Biological Strategies: Western Blot: MyD88 Antibody [NB100-56698] - The ability of PTX to induce the IL-1 Beta IL-6 cascade depends on the integrity of its multimeric structure and enzymatic activity.Western ...read more
Immunocytochemistry/ Immunofluorescence: MyD88 Antibody [NB100-56698] - Raw264.7 cells were fixed for 10 minutes using 10% formalin and then permeabilized for 5 minutes using 1X PBS + 0.5% Triton-X100. The cells were ...read more
Immunohistochemistry-Paraffin: MyD88 Antibody [NB100-56698] - Tissue section of human liver using at 1:100 dilution. This antibody generated a very specific cytoplasmic staining in the hepatocytes as well as the ...read more
Western Blot: MyD88 Antibody [NB100-56698] - Analysis of MyD88 in human spleen cell lysate using 0.5 ug/ml of NB100-56698.
Immunohistochemistry-Paraffin: MyD88 Antibody [NB100-56698] - Tissue section of human liver using at 1:100 dilution. This antibody generated a very specific cytoplasmic staining in the hepatocytes as well as the ...read more
Western Blot: MyD88 Antibody - BSA Free [NB100-56698] - TLR & other LPS-response elements in LPS-stimulated HSCs.(A) Microarray data show time-dependent changes in the indicated transcripts. For clarity control gene ...read more
myeloid differentiation primary response protein MyD88
Background
MyD88, a protein involved in interleukin-1 (IL-1) mediated signalling was originally isolated as myeloid differentiation primary response gene (3,4). MyD88 possesses a N-terminal death domain similar to cytoplasmic segments of TNF receptor 1, Fas, and C-terminal region related to IL-1 and Toll receptors. Overexpression of MyD88 induces activation the c-Jun N-terminal kinase and NF-kB through its death domain (1,2). The C-terminus of MyD88 interacts with the IL-1 receptor and blocks NF-kB activation induced by IL-1, but not by NF-kB.
Limitations
This product is for research use only and is not approved for use in humans or in clinical diagnosis. Primary Antibodies are guaranteed for 1 year from date of receipt.
Yoshikawa T, Takeichi T, Hirabayashi T et al. IL-17 axis is a significant driver of skin inflammation in Card14 mutant pityriasis rubra pilaris model mice Research Square 2023-02-02 (IHC, Mouse)
Toll-like receptors in the intestinal epithelial cells By Jamshed Arslan, Pharm. D., PhD. Toll-like receptors (TLRs) are microbe-sensing proteins that act as first responders to danger signals. TLRs help the intestinal epithelial cells (IECs) recognize commensal bacteria ... Read full blog post.
The role of TLR4 in breast cancer Toll like receptors (TLRs) are highly conserved proteins that are first known for their role in pathogen recognition and immune response activation. In order to elicit the necessary immune response in reaction to a foreign pathogen, TLRs trigger cy... Read full blog post.
MYD88 Expression and Tumorigenesis MyD88, also called myeloid differentiation primary response gene 88, encodes a cytosolic adapter protein that plays an essential role in innate and adaptive immune responses. The innate immune system recognizes the presence of bacterial pathogens thro... Read full blog post.
TLR7 and Immune Response Regulation Toll-like receptor 7 (TLR7) is a protein encoded by the TLR7 gene in humans and is a member of TLR family. TLRs controls host immune response against pathogens (e.g. viruses, bacteria and fungi) through recognition of pathogen-associated molecular pat... Read full blog post.
MYD88: Fanning Inflammation and Immune Responses Myeloid differentiation primary response gene 88 (MYD88) encodes a cytosolic adapter protein that plays an essential role in innate and adaptive immune responses. MYD88 protein functions as an essential signal transducer in the interleukin-1 and in To... Read full blog post.
MyD88 Antibodies for IL Signaling and Immunity Research The myeloid differentiation protein MyD88 (myeloid differentiation primary response protein) was originally identified and characterized as a primary upregulated response gene in interleukin-6 mediated myeloid differentiation. Now, MyD88 is known to b... Read full blog post.
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