MyD88 Antibody - #DF6162

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Product: MyD88 Antibody
Catalog: DF6162
Description: Rabbit polyclonal antibody to MyD88
Application: WB IHC
Reactivity: Human, Mouse, Rat
Prediction: Bovine, Horse, Sheep, Rabbit, Dog
Mol.Wt.: 33kDa; 33kD(Calculated).
Uniprot: Q99836
RRID: AB_2838129

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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
*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:
Bovine(88%), Horse(100%), Sheep(88%), Rabbit(100%), Dog(100%)
Clonality:
Polyclonal
Specificity:
MyD88 Antibody detects endogenous levels of total MyD88.
RRID:
AB_2838129
Cite Format: Affinity Biosciences Cat# DF6162, RRID:AB_2838129.
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

Mutant myeloid differentiation primary response 88; MYD 88; Myd88; MYD88_HUMAN; MYD88D; Myeloid differentiation marker 88; Myeloid differentiation primary response 88; Myeloid differentiation primary response gene (88); Myeloid differentiation primary response gene 88; Myeloid differentiation primary response gene; Myeloid differentiation primary response protein MyD88; OTTHUMP00000161718; OTTHUMP00000208595; OTTHUMP00000209058; OTTHUMP00000209059; OTTHUMP00000209060;

Immunogens

Immunogen:
Uniprot:

Q99836(MYD88_HUMAN) >>Visit HPA database.

Gene(ID):
MYD88(4615)
Expression:
Q99836 MYD88_HUMAN:

Ubiquitous.

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. MyD88 was originally isolated as a myeloid differentiation primary response gene that is rapidly induced upon IL-6 stimulated differentiation of M1 myeloleukemic cells into macrophages (4-6). It contains an amino-terminal death domain separated from a carboxyl-terminal TIR domain and functions as an adaptor in TLR/IL-1 receptor signaling (7). The death domain of MyD88 mediates interactions with the IRAK complex triggering a signaling cascade that includes the activation of NF-κB (8,9).
Sequence:
MAAGGPGAGSAAPVSSTSSLPLAALNMRVRRRLSLFLNVRTQVAADWTALAEEMDFEYLEIRQLETQADPTGRLLDAWQGRPGASVGRLLELLTKLGRDDVLLELGPSIEEDCQKYILKQQQEEAEKPLQVAAVDSSVPRTAELAGITTLDDPLGHMPERFDAFICYCPSDIQFVQEMIRQLEQTNYRLKLCVSDRDVLPGTCVWSIASELIEKRCRRMVVVVSDDYLQSKECDFQTKFALSLSPGAHQKRLIPIKYKAMKKEFPSILRFITVCDYTNPCTKSWFWTRLAKALSLP

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
Horse
100
Dog
100
Rabbit
100
Bovine
88
Sheep
88
Pig
75
Xenopus
75
Zebrafish
0
Chicken
0
Model Confidence:
High(score>80) Medium(80>score>50) Low(score<50) No confidence

PTMs - Q99836 As Substrate

Site PTM Type Enzyme
K95 Ubiquitination
C113 S-Nitrosylation
K115 Ubiquitination
K119 Ubiquitination
K127 Ubiquitination
K190 Ubiquitination
K214 Ubiquitination
C216 S-Nitrosylation
K231 Ubiquitination
K238 Ubiquitination
S244 Phosphorylation
K250 Ubiquitination
K256 Ubiquitination
Y257 Phosphorylation
K262 Ubiquitination
Y276 Phosphorylation
K282 Ubiquitination
K291 Ubiquitination

Research Backgrounds

Function:

Adapter protein involved in the Toll-like receptor and IL-1 receptor signaling pathway in the innate immune response. Acts via IRAK1, IRAK2, IRF7 and TRAF6, leading to NF-kappa-B activation, cytokine secretion and the inflammatory response. Increases IL-8 transcription. Involved in IL-18-mediated signaling pathway. Activates IRF1 resulting in its rapid migration into the nucleus to mediate an efficient induction of IFN-beta, NOS2/INOS, and IL12A genes. MyD88-mediated signaling in intestinal epithelial cells is crucial for maintenance of gut homeostasis and controls the expression of the antimicrobial lectin REG3G in the small intestine (By similarity).

PTMs:

Ubiquitinated; undergoes 'Lys-63'-linked polyubiquitination. OTUD4 specifically hydrolyzes 'Lys-63'-linked polyubiquitinated MYD88.

Subcellular Location:

Cytoplasm. Nucleus.

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

Ubiquitous.

Subunit Structure:

Homodimer. Also forms heterodimers with TIRAP. Binds to TLR2, TLR4, TLR5, IRAK1, IRAK2 and IRAK4 via their respective TIR domains. Interacts with IL18R1. Interacts with BMX, IL1RL1, IKBKE and IRF7. Interacts with LRRFIP1 and LRRFIP2; this interaction positively regulates Toll-like receptor (TLR) signaling in response to agonist. Interacts with FLII. LRRFIP1 and LRRFIP2 compete with FLII for MYD88-binding. Interacts with IRF1. Upon IL1B treatment, forms a complex with PELI1, IRAK1, IRAK4 and TRAF6; this complex recruits MAP3K7/TAK1, TAB1 and TAB2 to mediate NF-kappa-B activation. Direct binding of SMAD6 to PELI1 prevents the complex formation and hence negatively regulates IL1R-TLR signaling and eventually NF-kappa-B-mediated gene expression. May interact with PIK3AP1. Interacts (via TIR domain) with DHX9 (via H2A and OB-fold regions); this interaction is direct. Interacts with OTUD4 deubiquitinase; the interaction is direct.

(Microbial infection) In case of infection, interacts with uropathogenic E.coli protein TcpC; suppressing Toll-like receptor (TLR)-mediated cytokine production.

(Microbial infection) In case of infection, interacts with uropathogenic E.faecalis protein TcpF; suppressing Toll-like receptor (TLR)-mediated cytokine production.

Family&Domains:

The intermediate domain (ID) is required for the phosphorylation and activation of IRAK.

Research Fields

· Environmental Information Processing > Signal transduction > MAPK signaling pathway.   (View pathway)

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

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Pertussis.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > Leishmaniasis.

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

· Human Diseases > Infectious diseases: Parasitic > African trypanosomiasis.

· Human Diseases > Infectious diseases: Parasitic > Malaria.

· Human Diseases > Infectious diseases: Parasitic > Toxoplasmosis.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

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

· Human Diseases > Infectious diseases: Viral > Measles.

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

· 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). Demethyleneberberine alleviated the inflammatory response by targeting MD-2 to inhibit the TLR4 signaling. Frontiers in Immunology (PubMed: 37168866) [IF=7.3]

Application: WB    Species: Mouse    Sample: colonic tissue

Figure 3 DMB inhibited TLR4 signaling in a MyD88-dependent and -independent manner. (A) The protein expressions were assessed by immunoblotting for IL-1β, IκB, and p-IκB (Ser32) in colonic tissue; GAPDH served as reference. (B) The grayscale analysis of IL-1β and the ratio of p-IκB/IκB. (C) The protein expression of MyD88, TRAF6, and IRF3 in colonic tissue; GAPDH served as reference. (D) The grayscale analysis of MyD88, TTRAF6, and IRF3. (E–G) The mRNA levels of IL-1β, TNF-α, and IFN-α in colonic tissues. Statistical analysis was performed using one-way ANOVA. n = 3. #p < 0.05, ##p < 0.01, ###p < 0.005 (#: TNBS group versus the CON group) and *p < 0.05, **p < 0.01, ***p < 0.005, ns, non-significantly (*: the DMB or BBR group versus the TNBS group).
2). Inhibition of murine herpesvirus-68 replication by IFN-gamma in macrophages is counteracted by the induction of SOCS1 expression. PLOS Pathogens (PubMed: 30075008) [IF=6.7]

Application: WB    Species: mouse    Sample: macrophages

Fig 6.| TLR3 mediates the MHV-68-induced SOCS1 production.(D) BMMs were transfected with si-MyD88 or si-Control. Forty-eight hours post-transfection, the cells were infected with MHV-68. At 8 hpi, the SOCS1 mRNA levels and protein levels were determined. The SOCS1 mRNA levels are expressed as values relative to the MHV-68 infected, si-Control transfected cells.
3). β-patchoulene simultaneously ameliorated dextran sulfate sodium-induced colitis and secondary liver injury in mice via suppressing colonic leakage and flora imbalance. Biochemical Pharmacology (PubMed: 33017576) [IF=5.8]

Application: WB    Species: mouse    Sample: colon

Fig.4.| Effect of β-PAE on TLR4/MyD88/NF-κB and ROCK/MLC signalling pathway.(A) Representative bands of TLR4, MyD88, phospho-IκBα, IκBα and p65. (B)Quantitative results of band densities of TLR4, MyD88, phospho-IκBα, IκBα and p65.(C) Representative bands of ROCK1, phospho-MLC2 and MLC2.

Application: WB    Species: mouse    Sample: Colons

Fig.4. |Effect of β-PAE on TLR4/MyD88/NF-κB and ROCK/MLC signalling pathway. (A) Representative bands of TLR4, MyD88, phospho-IκBα, IκBα and p65.
4). Protective Effects of Oxyberberine in 5-Fluorouracil-Induced Intestinal Mucositis in the Mice Model. Evidence-based Complementary and Alternative Medicine (PubMed: 35677366)

Application: WB    Species: Mice    Sample:

Figure 7 The effect of OBB on the TLR4/NF-κB signaling pathway in 5-FU-induced IM mice. (a) Representative western blotting band, (b) TLR4, (c) MYD88, (d) IRAK-1, (e) the p-IκBα/IκBα ratio, and (f) the p-p65/p65 ratio. The results were expressed as mean ± SEM (n = 3). ##P < 0.01 vs. the control group; ∗P < 0.05 and ∗∗P < 0.01 vs. the 5-FU group; &P < 0.05 and &&P < 0.01vs. the BBR group.
5). DMB Alleviated Inflammatory Bowel Disease by Targeting MD-2 to Inhibit TLR4-NLRP3-IL-1β Signaling.

Application: WB    Species: Rat    Sample: colonic tissue

Figure.2 DMB inhibited TLR4 signaling in MyD88-dependent and independent ways.

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