Description
Key facts
Cell type:HEK-293T,
Species or organism:Human,
Tissue:Kidney,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, 10 bp deletion in exon2.
Product details:
Knockout cell lysate achieved by CRISPR/Cas9.
REACH authorisation
Abcam has not and does not intend to apply for the REACH Authorisation of customers' uses of products that contain European Authorisation list (Annex XIV) substances.
It is the responsibility of our customers to check the necessity of application of REACH Authorisation, and any other relevant authorisations, for their intended uses.
Lysate preparation:
Our lysates are made using RIPA buffer to which we add a protease inhibitor cocktail and phosphatase inhibitor cocktail (ratio: 300:100:10).
This means that the protein of interest is denatured.
If you require a native form of the protein please use the live cell version. Please refer to our lysis protocol for further details on how our lysates are prepared.
User storage instructions:
Lyophilizate may be stored at 4°C. After reconstitution, store at -20°C for short-term storage or -80°C for long-term storage.
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-CBX1, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions--20°C, Appropriate long-term storage conditions--20°C
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
CBX1 also known as HP1 beta is a chromatin-associated protein that plays an important role in chromatin organization and epigenetic regulation. This protein has a mass of approximately 22 kDa and localizes within the nucleus where it participates in heterochromatin formation. CBX1 recognizes and binds to histone H3 when it is methylated at lysine 9 (H3K9me3) a modification integral to forming tightly packed DNA regions. Expression of CBX1 occurs widely in many tissue types reflecting its fundamental role in genomic maintenance and cell cycle regulation.
Biological function summary
The CBX1 protein acts as an integral component of the chromatin remodeling complex. By binding to methylated histones CBX1 helps stabilize chromatin architecture and repress transcription of genes within heterochromatic regions. This function is essential for maintaining gene silencing which is critical for processes like development and differentiation. CBX1 collaborates with other HP1 isoforms such as HP1 alpha and HP1 gamma as part of the family of heterochromatin proteins that contribute collectively to chromatin dynamics and gene expression control.
Pathways
CBX1 plays a part in the epigenetic transcriptional repression and cell cycle regulation pathways. It associates with SUV39H1 a methyltransferase to recognize and bind the H3K9me3 mark adding stability to the methylation signal and contributing to gene silencing. Additionally CBX1 interacts with other proteins like DNMT1 a DNA methyltransferase reinforcing its role in sustaining repressive chromatin states and preserving genome integrity during DNA replication.
CBX1 holds a significant association with cancer and neurological disorders. Aberrant expression or mutations in CBX1 can lead to disrupted chromatin states influencing oncogene activation or tumor suppressor gene silencing which are common events in cancer development. Furthermore altered CBX1 function links to neurological disorders where inappropriate chromatin remodeling contributes to disease pathology. Changes in the expression and interaction with other proteins including HP1 alpha highlight its potential role in disease mechanisms making CBX1 a relevant target for therapeutic research.
