https://www.selleckchem.com/btk.html
The RB1 tumor suppressor gene is mutated in highly aggressive tumors including small cell lung cancer (SCLC), where its loss, along with TP53, is required and sufficient for tumorigenesis. While RB1 mutant cells fail to arrest at G1/S in response to cell cycle restriction point signals, this information has not led to effective strategies to treat RB1-deficient tumors, as it is challenging to develop targeted drugs for tumors that are driven by the loss of gene function. Our group previously identified Skp2, a substrate recruiting subunit of the SCF