MYD88 Antibodies

Background

MYD88 gene encoding a protein critical cohesion, mainly involved in toll-like receptors in the innate immune system and interleukin 1 receptor signaling pathways. This protein plays a core role in inflammatory responses and immune defense by forming complexes to activate downstream transcription factors such as NF-κB. First identified by Bruce Beutler's team in 1990, its functional abnormality is closely related to a variety of autoimmune diseases and B-cell lymphoma. In 2011, a study found that the MYD88 L265P mutation is an important molecular marker of waldenstrom macroglobulinemia. This discovery significantly promoted the research and development of related targeted therapies. As a central molecule for immune signal transduction, MYD88 has become an important research object for understanding the immune regulatory mechanism and developing new immunotherapies. The study of its mechanism of action has provided new ideas for the treatment of various diseases.

Structure Function Application Advantage Our Products

Structure of MYD88

MYD88 is a key adaptor protein with a molecular weight of approximately 33 kDa, and its molecular weight varies slightly among different species:

Species Human Mouse Rat Zebrafish
Molecular Weight (kDa) 33.0 33.2 33.1 32.8
Primary Structural Differences Highly conserved death domains (DD) and TIR domains Highly homologous to human MYD88 (~90%) Similar signal transmission function Retain the core immune regulatory function

MYD88 is composed of 296 amino acids, and its structure includes the N-terminal death domain (DD) and the C-terminal Toll/IL-1 receptor (TIR) domain. DD mediates protein-protein interactions, while the TIR domain participates in downstream signal transduction. This protein activates IRAK kinase by forming a polymeric complex, thereby triggering the NF-κB and MAPK pathways and regulating inflammatory and immune responses. Its functional abnormalities (such as the L265P mutation) are closely related to various lymphomas and autoimmune diseases.

Fig. 1:MyD88 and immune escape. Fig. 1 MyD88 is associated with immune escape.1

Key structural properties of MYD88:

  • Dual-domain architecture
  • Conserved protein-protein interaction interfaces
  • Iron ion independent
  • Key functional residues

Functions of MYD88

The core function of the MYD88 gene is to mediate innate immune signal transduction, and it also plays a key role in various pathological processes.

Function Description
Immune signal transduction As a key adaptor protein of the Toll-like receptor (TLR) and IL-1 receptor family, it recruits downstream signaling molecules through the TIR domain.
Regulation of inflammatory response Activate the IRAK4/NF-κB signaling pathway and induce the production of pro-inflammatory factors (TNF-α, IL-6, etc.).
Promotion of B cell survival Cell survival is maintained in B-cell receptor (BCR) signaling, whose mutation (L265P) results in constitutive activation.
Tumorigenesis participation Carcinogenic mutations occur in 90% of cases of Waldenstrom macroglobulinemia and some diffuse large B-cell lymphomas.
Association with autoimmune diseases Abnormal activation is closely related to autoimmune diseases such as rheumatoid arthritis and systemic lupus erythematosus.

Unlike multi-step activated immune receptors, MYD88 achieves rapid response through a "signal hub" mode, and its activation threshold directly affects the intensity and duration of the inflammatory response. This property makes it a key molecule for regulating immune balance and a potential target for the treatment of various diseases.

Applications of MYD88 and MYD88 Antibody in Literature

1. Song, Jiali, et al. "MyD88 and its inhibitors in cancer: prospects and challenges." Biomolecules 14.5 (2024): 562. https://doi.org/10.3390/biom14050562

The article indicates that MyD88 is a key molecule of innate immunity. It promotes immune escape and tumor progression by regulating inflammatory factors and the tumor microenvironment, and its abnormal signals are associated with poor prognosis. Targeting MyD88 (such as inhibiting signaling pathways or protein polymerization) has significant potential in cancer treatment, but the specific mechanisms still need to be explored. Current inhibitor research provides a new direction for tumor treatment.

2. Saikh, Kamal U. "MyD88 and beyond: a perspective on MyD88-targeted therapeutic approach for modulation of host immunity." Immunologic Research 69.2 (2021): 117-128. https://doi.org/10.1007/s12026-021-09188-2

The article indicates that MyD88 is a key adaptor protein of innate immunity, regulating pathways such as TLR/IL-1R. However, its excessive activation can trigger inflammatory diseases and inhibit the antiviral response of type I interferon. Small molecule inhibitors targeting MyD88 BB-loop can reduce inflammation and enhance antiviral immunity by blocking dimerization in the TIR domain, thus becoming a new strategy for broad-spectrum anti-infection treatment.

3. Liu, Yu, et al. "MyD88 in myofibroblasts enhances nonalcoholic fatty liver disease-related hepatocarcinogenesis via promoting macrophage M2 polarization." Cell Communication and Signaling 22.1 (2024): 86. https://doi.org/10.1186/s12964-024-01489-x

The article indicates that MyD88 in myofibroblasts drives M2 polarization of macrophages through the CCL9-CCR1 axis, promoting the progression of NAFLD-related liver cancer. Inhibiting MyD88 or CCR1 can reduce fat accumulation and tumor growth. The human homologous protein CCL15 is associated with a poor prognosis of liver cancer, suggesting that MyD88 is a potential therapeutic target.

4. Lacey, Carolyn A., et al. "MyD88-dependent glucose restriction and itaconate production control Brucella infection." Infection and Immunity 89.10 (2021). https://doi.org/10.1128/iai.00156-21

The article indicates that MyD88 inhibits Brucella infection by regulating glycolysis and itaconic acid production in macrophages. Its absence leads to abnormal glucose metabolism in the host and promotes bacterial proliferation. Itaconic acid has direct antibacterial effects and regulates inflammatory responses, revealing a new mechanism by which MyD88 defuses intracellular pathogens through metabolic reprogramming.

5. Cucos, Catalina Anca, et al. "Increased MYD88 blood transcript in a mouse model of Alzheimer's disease." BMC neuroscience 23.1 (2022): 13. https://doi.org/10.1186/s12868-022-00699-8

The article indicates that the level of MYD88 mRNA in the peripheral blood of Alzheimer's disease (AD) model mice is significantly elevated and continues to rise with the progression of the disease, suggesting that MYD88 may serve as a plasma biomarker for monitoring the progression of AD. However, treatment with the cholinesterase inhibitor carbapatine did not change its expression level.

Creative Biolabs: MYD88 Antibodies for Research

Creative Biolabs specializes in the production of high-quality MYD88 antibodies for research and industrial applications. Our portfolio includes monoclonal antibodies tailored for ELISA, Flow Cytometry, Western blot, immunohistochemistry, and other diagnostic methodologies.

  • Custom MYD88 Antibody Development: Tailor-made solutions to meet specific research requirements.
  • Bulk Production: Large-scale antibody manufacturing for industry partners.
  • Technical Support: Expert consultation for protocol optimization and troubleshooting.
  • Aliquoting Services: Conveniently sized aliquots for long-term storage and consistent experimental outcomes.

For more details on our MYD88 antibodies, custom preparations, or technical support, contact us at email.

Reference

  1. Song, Jiali, et al. "MyD88 and its inhibitors in cancer: prospects and challenges." Biomolecules 14.5 (2024): 562. https://doi.org/10.3390/biom14050562
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Anti-MYD88 antibodies

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Target: MYD88
Host: Mouse
Antibody Isotype: IgG1
Specificity: Human, Dog
Clone: CBFYM-2903
Application*: F, IF
Target: MYD88
Host: Mouse
Antibody Isotype: IgG
Specificity: Human, Mouse
Clone: A1270
Application*: ELISA, IHC, WB
Target: MYD88
Host: Mouse
Antibody Isotype: IgG2b, κ
Specificity: Human
Clone: A1269
Application*: Dot blot, ELISA, WB
Target: MYD88
Host: Mouse
Antibody Isotype: IgG1
Specificity: Human, Mouse, Rat
Clone: CF296
Application*: ELISA, WB
Target: MYD88
Host: Rabbit
Antibody Isotype: IgG
Specificity: Human
Clone: RM306
Application*: IHC, WB
Target: MYD88
Host: Rabbit
Antibody Isotype: IgG
Specificity: Human, Mouse, Rat, Monkey
Clone: D80F5
Application*: WB, IP
Target: MYD88
Host: Mouse
Specificity: Rat
Clone: CBFYM-2905
Application*: WB, IC, P, C, E
Target: MYD88
Host: Rabbit
Antibody Isotype: IgG
Specificity: Human, Monkey, Mouse, Rat
Clone: CBFYM-2904
Application*: IP, WB
Target: MYD88
Host: Mouse
Antibody Isotype: IgG2b
Specificity: Human, Dog
Clone: CBFYM-2902
Application*: F, IH, P, C
Target: MYD88
Host: Mouse
Specificity: Human
Clone: CBFYM-2901
Application*: E, WB
Target: MYD88
Host: Mouse
Antibody Isotype: IgG2a
Specificity: Human
Clone: CBFYM-2900
Application*: F, IF, IH, WB
Target: MYD88
Host: Mouse
Antibody Isotype: IgG2b
Specificity: Human
Clone: CBFYM-2899
Application*: E, IF, IH, WB
Target: MYD88
Host: Mouse
Antibody Isotype: IgG1, κ
Specificity: Human, Mouse
Clone: CBFYM-0164
Application*: F, IC, IF, WB
Target: MYD88
Host: Rat
Antibody Isotype: IgG2a
Specificity: Human
Clone: CBFYM-0124
Application*: IC
Target: MYD88
Host: Mouse
Antibody Isotype: IgG2b, κ
Specificity: Human
Clone: CBFYM-0092
Application*: WB, F, E, IF
Target: MYD88
Host: Mouse
Antibody Isotype: IgG2b
Specificity: Human, Mouse
Clone: 2E9C2
Application*: IF, IH, WB
Target: MYD88
Host: Mouse
Antibody Isotype: IgG1
Specificity: Human
Clone: E9K4E
Application*: WB, IP
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Submit A Review Fig.3 Signaling pathways in cancers. (Creative Biolabs Authorized) Fig.4 Protocols troubleshootings & guides. (Creative Biolabs Authorized) Submit A Review Fig.3 Signaling pathways in cancers. (Creative Biolabs Authorized) Fig.4 Protocols troubleshootings & guides. (Creative Biolabs Authorized)
For Research Use Only. Not For Clinical Use.
(P): Predicted
* Abbreviations
  • AActivation
  • AGAgonist
  • APApoptosis
  • BBlocking
  • BABioassay
  • BIBioimaging
  • CImmunohistochemistry-Frozen Sections
  • CIChromatin Immunoprecipitation
  • CTCytotoxicity
  • CSCostimulation
  • DDepletion
  • DBDot Blot
  • EELISA
  • ECELISA(Cap)
  • EDELISA(Det)
  • ESELISpot
  • EMElectron Microscopy
  • FFlow Cytometry
  • FNFunction Assay
  • GSGel Supershift
  • IInhibition
  • IAEnzyme Immunoassay
  • ICImmunocytochemistry
  • IDImmunodiffusion
  • IEImmunoelectrophoresis
  • IFImmunofluorescence
  • IGImmunochromatography
  • IHImmunohistochemistry
  • IMImmunomicroscopy
  • IOImmunoassay
  • IPImmunoprecipitation
  • ISIntracellular Staining for Flow Cytometry
  • LALuminex Assay
  • LFLateral Flow Immunoassay
  • MMicroarray
  • MCMass Cytometry/CyTOF
  • MDMeDIP
  • MSElectrophoretic Mobility Shift Assay
  • NNeutralization
  • PImmunohistologyp-Paraffin Sections
  • PAPeptide Array
  • PEPeptide ELISA
  • PLProximity Ligation Assay
  • RRadioimmunoassay
  • SStimulation
  • SESandwich ELISA
  • SHIn situ hybridization
  • TCTissue Culture
  • WBWestern Blot
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