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BRAND / VENDOR: Abcam

Abcam, ab300217, Human GNC5 knockout U2-OS cell line

CATALOG NUMBER: ab300217
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Product Description

Size: 1000000Cells / vial / 2 x 1000000Cells / vial
GNC5 KO cell line available to order. KO validated by Western blot. Free of charge wild type control available. KO cell line generated by CRISPR/Cas9 system. Individual gRNAs were subcloned into pSpCas9 (BB)-2A-Puro and then stably transfected into U2OS cells. Transfected cells were selected by puromycin. 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:U-2 OS,
Species or organism:Human,
Tissue:Bone,
Form:LiquidSee storage information,
Knockout validation:Western blot,
Mutation description:KO cell line generated by CRISPR/Cas9 system. Individual gRNAs were subcloned into pSpCas9 (BB)-2A-Puro and then stably transfected into U2OS cells. Transfected cells were selected by puromycin.,
Disease:Osteosarcoma

Product details:
For more information about this cell line please see publication: PMID: 31753913.
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.
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-GNC5, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Western blot, Shipped at conditions-Dry Ice, Appropriate short-term storage duration-A few days, 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.
KAT2A also known as GCN5 is a lysine acetyltransferase enzyme with a molecular mass of approximately 92 kDa. It mainly acetylates histone proteins and affects transcriptional regulation by modifying chromatin structure. KAT2A/GCN5 is expressed in various tissues with significant expression in the nucleus of eukaryotic cells. Its role as a histone acetyltransferase places it as an important player in transcriptional activation by modifying the chromatin to a more open conformation facilitating access by transcription machinery.
Biological function summary
KAT2A/GCN5 participates in several cellular processes as part of larger protein complexes. It is a component of the SAGA (Spt-Ada-Gcn5 acetyltransferase) and TFTC (TBP-free TAF-containing complex) both involved in transcription regulation. Through these complexes KAT2A influences gene expression by acetylating histone residues which in turn affects the recruitment of other transcriptional activators or repressors. This activity also links it to non-histone substrates that support DNA damage repair and cellular senescence.
Pathways
KAT2A/GCN5 is integrally connected to the regulation of transcription and chromatin remodeling pathways. It interacts closely with the transcription factor c-Myc assisting in cell cycle regulation and proliferation. Additionally its presence in the p53 signaling pathway highlights its involvement in controlling cell growth and apoptosis. KAT2A/GCN5 activity influences downstream events in these pathways by affecting the acetylation state of specific histones and non-histone proteins.
The dysregulation of KAT2A/GCN5 is linked to cancer particularly in breast and colorectal cancers. Its role in acetylating key proteins like c-Myc and affecting pathways like p53 can lead to unchecked cell growth when improperly regulated. Furthermore KAT2A is connected to neurodegenerative diseases through its interactions with other histone modifiers such as HDAC1 and HDAC2 implicating it in conditions where neural cell function or maintenance goes awry.


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Collaboration

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