REL KO cell line available to order. KO validated by Next Generation Sequencing. Free of charge wild type control provided.
Avian reticuloendotheliosis, C REL, C Rel protein, Oncogene REL, Oncogene REL avian reticuloendotheliosis, Proto-oncogene c-Rel, REL_HUMAN, V rel reticuloendotheliosis viral oncogene homolog (avian), c Rel proto oncogene protein, v rel avian reticuloendotheliosis viral oncogene homolog, v rel reticuloendotheliosis viral oncogene homolog
REL KO cell line available to order. KO validated by Next Generation Sequencing. 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.
Recommended control: 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.
The c-Rel protein also known as REL is a member of the NF-kappaB (nuclear factor kappa-light-chain-enhancer of activated B cells) family of transcription factors. It has a mass of approximately 65 kDa and is expressed in a variety of tissues with high levels seen in immune cells such as T and B lymphocytes. Being a transcription factor c-Rel regulates the expression of genes involved in immune responses cell proliferation and apoptosis. Its activity depends on its ability to translocate to the nucleus where it binds specific DNA sequences to modulate transcription.
C-Rel functions to regulate immune system processes and is integral in lymphocyte activation. c-Rel functions as part of both homodimer and heterodimer complexes often partnering with other members of the NF-kappaB family to exert its effects. Through these complexes c-Rel influences the transcription of cytokines growth factors and other molecules critical for immune function. The protein’s role extends to influencing the differentiation and survival of lymphocytes instrumental in mounting adequate immune responses.
C-Rel plays a significant role in the regulation of the NF-kappaB signaling pathway and the MAPK (mitogen-activated protein kinase) pathway. The NF-kappaB pathway is activated by inflammatory stimuli and stress which leads to the translocation of c-Rel to the nucleus. Here c-Rel regulates genes important for immune and inflammatory responses alongside other proteins like RelA and p50. In conjunction with the MAPK pathway c-Rel contributes to cellular responses to growth signals and stress collaborating with proteins such as JNK (c-Jun N-terminal kinase) and ERK (extracellular signal-regulated kinase).
C-Rel’s dysregulation is associated with autoimmune diseases and lymphoid malignancies. Abnormal c-Rel activity contributes to diseases like rheumatoid arthritis where enhanced expression can lead to excessive inflammation and immune response. In certain lymphomas and leukemias overactive c-Rel promotes uncontrolled cell proliferation and survival. P53 a protein known for its role in tumor suppression may interact with pathways involving c-Rel influencing cancer progression and immune response dynamics. Understanding c-Rel and its interactions offers potential therapeutic targets for these and other related conditions.
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Terms & Conditions.
48 bp deletion (allele 1), and 48 bp deletion with 2 bp insertion (allele 2) after Gln15 of the WT protein
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