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Newkirk, S.

Publications and source records attributed to Newkirk, S..

2 recordsLinked to original sources

Molecular Determinants Governing the Antitubercular Activity of Griselimycin

The emergence of drug-resistant strains of Mycobacterium tuberculosis makes anti-tubercular drug development a critical priority. Griselimycin is a cyclic peptide that targets the essential DNA sliding clamp of M. tuberculosis. While griselimycin is a promising antimycobacterial compound, its poorly understood structure-activity relationship has stalled derivatization. To investigate the contribution of each amino acid towards its activity, we assessed the antibiotic activity of an alanine scan library in M. tuberculosis. Incorporation of an N-terminal fluorophore enabled visualization of griselimycin accumulation inside of mycobacteria-infected macrophage cells. Derivatives containing altered cyclization chemistries, unnatural amino acids, expanded proline side chains, and alkyne handles were assessed, with a final design combining the most potent edits showing increased antibiotic activity. These findings present the comprehensive structure-activity investigation of griselimycin and can be used to rationally design future analogues.

pharmacology and toxicology↗

Non-Enzymatic Structural Modifications Reshape Peptide Presentation and Antigen Recognition

Cytotoxic T lymphocytes recognize infected and transformed cells through peptide antigens presented by MHC-I. Peptide sequence is assumed to dictate recognition, yet non-enzymatic post-translational modifications (PTMs) installed by reactive electrophiles can render a peptide chemically distinct from the form against which tolerance was established. Here we show that non-enzymatic PTMs arising from oxidative, inflammatory, metabolic, and carbonyl stress alter peptide-MHC-I stability and frequently disrupt recognition by a cognate TCR despite preserved MHC-I binding. Using a thioester probe, we demonstrate proof-of-concept capture of acylation-susceptible MHC-I ligands from the cellular immunopeptidome. Environmental chemicals, pharmaceuticals, and dietary isothiocyanates likewise modify antigenic peptides and impair T cell activation, and chemically distinct adducts at a single residue span the range from complete loss to full retention. Finally, methylglyoxal glycation impairs antigen-specific activation, and scavenging by creatine prevents it. Antigenic identity therefore reflects not only sequence but a peptides cumulative chemical history.

immunology↗