MYD88 KO cell line available to order. Free of charge wild type control provided.
MYD88D, MYD88_HUMAN, Mutant myeloid differentiation primary response 88, Myeloid differentiation marker 88, Myeloid differentiation primary response 88, Myeloid differentiation primary response gene, Myeloid differentiation primary response gene (88), Myeloid differentiation primary response gene 88, Myeloid differentiation primary response protein MyD88, OTTHUMP00000161718, OTTHUMP00000208595, OTTHUMP00000209058, OTTHUMP00000209059, OTTHUMP00000209060
MYD88 KO cell line available to order. Free of charge wild type control provided.
Upon arrival, the vial should be stored in liquid nitrogen vapor phase and not at -80°C. Storage at -80°C may result in loss of viability.
1. Thaw the vial in 37°C water bath for approximately 1-2 minutes.
2. Transfer the cell suspension (0.8 mL) to a 15 mL/50 mL conical sterile polypropylene centrifuge tube containing 8.4 mL pre-warmed culture medium, wash vial with an additional 0.8 mL culture medium (total volume 10 mL) to collect remaining cells, and centrifuge at 201 x g (rcf) for 5 minutes at room temperature. 10 mL represents minimum recommended dilution. 20 mL represents maximum recommended dilution.
3. Resuspend the cell pellet in 5 mL pre-warmed culture medium and count using a haemocytometer or alternative cell counting method seed all remaining cells into a T25.
4. Incubate the culture at 37°C incubator with 5% CO2. Check the culture one day after revival and continue to check until 80% confluent. Media change can be given if needed.
5. Once confluent passage into an appropriate flask at a density of 2x104 cells/cm2. Seeding density is given as a guide only and should be scaled to align with individual lab schedules. Cultures should be monitored daily.
Although we aim to provide customers with a homozygous clone, feasibility will be dependent on the biology of the protein. Should only heterozygous edits be achieved, you will be notified of the outcome and be asked to confirm whether the cell line is acceptable. All clones will be accompanied with DNA sequencing data, and the mutation description.
Recommended control: Human wild-type HCT116 cell line (Human wild-type HCT116 cell line ab288559). Please note a wild-type cell line is not automatically included with a knockout cell line order, if required please add recommended wild-type cell line at no additional cost using the code WILDTYPE-TMTK1.
We will provide viable cells that proliferate on revival.
This product is subject to limited use licenses from The Broad Institute and ERS Genomics Limited, and is developed with patented technology. For full details of the limited use licenses and relevant patents please refer to our limited use license and patent pages.
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.
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.
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.
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