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BRAND / VENDOR: Abcam

Abcam, ab289221, Human FOXP3 knockout HCT116 cell line

CATALOG NUMBER: ab289221
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Product Description

Size: 1000000Cells / vial
FOXP3 KO cell line available to order. KO validated by Next Generation Sequencing. Free of charge wild type control available. 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:HCT116,
Species or organism:Human,
Tissue:Colon,
Form:LiquidSee storage information,
Knockout validation:Next Generation Sequencing,
Disease:Carcinoma

Product details:
There is evidence in literature (PMID: 28591725) that detects the expression of FOXP3 in WT HCT116 cell line.
We will provide viable cells that proliferate on revival.
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.
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-FOXP3, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Next Generation Sequencing, 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.
FOXP3 also recognized as Forkhead box P3 is a transcription factor critical for immune system function. It weighs approximately 47 kDa. FOXP3 is mainly expressed in regulatory T cells (Tregs) which play a role in maintaining immune tolerance. Scientists primarily identify its presence in the nucleus where it facilitates transcriptional regulation. Methods like 'FOXP3 IHC' and 'FOXP3 IHC mouse' are useful for detecting this protein in tissue samples while 'FOXP3 antibodies' aid in research on this target. Techniques like 'FOXP3 staining' and 'FOXP3 flow cytometry' further allow for the analysis of its expression and function.
Biological function summary
This transcription factor operates by regulating the expression of a variety of genes involved in Treg cell development and function. FOXP3 can interact with other proteins to form complexes that modulate gene expression. Its role is essential in enabling Tregs to suppress immune responses a process necessary for preventing autoimmunity. The interaction extends to other key regulators within Tregs such as the protein complex 221D which may have overlapping functional responsibilities. 'FOXP3 236a/E7' reflects its genetic variants detectable in different studies providing insights into its biological functions.
Pathways
FOXP3 is a significant player within the immune regulation pathway. It integrates into the TGF-beta signaling pathway in which it controls the expression of genes important for Treg functions. The protein recruits other transcription factors like NF-kB coordinating intricate network regulations within immune cells. FOXP3's activity orchestrates the balance between immune activation and suppression ensuring a well-functioning immune response that prevents overreactions leading to autoimmune conditions.
FOXP3 mutations or dysregulation can link to autoimmune diseases like immune dysregulation polyendocrinopathy enteropathy X-linked syndrome (IPEX). This transcription factor's malfunction implicates cancer where inadequate Treg function can either suppress antitumor immunity or result in tumor progression. Proteins such as CTLA-4 which is also involved in immune regulation connect to FOXP3 in these contexts emphasizing FOXP3’s significant role in maintaining immune homeostasis and its impact on disease development.


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Collaboration

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