MYD88 Monoclonal antibody

MYD88 Monoclonal Antibody for WB, ELISA

Host / Isotype

Mouse / IgG1

Reactivity

Human, rat, mouse and More (1)

Applications

WB, IHC, ELISA

Conjugate

Unconjugated

CloneNo.

1B10E12

Cat no : 66660-1-Ig

Synonyms

MYD88, MYD88D



Tested Applications

Positive WB detected inHSC-T6 cells, HepG2 cells, PC-12 cells, NIH/3T3 cells, 4T1 cells, SP2/0 cells

Recommended dilution

ApplicationDilution
Western Blot (WB)WB : 1:2000-1:10000
Sample-dependent, check data in validation data gallery

Product Information

66660-1-Ig targets MYD88 in WB, IHC, ELISA applications and shows reactivity with Human, rat, mouse samples.

Tested Reactivity Human, rat, mouse
Cited Reactivityhuman, mouse
Host / Isotype Mouse / IgG1
Class Monoclonal
Type Antibody
Immunogen MYD88 fusion protein Ag19770 相同性解析による交差性が予測される生物種
Full Name myeloid differentiation primary response gene (88)
Calculated molecular weight 33 kDa
Observed molecular weight 33-36 kDa
GenBank accession numberBC013589
Gene symbol MYD88
Gene ID (NCBI) 4615
Conjugate Unconjugated
Form Liquid
Purification Method Protein A purification
Storage Buffer PBS with 0.02% sodium azide and 50% glycerol pH 7.3.
Storage ConditionsStore at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.

Background Information

Background

Myeloid differentiation primary response 88 (MYD88) is an adapter protein critical to the innate and adaptive immune response.

 

What is the molecular weight of MYD88?

The molecular weight of MYD88 is 33 kDa.

 

What is the cellular localization of MYD88?

The subcellular localization of MYD88 is largely confined to the cytoplasm as condensed forms or aggregated structures.

 

What is the role of MYD88 in the IL-1R signaling pathway?

MYD88 plays a major role in the inflammatory signaling pathways downstream of Toll-like receptor (TLR) and interleukin-1 receptor (IL-1R) families. MYD88 links these receptors to IL-1R-associated kinases (IRAK), such as IRAK1 and IRAK2, via protein-protein interactions. The C-terminal TIR domain of MYD88 mediates the interaction with the receptors, whereas the N-terminal death domain of MYD88 associates with IRAK family members (PMID: 25580251). MYD88 acts via its intermediate domain to phosphorylate and thus activate IRAK1, IRAK2, IRF7, and TRAF6 to trigger NF-kappa-B signaling and cytokine secretion as part of the inflammatory response (PMID: 19679662).

 

What is MYD88's involvement in disease?

Defects in MYD88 due to deficiency of the protein leads to recurrent pyogenic bacterial infections, including invasive pneumococcal disease. Patients usually die between 1 and 11 months of age, but surviving patients are otherwise healthy with normal resistance to other microbes (PMID: 18669862). Mutations in the MYD88 gene also lead to the development of cancers such as lymphoma (PMID: 21179087) and some autoimmune disorders like ulcerative colitis (PMID: 24189845).


Protocols

Product Specific Protocols
WB protocol for MYD88 antibody 66660-1-IgDownload protocol
Standard Protocols
Click here to view our Standard Protocols

Publications

SpeciesApplicationTitle
mouseWB

ACS Nano

Bacteria-Anchoring Hybrid Liposome Capable of Absorbing Multiple Toxins for Antivirulence Therapy of Escherichia coli Infection.

Authors - Lixian Jiang
mouseWB

Theranostics

Fibrinogen-like protein 2 aggravates nonalcoholic steatohepatitis via interaction with TLR4, eliciting inflammation in macrophages and inducing hepatic lipid metabolism disorder.

Authors - Junjian Hu
mouseWB

Food Funct

Salvianolic acid B prevents body weight gain and regulates gut microbiota and LPS/TLR4 signaling pathway in high-fat diet-induced obese mice.

Authors - Lin Li
mouseWB

Pharm Biol

Catalpol relieved angiotensin II-induced blood–brain barrier destruction via inhibiting the TLR4 pathway in brain endothelial cells

Authors - Yu Xia
mouseWB

Life Sci

Salvianolate reduces neuronal apoptosis by suppressing OGD-induced microglial activation.

Authors - Pengwei Luan
mouseWB

Oncol Rep

α7‑nAchR agonist GTS‑21 reduces radiation‑induced lung injury.

Authors - Zijie Mei