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Biology subjects

Michelsen, K.

Publications and source records attributed to Michelsen, K..

2 recordsLinked to original sources

Unlocking Scalable Ligand Residence Time Predictions with Koffee Unbinding Kinetics Simulations

A great number of drug discovery programs fail due to poor in vivo efficacy and ADMET liabilities. On- and off-target ligand residence times can act as important drivers of these problems. While modern experimental techniques have made measuring compound kinetics data more routine, there is a lack of accurate, high-throughput simulation techniques to guide compound prioritization by residence time. In this work, we introduce Koffee Unbinding Kinetics as a solution to the hitherto unanswered problem of scalable ligand-protein residence time prediction. By bypassing conventional approaches based on molecular dynamics simulations, Koffee Unbinding Kinetics performs physics-based residence time screening at the atomistic level in {approx} 1 GPU minute per complex using inexpensive hardware, a speed-up of at least 3 - 5 orders of magnitude compared to current state-of-the-art simulation approaches. Koffee Unbinding Kinetics can enhance compound selection to mitigate costly future program failures by adding fast, predictive residence time simulations to early-stage computational drug discovery pipelines. TOC Graphic O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=111 SRC="FIGDIR/small/686759v3_ufig1.gif" ALT="Figure 1"> View larger version (16K): org.highwire.dtl.DTLVardef@120d5dcorg.highwire.dtl.DTLVardef@b86b67org.highwire.dtl.DTLVardef@193554forg.highwire.dtl.DTLVardef@1c5c6c1_HPS_FORMAT_FIGEXP M_FIG C_FIG

biophysics↗

TL1A overexpression in Crohn's Disease and mice alters Paneth cells and microbiota promoting ileal inflammation

Paneth cells regulate host-microbial homeostasis and defects in autophagy and host defense pathways have been associated with inflammatory bowel diseases (IBD). Genetic variants in TL1A (TNFSF15) and its receptor DR3 (TNFRSF25) have been associated with IBD. TL1A expression is increased in IBD patients, particularly in TL1A risk allele carriers. However, effects of TL1A on Paneth cells, resident microbiota, and development of ileitis remain unknown. TL1A overexpression in mice induces Paneth cell hyperplasia and morphological abnormalities preceding the development of ileitis. In Crohns disease (CD) patients, ileal TL1A expression was associated with abnormal Paneth cell phenotypes. We confirmed direct effects of TL1A on Paneth cells in human iPSC-derived human intestinal organoids and mouse Paneth cell-enriched organoids. Resident microbiota was required for TL1A-mediated Paneth cell dysfunction, and ileitis. Tl1a-tg mice were enriched in short chain fatty acid-producing bacteria and the metabolite acetate. Acetate supplementation in WT or Tl1a-tg mice caused ileal inflammation, suggesting that acetate is sufficient to cause ileitis. DR3-deficiency in Paneth cells resulted in Paneth cell abnormalities and microbiome composition changes. Our findings provide a mechanistic link between overexpression of TL1A in CD patients, Paneth cell dysfunction, and enrichment of acetate-producing bacteria and acetate that promotes ileal inflammation. Brief SummaryOverexpression of TL1A drives Paneth cell dysfunction in Crohns Disease and mice leading to microbial and metabolomic changes that promote small bowel inflammation.

immunology↗