Description
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Knockout validation:Sanger Sequencing,Western blot,
Mutation description:Knockout achieved by using CRISPR/Cas9, Homozygous: 5 bp deletion in exon 2.,
Disease:Adenocarcinoma
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-BAZ1B, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger Sequencing, Western blot, Zygosity-Homozygous, 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.
WSTF also known as Williams Syndrome Transcription Factor or BAZ1B is a versatile protein with an estimated mass around 175 kDa. It is a component of the nucleosome remodeling factor (NURF) and the Williams-Beuren syndrome chromosome region 17 (WBSCR17) complex. WSTF has widespread expression in various tissues including the brain and heart which highlights its involvement in diverse cellular processes. Functionally it facilitates chromatin remodeling by altering the structure of nucleosomes which is vital for DNA accessibility in transcription DNA repair and replication.
Biological function summary
Since WSTF participates in chromatin structure modulation it plays a considerable role in transcriptional regulation. It is a part of the NURF complex which makes it essential for DNA accessibility and gene expression. The complex interacts with other proteins to allow chromatin to accommodate active transcription by repositioning nucleosomes. WSTF also has a kinase domain that phosphorylates histone H2A. This phosphorylation integrates signals that coordinate transcription and DNA damage repair mechanisms highlighting its multifunctional nature in maintaining genomic stability.
Pathways
WSTF has pivotal roles in the chromatin remodeling and DNA repair pathways. The chromatin remodeling pathway involves WSTF's interaction with the transcription factor complex influencing gene accessibility and expression. WSTF in the DNA repair pathway ensures proper genomic integrity through its association with proteins like BRCA1 highlighting its participation in the cellular response to DNA damage. By engaging with these pathways WSTF contributes to the cell's ability to regulate the genome and respond to damage efficiently.
WSTF is significantly connected to Williams-Beuren syndrome and certain cancers. Williams-Beuren syndrome a developmental disorder arises from the deletion of the region on chromosome 7 involving the WSTF gene affecting brain and heart function. In certain cancers aberrant expression or mutations within the WSTF gene are associated with uncontrolled chromatin remodeling contributing to tumorigenesis. Through these disorders WSTF shows its interaction with proteins like SMARCA1 in chromatin remodeling anomalies emphasizing its importance in disease progression and cellular dysfunction.
