclonal antibody to TICAM1
Application: WB IHC IF/ICC
Reactivity: Human, Mouse, Rat
Prediction: Pig, Zebrafish, Bovine, Horse, Sheep, Dog, Chicken
Mol.Wt.: 76kDa; 76kD(Calculated).
Uniprot: Q8IUC6
RRID: AB_2838255

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Related Downloads
MS Report
HPLC Report
MSDS
Data Sheet
COA
Protocols
WB Handbook
IHC Protocol
IF/ICC Protocol

Product Info

Source:
Rabbit
Application:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

Reactivity:
Human,Mouse,Rat
Prediction:
Pig(100%), Zebrafish(88%), Bovine(100%), Horse(100%), Sheep(100%), Dog(100%), Chicken(100%)
Clonality:
Polyclonal
Specificity:
TICAM1 Antibody detects endogenous levels of total TICAM1.
RRID:
AB_2838255
Cite Format: Affinity Biosciences Cat# DF6289, RRID:AB_2838255.
Conjugate:
Unconjugated.
Purification:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
Storage:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
Alias:

Fold/Unfold

IIAE6; MGC35334; MyD88 3; Proline rich vinculin and TIR domain containing protein B; Proline-rich; PRVTIRB; Putative NF kappa B activating protein 502H; Putative NF-kappa-B-activating protein 502H; Putative NFkB activating protein; TCAM1_HUMAN; TICAM 1; TICAM-1; Ticam1; TIR domain containing adapter molecule 1; TIR domain containing adapter protein inducing IFN beta; TIR domain containing adaptor inducing interferon beta; TIR domain-containing adapter molecule 1; TIR domain-containing adapter protein inducing IFN-beta; Toll interleukin 1 receptor domain containing adapter protein inducing interferon beta; Toll like receptor adaptor molecule 1; Toll-interleukin-1 receptor domain-containing adapter protein inducing interferon beta; TRIF; TRIF protein; vinculin and TIR domain-containing protein B;

Immunogens

Immunogen:
Uniprot:

Q8IUC6(TCAM1_HUMAN) >>Visit HPA database.

Gene(ID):
TICAM1(148022)
Expression:
Q8IUC6 TCAM1_HUMAN:

Ubiquitously expressed but with higher levels in liver.

Description:
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 (1-3). TLRs recognize conserved motifs found in various pathogens and mediate defense responses. Triggering of the TLR pathway leads to the activation of NF-κB and subsequent regulation of immune and inflammatory genes. The TLRs and members of the IL-1 receptor family share a conserved stretch of approximately 200 amino acids known as the TIR domain. Upon activation, TLRs associate with a number of cytoplasmic adaptor proteins containing TIR domains including MyD88 (myeloid differentiation factor), MAL/TIRAP (MyD88-adaptor-like/TIR-associated protein), TRIF (Toll-receptor-associated activator of interferon), and TRAM (Toll-receptor-associated molecule). This association leads to the recruitment and activation of IRAK1 and IRAK4, which form a complex with TRAF6 to activate TAK1 and IKK. Activation of IKK leads to the degradation of IκB that normally maintains NF-κB inactivity by sequestering it in the cytoplasm.
Sequence:
MACTGPSLPSAFDILGAAGQDKLLYLKHKLKTPRPGCQGQDLLHAMVLLKLGQETEARISLEALKADAVARLVARQWAGVDSTEDPEEPPDVSWAVARLYHLLAEEKLCPASLRDVAYQEAVRTLSSRDDHRLGELQDEARNRCGWDIAGDPGSIRTLQSNLGCLPPSSALPSGTRSLPRPIDGVSDWSQGCSLRSTGSPASLASNLEISQSPTMPFLSLHRSPHGPSKLCDDPQASLVPEPVPGGCQEPEEMSWPPSGEIASPPELPSSPPPGLPEVAPDATSTGLPDTPAAPETSTNYPVECTEGSAGPQSLPLPILEPVKNPCSVKDQTPLQLSVEDTTSPNTKPCPPTPTTPETSPPPPPPPPSSTPCSAHLTPSSLFPSSLESSSEQKFYNFVILHARADEHIALRVREKLEALGVPDGATFCEDFQVPGRGELSCLQDAIDHSAFIILLLTSNFDCRLSLHQVNQAMMSNLTRQGSPDCVIPFLPLESSPAQLSSDTASLLSGLVRLDEHSQIFARKVANTFKPHRLQARKAMWRKEQDTRALREQSQHLDGERMQAAALNAAYSAYLQSYLSYQAQMEQLQVAFGSHMSFGTGAPYGARMPFGGQVPLGAPPPFPTWPGCPQPPPLHAWQAGTPPPPSPQPAAFPQSLPFPQSPAFPTASPAPPQSPGLQPLIIHHAQMVQLGLNNHMWNQRGSQAPEDKTQEAE

Predictions

Predictions:

Score>80(red) has high confidence and is suggested to be used for WB detection. *The prediction model is mainly based on the alignment of immunogen sequences, the results are for reference only, not as the basis of quality assurance.

Species
Results
Score
Pig
100
Horse
100
Bovine
100
Sheep
100
Dog
100
Chicken
100
Zebrafish
88
Xenopus
0
Rabbit
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q8IUC6 As Substrate

Site PTM Type Enzyme
K65 Ubiquitination
S196 Phosphorylation
S199 Phosphorylation
S205 Phosphorylation
S210 Phosphorylation
S212 Phosphorylation
S223 Phosphorylation
S388 Phosphorylation
S389 Phosphorylation
S390 Phosphorylation
S500 Phosphorylation
Y570 Phosphorylation
Y573 Phosphorylation
Y577 Phosphorylation
K707 Ubiquitination

Research Backgrounds

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. 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. 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. 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 proinflammatory cytokines (By similarity).

PTMs:

Phosphorylated by TBK1. Following activation, phosphorylated by TBK1 at Ser-210 in the pLxIS motif. The phosphorylated pLxIS motif constitutes an IRF3-binding motif, leading to recruitment of the transcription factor IRF3 to induce type-I interferons and other cytokines.

Polyubiquitinated by TRIM38 with 'Lys-48'-linked chains, leading to proteasomal degradation.

(Microbial infection) Cleaved and degraded by hepatitis A virus (HAV) protein 3CD allowing the virus to disrupt host TLR3 signaling.

(Microbial infection) Cleaved by CVB3 protease 3C allowing the virus to disrupt host TLR3 signaling.

(Microbial infection) Cleaved by Seneca Valley virus protease 3C allowing the virus to disrupt host TLR3 signaling.

(Microbial infection) Cleaved by protease 3C of human enterovirus D68 (EV68) allowing the virus to disrupt host TLR3 signaling.

Subcellular Location:

Cytoplasmic vesicle>Autophagosome. Cytoplasm>Cytosol. Mitochondrion.
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).

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
Tissue Specificity:

Ubiquitously expressed but with higher levels in liver.

Subunit Structure:

Homodimer. Found in a multi-helicase-TICAM1 complex at least composed of DHX36, DDX1, DDX21 and TICAM1; this complex exists in resting cells with or without poly(I:C) RNA ligand stimulation. Interacts (via TIR domain) with DDX21 (via C-terminus). Interacts (via TIR domain) with DHX36 (via C-terminus) (By similarity). Interacts with AZI2 and IRF7. Interacts with TICAM2 in TLR4 recruitment. Interaction with PIAS4 inhibits the TICAM1-induced NF-kappa-B, IRF and IFNB1 activation. Interacts with IKBKB and IKBKE. Interaction with SARM1 blocks TICAM1-dependent transcription factor activation. Interacts with TRAF3 (By similarity). Interacts (when phosphorylated) with IRF3; following activation and phosphorylation on the pLxIS motif by TBK1, recruits IRF3. Interacts with TBK1, TRAF6 and RIPK1 and these interactions are enhanced in the presence of WDFY1. Interacts with TRAFD1 (By similarity). Interacts with UBQLN1 (via UBA domain). Interacts with TLR4 in response to LPS in a WDFY1-dependent manner (By similarity). Interacts with WDFY1 in response to poly(I:C) (By similarity). Interacts (via the TIR domain) with TLR3 in response to poly(I:C) and this interaction is enhanced in the presence of WDFY1. Interacts with TRIM56. 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 proinflammatory cytokines (By similarity). Interacts (via the TIR domain) with TLR5.

(Microbial infection) Interacts with Seneca Valley virus protease 3C; this interaction allows the cleavage of TICAM1/TRIF and subsequent suppression of host innate immunity.

(Microbial infection) Interacts (via C-terminus) with coxsackievirus B3 (CVB3) protease 3C.

Family&Domains:

The pLxIS motif constitutes an IRF3-binding motif: following phosphorylation by TBK1, the phosphorylated pLxIS motif of TICAM1 recruits IRF3 (PubMed:25636800). IRF3 is then phosphorylated and activated by TBK1 to induce type-I interferons and other cytokines (PubMed:25636800).

The N-terminal region is essential for activation of the IFNB promoter activity.

The N-terminal domain (TRIF-NTD) is globular and consists of two alpha-helical subdomains connected by a 14-residue linker. It shares structural similarity with IFIT family members N-terminal regions.

Research Fields

· Cellular Processes > Cell growth and death > Necroptosis.   (View pathway)

· Environmental Information Processing > Signal transduction > NF-kappa B signaling pathway.   (View pathway)

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Parasitic > Chagas disease (American trypanosomiasis).

· Human Diseases > Infectious diseases: Viral > Hepatitis C.

· Human Diseases > Infectious diseases: Viral > Hepatitis B.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Infectious diseases: Viral > Human papillomavirus infection.

· Human Diseases > Infectious diseases: Viral > Herpes simplex infection.

· Organismal Systems > Immune system > Toll-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

References

1). Chronic low-grade inflammation is involved in TLR4 knockout-induced spontaneous obesity in aged mice. BIOMEDICINE & PHARMACOTHERAPY, 2022 (PubMed: 35093760) [IF=7.5]

Application: WB    Species: Mouse    Sample: liver

Fig. 5. TLR4 KO activated the TRIF pathway in the liver. a mRNA expression of TRIF and IRF3, n = 6. b Protein expression of hepatic TRIF, IRF3 and pIRF3, and the relative TRIF, IRF3 and pIRF3 protein levels is shown in bar graph. c Immunoreactivities of pIRF3 were detected by immunohistochemistry and relative optical density of immunoreactivities, n = 6. Scale bar is 50 µm. Data are presented as mean ± S.E.M. *P 

Application: IHC    Species: Mouse    Sample: liver

Fig. 5. TLR4 KO activated the TRIF pathway in the liver. a mRNA expression of TRIF and IRF3, n = 6. b Protein expression of hepatic TRIF, IRF3 and pIRF3, and the relative TRIF, IRF3 and pIRF3 protein levels is shown in bar graph. c Immunoreactivities of pIRF3 were detected by immunohistochemistry and relative optical density of immunoreactivities, n = 6. Scale bar is 50 µm. Data are presented as mean ± S.E.M. *P 
2). Emodin Attenuates Lipopolysaccharide-Induced Acute Liver Injury via Inhibiting the TLR4 Signaling Pathway in vitro and in vivo. Frontiers in Pharmacology, 2018 (PubMed: 30186181) [IF=5.6]

Application: WB    Species: mouse    Sample: RAW264.7cell

FIGURE 5 | Effect of emodin on TLR4 and downstream molecules after TLR4 knock-down. Expression of TLR4 was observed with a fluorescence microscope after siRNA was introduced into cells for 48 h, and then the cells were treated with different drug intervention for 24 h.(D) Expression of protein was assayed by western blotting. Data are shown as the mean ± SD. $P < 0.05 compared with the normal group; #P < 0.05 compared with the Si-TLR4 group;∗P < 0.05, ∗∗P < 0.01, compared with the Si-TLR4-LPS group; MP < 0.05, MMP < 0.01, compared with the DEX group. si-TLR4: TLR4 was knocked down in Raw264.7 cells by siRNA. si-NC: SiRNA negative control group.
3). Protecting effect of emodin in experimental autoimmune encephalomyelitis mice by inhibiting microglia activation and inflammation via Myd88/PI3K/Akt/NF-κB signalling pathway. Bioengineered, 2022 (PubMed: 35287559) [IF=4.9]

Application: WB    Species: Mice    Sample: cerebral cortex tissues

Figure 10. The effects of emodin on TLR4, Myd88, Ticam1, and NFKB1 mRNA relative expression and protein expression. Mice were sacrificed on 21 dpi. The cerebral cortex tissues are collected. The relative mRNA relative expression of TLR4 (a), Myd88 (b), Ticam1 (c), and NFKB1(d) was analyzed by qRT-PCR. The protein expression of TLR4, Myd88, Ticam1, and NFKB1 was analyzed by western blot. All data were expressed as mean ± S.D (n = 6). *P < 0.05, **P < 0.01 versus NC group, #P < 0.05, ##P < 0.01 versus EAE group. Comparisons among each group were analyzed by one-way ANOVA in A, B, C, D, and F.
4). Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex Encephalitis. Frontiers in Molecular Neuroscience, 2019 (PubMed: 31080403) [IF=4.8]

Application: WB    Species: mouse    Sample: BV-2 cells

Figure 4.| Lentiviral vector-mediated overexpression of TLR3 in BV-2 cells. The lentivirus (10 MOI) was incubated with the BV-2 cells for 72 h. (A) The expression of GFP was observed with a fluorescence microscope after lentivirus was introduced into the BV-2 cells. (B) The mRNA levels of TLR3 and its downstream molecules were measured by RT-PCR. (C) The protein levels were detected by western blotting. Data are shown as the mean ± SD of three independent experiments of triplicate samples.**P < 0.01 for lentivirus-up vs. normal; *P < 0.05 for lentivirus-up vs. normal (by Student’s t-test).
5). The intervention mechanism of emodin on TLR3 pathway in the process of central nervous system injury caused by herpes virus infection. NEUROLOGICAL RESEARCH, 2021 (PubMed: 33274693) [IF=1.9]

Application: WB    Species: Mice    Sample: brain tissues

Figure 4. The protein expression of TLR3 and its downstream protein in brain tissues of mice.
6). Immunofluorescent Labeling in Nasal Mucosa Tissue Sections of Allergic Rhinitis Rats via Multicolor Immunoassay. Journal of visualized experiments : JoVE, 2023 (PubMed: 37811950) [IF=1.2]

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