BTRC KO cell line available to order. Free of charge wild type control provided.
BETA-TRCP, Beta transducin repeat containing E3 ubiquitin protein ligase, E3RSIkappaB, F-box and WD repeats protein beta-TrCP, F-box/WD repeat protein 1A, F-box/WD repeat-containing protein 1A, FBW1A_HUMAN, FBXW1, FBXW1A, FWD1, HOS, Slimb, bTrCP, bTrCP1, beta TrCP1, beta-transducin repeat containing, btrC, mKIAA4123, pIkappaBalpha-E3 receptor subunit
BTRC 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 PC-3 cell line (ab290718). 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.
Beta TRCP also known as B-TRCP Beta-TRCP or BTRC is an E3 ubiquitin ligase subunit. It has a mass of about 63 kDa and shows expression in various human tissues such as the liver brain and muscle. The BTRC domain in beta TRCP recognizes specific phosphodegron sequences in target proteins tagging them for ubiquitination and subsequent proteasomal degradation. This process helps regulate the turnover of proteins important for cell cycle progression and signal transduction.
Beta TRCP participates in essential functions by being a component of the SCF (Skp1-Cullin-F-box) complex which facilitates the ubiquitination of its substrates. SCF complexes regulate various cellular processes by targeting proteins that need timely degradation. As a part of the complex beta TRCP controls the stability of pivotal substrates ensuring proper regulation of biological events like DNA replication and repair.
Beta TRCP plays critical roles in the Wnt and NF-kB signaling pathways. These pathways depend on the precise regulation of protein levels allowing for proper cellular responses. Beta TRCP interacts with key proteins such as IkB in the NF-kB pathway and beta-catenin in the Wnt pathway controlling their ubiquitination and stability. The degradation of these proteins is necessary for pathway activation or repression influencing cell proliferation and survival decisions.
Beta TRCP has associations with cancer and inflammatory diseases. Abnormal beta TRCP function can lead to dysregulation of the NF-kB and Wnt pathways contributing to tumorigenesis and chronic inflammation. In cancers for example its relationship with proteins like beta-catenin influences tumor growth due to improper degradation. In inflammatory diseases disrupted interaction with IkB leads to excessive activation of NF-kB promoting inflammatory responses. Understanding these interactions can provide insights into therapeutic strategies.
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