MyD88 Antibody - #DF6162

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产品: MyD88 抗体
货号: DF6162
描述: Rabbit polyclonal antibody to MyD88
应用: WB IHC
文献验证: WB
反应: Human, Mouse, Rat
预测: Bovine, Horse, Sheep, Rabbit, Dog
蛋白号: Q99836
RRID: AB_2838129

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   规格 价格 库存
 50ul RMB¥ 1250 现货
 100ul RMB¥ 2300 现货
 200ul RMB¥ 3000 现货

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产品描述

来源:
Rabbit
应用:
WB 1:500-1:2000, IHC 1:50-1:200
*The optimal dilutions should be determined by the end user.
*Tips:

WB: 适用于变性蛋白样本的免疫印迹检测. IHC: 适用于组织样本的石蜡(IHC-p)或冰冻(IHC-f)切片样本的免疫组化/荧光检测. IF/ICC: 适用于细胞样本的荧光检测. ELISA(peptide): 适用于抗原肽的ELISA检测.

反应:
Human, Mouse, Rat
克隆:
Polyclonal
特异性:
MyD88 Antibody detects endogenous levels of total MyD88.
RRID:
AB_2838129
引用格式: Affinity Biosciences Cat# DF6162, RRID:AB_2838129.
偶联:
Unconjugated.
纯化:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
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.
别名:

展开/折叠

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;

抗原和靶标

免疫原:

A synthesized peptide derived from human MyD88, corresponding to a region within C-terminal amino acids.

基因/基因ID:
MYD88(4615)
描述:
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).

研究领域

· 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)

文献引用

1). Demethyleneberberine alleviated the inflammatory response by targeting MD-2 to inhibit the TLR4 signaling. Frontiers in Immunology, 2023 (PubMed: 37168866) [IF=5.7]

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). Morinda officinalis oligosaccharides mitigate chronic mild stress-induced inflammation and depression-like behaviour by deactivating the MyD88/PI3K pathway via E2F2. Frontiers in pharmacology, 2022 (PubMed: 36052143) [IF=5.6]

Application: WB    Species: Mouse    Sample: hippocampus

FIGURE 1. Protein expression of MyD88, p-PI3K, p-AKT and p-NF-κB p65 in the hippocampus of CMS-exposed mice. (A) Mice were subjected to the CMS protocol for 4 weeks, then sucrose preference test was performed. (B) Densitometric analysis and representative western blots of MyD88, p-PI3K, p-AKT and p-NF-κB p65 expressed in the hippocampus. Data are expressed as means ± SD (n = 3). #p < 0.05; ##p < 0.01.
3). Inhibition of murine herpesvirus-68 replication by IFN-gamma in macrophages is counteracted by the induction of SOCS1 expression. PLOS Pathogens, 2023 (PubMed: 30075008) [IF=5.5]

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.
4). β-patchoulene simultaneously ameliorated dextran sulfate sodium-induced colitis and secondary liver injury in mice via suppressing colonic leakage and flora imbalance. Biochemical Pharmacology, 2020 (PubMed: 33017576) [IF=5.3]

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.
5). DMB Alleviated Inflammatory Bowel Disease by Targeting MD-2 to Inhibit TLR4-NLRP3-IL-1β Signaling. , 2022

Application: WB    Species: Rat    Sample: colonic tissue

Figure.2 DMB inhibited TLR4 signaling in MyD88-dependent and independent ways.
6). Protective Effects of Oxyberberine in 5-Fluorouracil-Induced Intestinal Mucositis in the Mice Model. Evidence-based Complementary and Alternative Medicine, 2022 (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.

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