Publications
(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) Antigenic drift expands influenza viral escape pathways from recalled humoral immunity. Immunity. 58, 716-727.e6
(2025) Antitoxin control of optimal transcriptional repression in the atypical HigB-HigA toxin-antitoxin system from Proteus vulgaris. Nucleic Acids Res. 10.1093/nar/gkaf610
(2025) Antitoxin control of optimal transcriptional repression in the atypical HigB-HigA toxin-antitoxin system from Proteus vulgaris. Nucleic Acids Res. 10.1093/nar/gkaf610
(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) An asymmetric tetrabody is a potent and efficacious agonist of the erythropoietin receptor in vitro and in vivo. Protein Sci. 34, e70292
(2025) BBO-10203 inhibits tumor growth without inducing hyperglycemia by blocking RAS-PI3Kα interaction.. Science. 10.1126/science.adq2004
(2025) BBO-10203 inhibits tumor growth without inducing hyperglycemia by blocking RAS-PI3Kα interaction.. Science. 10.1126/science.adq2004
(2025) BBO-10203 inhibits tumor growth without inducing hyperglycemia by blocking RAS-PI3Kα interaction.. Science. 10.1126/science.adq2004
(2025) BBO-10203 inhibits tumor growth without inducing hyperglycemia by blocking RAS-PI3Kα interaction.. Science. 10.1126/science.adq2004
(2025) BBO-10203 inhibits tumor growth without inducing hyperglycemia by blocking RAS-PI3Kα interaction.. Science. 10.1126/science.adq2004
(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) Biophysical and structural analysis of KRAS switch-II pocket inhibitors reveals allele-specific binding constraints. J Biol Chem. 10.1016/j.jbc.2025.110331
(2025) Biophysical and structural analysis of KRAS switch-II pocket inhibitors reveals allele-specific binding constraints. J Biol Chem. 10.1016/j.jbc.2025.110331
(2025) Biophysical and structural analysis of KRAS switch-II pocket inhibitors reveals allele-specific binding constraints. J Biol Chem. 10.1016/j.jbc.2025.110331
(2025) A broad-spectrum lasso peptide antibiotic targeting the bacterial ribosome. Nature. 10.1038/s41586-025-08723-7
(2025) The C2 domain augments Ras GTPase-activating protein catalytic activity. Proc Natl Acad Sci U S A. 122, e2418433122

