Description
Key facts
Cell type:HeLa,
Species or organism:Human,
Tissue:Cervix,
Form:LiquidSee storage information,
Knockout validation:Sanger Sequencing,
Mutation description:Knockout achieved by using CRISPR/Cas9, 1 bp deletion in exon 3 and 1 bp insertion in exon 3,
Disease:Adenocarcinoma
Product details:
We will provide viable cells that proliferate on revival.
Western blot data indicates that the CRISPR gene edit may have resulted in a truncation of the protein of interest. Please see data images.
This product is subject to limited use licenses from The Broad Institute, ERS Genomics Limited and Sigma-Aldrich Co. LLC, and is developed with patented technology. For full details of the licenses and patents please refer to our
limited use license
patent pages
Properties and Storage Information:
Gene name-ABL1, Gene editing type-Knockout, Gene editing method-CRISPR technology, Knockout validation-Sanger 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.
ABL1 also referred to as ABL-1 or ABL1 protein is a non-receptor tyrosine kinase with a mass of approximately 120 kDa. It is found throughout the body in diverse tissues with significant expression in the brain testes and hematopoietic cells. This protein consists of several functional domains including SH3 SH2 and a kinase domain that facilitate its interaction with various cellular components. ABL1 kinase plays a central role in cell differentiation division and stress response reflecting its mechanical versatility in cellular signaling.
Biological function summary
ABL1 functions by regulating key processes like cell cycle progression actin dynamics and cell adhesion. ABL1 participates as part of larger protein complexes that modulate cellular movement and gene transcription. When activated it phosphorylates a range of substrates that leads to various cellular outcomes. ABL1 operates in the cytoplasm and nucleus influencing both cytoskeletal rearrangement and DNA repair which highlights its critical function in maintaining cellular integrity and response to damage.
Pathways
ABL1 interacts in both the mitogenic and apoptotic pathways including involvement in the MAPK and PI3K/AKT pathways. ABL1 interfaces with proteins like CRK and GRB2 in these pathways integrating signals that determine cell fate decisions. Through its kinase activity ABL1 mediates signaling cascades that impact cellular growth and survival responding dynamically to internal and external cues.
ABL1 is notoriously implicated in chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL). The fusion protein BCR-ABL1 resulting from chromosomal translocation drives oncogenic signals that promote uncontrolled cell proliferation. The aberrant activity of BCR-ABL1 disrupts normal cellular regulation and interacts with proteins such as STAT5 enhancing leukemogenesis. Targeted therapies like tyrosine kinase inhibitors specifically hinder BCR-ABL1 activity demonstrating ABL1's importance in cancer pathology and treatment.
