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Granger, A.

Publications and source records attributed to Granger, A..

2 recordsLinked to original sources

De novo design of small cyclic peptide inhibitors from non-canonical amino acids by cofolding-guided search

Cyclic peptides can engage targets beyond the reach of small molecules, but their discovery typically relies on libraries reused across targets, diversification around a known interaction motif, or computational methods limited to a handful of non-canonical building blocks. Here, we present nCycle-Forge, a simulated annealing framework that designs cyclic peptide binders by iteratively substituting building blocks and scoring each proposal by cofolding with the target. We designed, synthesized, and screened 1,472 cyclic peptides against the active-site pocket of Thrombin and the shallow p53-binding surface of MDM2 from the target sequence alone and without fixing binding mo-tifs. The library yielded chemically diverse hits against both targets in a single round without experimental optimization, with hit rates comparable to or up to 24-fold higher than in larger experimental libraries. Purified designs reached sub- to low-micromolar potency, with the best Thrombin inhibitor at Ki 0.14 M and the best MDM2 binder at EC50 2.4 M. Surface plasmon resonance confirmed direct binding, competition with or-thosteric inhibitors at both sites, and weaker binding under conditions expected to linearize the designs. nCycle-Forge requires no building block-specific parameterization, conformer generation, or retraining, and provides a target-focused route to functional cyclic peptides beyond the canonical amino acid alphabet.

bioinformatics↗

Tamoxifen Suppresses Pancreatic β-Cell Proliferation in Mice

Tamoxifen is a mixed agonist/antagonist estrogen analogue that is frequently used to induce conditional gene deletion in mice using Cre-loxP mediated gene recombination. Tamoxifen is routinely employed in extremely high-doses relative to typical human doses to induce efficient gene deletion in mice. Although tamoxifen has been widely assumed to have no influence upon {beta}-cells, the acute developmental and functional consequences of high-dose tamoxifen upon glucose homeostasis and adult {beta}-cells are largely unknown. We tested if tamoxifen influences glucose homeostasis in male mice of various genetic backgrounds. We then carried out detailed histomorphometry studies of mouse pancreata. We also performed gene expression studies with islets of tamoxifen-treated mice and controls. Tamoxifen had modest effects upon glucose homeostasis of mixed genetic background (F1 B6129SF1/J) mice, with fasting hyperglycemia and improved glucose tolerance but without overt effects on fed glucose levels or insulin sensitivity. Tamoxifen inhibited proliferation of {beta}-cells in a dose-dependent manner, with dramatic reductions in {beta}-cell turnover at the highest dose (decreased by 66%). In sharp contrast, tamoxifen did not reduce proliferation of pancreatic acinar cells. {beta}-cell proliferation was unchanged by tamoxifen in 129S2 mice but was reduced in C57Bl6 genetic background mice (decreased by 59%). Gene expression studies revealed suppression of RNA for cyclins D1 and D2 within islets of tamoxifen-treated mice. Tamoxifen has a cytostatic effect on {beta}-cells, independent of changes in glucose homeostasis, in mixed genetic background and also in C57Bl6 mice. Tamoxifen should be used judiciously to inducibly inactivate genes in studies of glucose homeostasis.

developmental biology↗