Abcam, ab256997, Human MYD88 knockout A549 cell lysate

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MYD88 KO cell lysate available now. KO validated by. Free of charge wild type control included. Knockout achieved by using CRISPR/Cas9, 13 bp deletion in exon1 and 1 bp insertion in exon1 and 2 bp deletion in exon1.
Key facts
Cell type:A549,
Species or organism:Human,
Tissue:Lung,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 13 bp deletion in exon1 and 1 bp insertion in exon1 and 2 bp deletion in exon1.,
Disease:Carcinoma

Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Lysate preparation:
Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10).
This means that the protein of interest is denatured.
If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions:
Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages

Properties and Storage Information:
Gene name-MYD88, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
MyD88 standing for myeloid differentiation primary response 88 is a cytoplasmic adaptor protein with a molecular weight of approximately 33 kDa. This protein is expressed widely in immune cells including monocytes macrophages and dendritic cells. MyD88 serves a major role in the signaling pathways for the innate immune system. It acts as a linker transmitting signals from toll-like receptors (TLRs) and interleukin-1 receptors (IL-1Rs) to downstream signaling molecules ultimately activating transcription factors.
Biological function summary
MyD88 plays a significant role in mediating immune responses by forming part of a complex that includes IRAK kinases and TRAF6. When TLRs or IL-1Rs activate MyD88 this adaptor protein recruits IRAK4 which then phosphorylates IRAK1 or IRAK2. This cascade promotes the activation of NF-κB and MAPK pathways leading to the production of inflammatory cytokines. The MyD88-dependent pathway is integral to innate immunity influencing how the body responds to pathogen infection and inflammation.
Pathways
MyD88 integrates into both the TLR signaling and IL-1R signaling pathways. Key related proteins in these pathways include interleukin-1 receptor-associated kinase (IRAK) and tumor necrosis factor receptor-associated factor 6 (TRAF6). MyD88 initiates the recruitment and activation of IRAK1 and IRAK4 following receptor engagement leading to subsequent activation of downstream signals. As part of these pathways MyD88 mediates cellular responses important for immune system signaling and inflammatory response regulation.
MyD88 involvement is notable in the context of oncological and autoimmune diseases. Mutations or dysregulation of MyD88 are implicated in conditions like lymphoma and rheumatoid arthritis. In lymphoma the mutation usually results in constant activation of NF-κB leading to unchecked cell growth. As for rheumatoid arthritis an overactive immune response due to MyD88 can cause additional inflammation affecting joint tissues. In these conditions MyD88 interaction with IRAK4 is significant given their mutual role in immune and inflammatory pathways.