Abcam, ab265948, Human RELB (Rel B) knockout HeLa cell line

Size: 2 x 1000000Cells / vial / 1000000Cells / vial
RELB KO cell line available to order. KO validated by Western blot. Free of charge wild type control available. Knockout achieved by using CRISPR/Cas9, Homozygous: 65 bp deletion in exon 4. To order both knockout and wild-type control cells: select 2 x 1000000Cells/vial. To order only knockout cells: select 1000000Cells/vial.
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 65 bp deletion in exon 4,
Antibiotic resistance:Puromycin 1µg/mL,
Disease:Adenocarcinoma

Product details:
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
patent pages

Properties and Storage Information:
Gene name-RELB, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Zygosity-Homozygous, Shipped at conditions-Dry Ice, Appropriate short-term storage conditions--196°C, Appropriate long-term storage conditions--196°C

Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Rel B also known as RELB proto-oncogene is a member of the NF-κB family of transcription factors. This protein plays a significant role in regulating gene expression. Rel B has a molecular mass of approximately 68 kDa. It expresses in diverse tissues including lymphoid organs and epithelial cells. It generally resides in the cytoplasm and translocates to the nucleus upon activation.
Biological function summary
Rel B serves as a critical component of the alternative NF-κB signaling pathway. It often forms a complex with another NF-κB family member called p52. This complex controls the transcription of genes involved in the immune response cell survival and differentiation. Additionally Rel B contributes to the development of secondary lymphoid organs and modulation of immune responses.
Pathways
Rel B integrates into the non-canonical NF-κB signaling pathway also influencing the canonical pathway to a lesser extent. In the non-canonical pathway Rel B interacts with NIK and p100 to influence immune cell function. This involvement makes Rel B essential in processes like adaptive immunity and inflammatory responses. The protein p52 closely associates with Rel B aiding its activity in these pathways.
Rel B has connections to autoimmune diseases and certain cancers. Abnormal Rel B activity can lead to chronic inflammation and contribute to conditions like rheumatoid arthritis. In cancer its deregulation associates with lymphomas where it may interact with other NF-κB proteins like p50 and RelA affecting cell proliferation and survival. Understanding Rel B in these contexts could provide insights into therapeutic targets.