Publications
(2024) Structural basis for C-degron selectivity across KLHDCX family E3 ubiquitin ligases. Nat Commun. 15, 9899
(2024) Structural basis for C-degron selectivity across KLHDCX family E3 ubiquitin ligases. Nat Commun. 15, 9899
(2024) Structural basis for promiscuity in ligand recognition by yjdF riboswitch. Cell Discov. 10, 37
(2024) Structural basis of Cfr-mediated antimicrobial resistance and mechanisms to evade it. Nat Chem Biol. 20, 867-876
(2024) Structural basis of divergent substrate recognition and inhibition of human neurolysin. Sci Rep. 14, 18420
(2024) Structural insights into the DNA-binding mechanism of BCL11A: The integral role of ZnF6. Structure. 32, 2276-2286.e4
(2024) Structural Insights into the DNA-Binding Mechanism of BCL11A: The Integral Role of ZnF6. bioRxiv. 10.1101/2024.01.17.576058
(2024) Structural requirements for activity of Mind bomb1 in Notch signaling. Structure. 32, 1667-1676.e5
(2024) Structure of saguaro cactus virus 3' translational enhancer mimics 5' cap for eIF4E binding. Proc Natl Acad Sci U S A. 121, e2313677121
(2024) Structure-guided aminoacylation and assembly of chimeric RNAs. bioRxiv. 10.1101/2024.03.02.583109
(2024) Symmetry breaking of fluorophore binding to a G-quadruplex generates an RNA aptamer with picomolar KD. Nucleic Acids Res. 52, 8039-8051
(2024) ZNL0325, a Pyrazolopyrimidine-Based Covalent Probe, Demonstrates an Alternative Binding Mode for Kinases. J Med Chem. 67, 2837-2848
(2025) Allosteric inhibition of JAK2 with lysine-reactive compounds that bind the pseudokinase domain. Eur J Med Chem. 302, 118274
(2025) Allosteric inhibition of JAK2 with lysine-reactive compounds that bind the pseudokinase domain. Eur J Med Chem. 302, 118274
(2025) ApaH decaps NpN-capped RNAs in two alternative orientations. Nat Chem Biol. 10.1038/s41589-025-01991-4
(2025) An asymmetric tetrabody is a potent and efficacious agonist of the erythropoietin receptor in vitro and in vivo. Protein Sci. 34, e70292
(2025) Bi-allelic PRMT9 loss-of-function variants cause a syndromic form of intellectual disability. Am J Hum Genet. 10.1016/j.ajhg.2025.10.014
(2025) Bi-allelic PRMT9 loss-of-function variants cause a syndromic form of intellectual disability. Am J Hum Genet. 10.1016/j.ajhg.2025.10.014
(2025) Bi-allelic PRMT9 loss-of-function variants cause a syndromic form of intellectual disability. Am J Hum Genet. 10.1016/j.ajhg.2025.10.014
(2025) Bi-allelic PRMT9 loss-of-function variants cause a syndromic form of intellectual disability. Am J Hum Genet. 10.1016/j.ajhg.2025.10.014
(2025) Bi-allelic PRMT9 loss-of-function variants cause a syndromic form of intellectual disability. Am J Hum Genet. 10.1016/j.ajhg.2025.10.014
(2025) Bi-allelic PRMT9 loss-of-function variants cause a syndromic form of intellectual disability. Am J Hum Genet. 10.1016/j.ajhg.2025.10.014
(2025) Bi-allelic PRMT9 loss-of-function variants cause a syndromic form of intellectual disability. Am J Hum Genet. 10.1016/j.ajhg.2025.10.014
(2025) Bi-allelic PRMT9 loss-of-function variants cause a syndromic form of intellectual disability. Am J Hum Genet. 10.1016/j.ajhg.2025.10.014

