Discovery of a Potent and Highly Isoform-Selective Inhibitor of the Neglected Ribosomal Protein S6 Kinase Beta 2 (S6K2). Read more about Discovery of a Potent and Highly Isoform-Selective Inhibitor of the Neglected Ribosomal Protein S6 Kinase Beta 2 (S6K2).
Structural basis of the TAM domain of BAZ2A in binding to DNA or RNA independent of methylation status. Read more about Structural basis of the TAM domain of BAZ2A in binding to DNA or RNA independent of methylation status.
The human pseudouridine synthase PUS7 recognizes RNA with an extended multi-domain binding surface. Read more about The human pseudouridine synthase PUS7 recognizes RNA with an extended multi-domain binding surface.
Selectivity aspects of activity-based (chemical) probes. Read more about Selectivity aspects of activity-based (chemical) probes.
Mutation in Abl kinase with altered drug-binding kinetics indicates a novel mechanism of imatinib resistance. Read more about Mutation in Abl kinase with altered drug-binding kinetics indicates a novel mechanism of imatinib resistance.
A chemical probe targeting the PWWP domain alters NSD2 nucleolar localization. Read more about A chemical probe targeting the PWWP domain alters NSD2 nucleolar localization.
Inhibitors of the Hippo Pathway Kinases STK3/MST2 and STK4/MST1 Have Utility for the Treatment of Acute Myeloid Leukemia. Read more about Inhibitors of the Hippo Pathway Kinases STK3/MST2 and STK4/MST1 Have Utility for the Treatment of Acute Myeloid Leukemia.
Structure-Based Design of Dual Partial Peroxisome Proliferator-Activated Receptor γ Agonists/Soluble Epoxide Hydrolase Inhibitors. Read more about Structure-Based Design of Dual Partial Peroxisome Proliferator-Activated Receptor γ Agonists/Soluble Epoxide Hydrolase Inhibitors.
NUAK family kinase 2 is a novel therapeutic target for prostate cancer. Read more about NUAK family kinase 2 is a novel therapeutic target for prostate cancer.
FOXN1 forms higher-order nuclear condensates displaced by mutations causing immunodeficiency. Read more about FOXN1 forms higher-order nuclear condensates displaced by mutations causing immunodeficiency.
