BCAR1 Human
Description
Product Specs
Product Science Overview
Breast Cancer Anti-Estrogen Resistance 1 (BCAR1), also known as p130Cas, is a protein encoded by the BCAR1 gene in humans. This protein plays a crucial role in cell signaling and has been implicated in the development of resistance to anti-estrogen therapies in breast cancer. BCAR1 is an adapter protein that interacts with various signaling molecules, influencing cell adhesion, migration, and survival. Its overexpression has been associated with poor prognosis in breast cancer patients, particularly those undergoing anti-estrogen treatments such as tamoxifen.
The recombinant form of BCAR1 can be produced using bacterial expression systems. A common method involves cloning the BCAR1 gene into an expression vector, which is then introduced into bacterial cells, such as Escherichia coli. The bacteria are cultured, and the expression of BCAR1 is induced using specific inducers like IPTG (Isopropyl β-D-1-thiogalactopyranoside). The recombinant BCAR1 protein is then purified from the bacterial lysate using affinity chromatography techniques, such as nickel-nitrilotriacetic acid (Ni-NTA) chromatography, which exploits the histidine tags often added to recombinant proteins for purification purposes.
BCAR1 is involved in various signaling pathways that regulate cell behavior. One of the key interactions is with focal adhesion kinase (FAK), which is crucial for cell adhesion and migration. BCAR1 can be phosphorylated on tyrosine residues, which creates binding sites for SH2 domain-containing proteins, further propagating signaling cascades. These interactions can lead to the activation of downstream pathways such as the MAPK/ERK pathway, which promotes cell proliferation and survival.
In the context of breast cancer, BCAR1 overexpression can lead to resistance to anti-estrogen therapies. This resistance is thought to arise from the activation of alternative survival pathways that bypass the estrogen receptor signaling. For example, BCAR1 can activate the PI3K/AKT pathway, which promotes cell survival and growth independently of estrogen signaling. This mechanism highlights the complexity of cancer cell signaling and the challenges in overcoming therapeutic resistance.
