Errata: Continuous directed evolution of aminoacyl-tRNA synthetases

January 16th, 2018 by David I Bryson

Errata: Continuous directed evolution of aminoacyl-tRNA synthetases

Errata: Continuous directed evolution of aminoacyl-tRNA synthetases, Published online: 16 January 2018; doi:10.1038/nchembio0218-186

Errata: Continuous directed evolution of aminoacyl-tRNA synthetases

Synthetic biology: License to kill

January 16th, 2018 by Caitlin Deane

Synthetic biology: License to kill

Synthetic biology: License to kill, Published online: 16 January 2018; doi:10.1038/nchembio.2561

Synthetic biology: License to kill

Natural products: Tapping into personalized chemistry

January 16th, 2018 by Jack R Davison

Natural products: Tapping into personalized chemistry

Natural products: Tapping into personalized chemistry, Published online: 16 January 2018; doi:10.1038/nchembio.2560

By integrating metagenomics, spectroscopy and synthetic biology, the individualized chemistry of small reef-dwelling organisms and their associated microbiota can be characterized in exquisite detail, unlocking a wealth of structural diversity for the development of new drugs.

Identifying Novel Enhancer Elements with CRISPR-Based Screens

January 10th, 2018 by Jason C. Klein, Wei Chen, Molly Gasperini and Jay Shendure

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ACS Chemical Biology
DOI: 10.1021/acschembio.7b00778

Metabolic Feedback Circuits Provide Rapid Control of Metabolite Dynamics

January 8th, 2018 by Di Liu and Fuzhong Zhang

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ACS Synthetic Biology
DOI: 10.1021/acssynbio.7b00342

Na<sup>+</sup>-mimicking ligands stabilize the inactive state of leukotriene B<sub>4</sub> receptor BLT1

January 8th, 2018 by Tetsuya Hori

Na+-mimicking ligands stabilize the inactive state of leukotriene B4 receptor BLT1

Na<sup>+</sup>-mimicking ligands stabilize the inactive state of leukotriene B<sub>4</sub> receptor BLT1, Published online: 08 January 2018; doi:10.1038/nchembio.2547

A structure of leukotriene B4 receptor BLT1 bound with a benzamidine-containing compound, BIIL260, reveals an inverse-agonist mechanism involving ligand binding in the sodium ion-centered water cluster adjacent to the conserved orthosteric site of class A GPCRs.
  • Posted in Nat Chem Biol, Publications
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Mechanism of intersubunit ketosynthase–dehydratase interaction in polyketide synthases

January 8th, 2018 by Matthew Jenner

Mechanism of intersubunit ketosynthase–dehydratase interaction in polyketide synthases

Mechanism of intersubunit ketosynthase–dehydratase interaction in polyketide synthases, Published online: 08 January 2018; doi:10.1038/nchembio.2549

A combination of biochemical and structural techniques allows the characterization of a novel docking domain in polyketide synthases, which is structurally disordered and facilitates association of subunits at ketosynthase–dehydratase junctions.
  • Posted in Nat Chem Biol, Publications
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Employing a biochemical protecting group for a sustainable indigo dyeing strategy

January 8th, 2018 by Tammy M Hsu

Employing a biochemical protecting group for a sustainable indigo dyeing strategy

Employing a biochemical protecting group for a sustainable indigo dyeing strategy, Published online: 08 January 2018; doi:10.1038/nchembio.2552

An environmentally friendly approach to indigo production is facilitated by the characterization of a plant indoxyl glucosyltransferase, which converts the unstable indoxyl precursor into indican by addition of a glucose protecting group.
  • Posted in Nat Chem Biol, Publications
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Next-Generation DNA-Functionalized Quantum Dots as Biological Sensors

January 4th, 2018 by Ganglin Wang, Zhi Li and Nan Ma

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ACS Chemical Biology
DOI: 10.1021/acschembio.7b00887

Toxoplasma gondii disrupts {beta}1 integrin signaling and focal adhesion formation during monocyte hypermotility [Immunology]

January 2nd, 2018 by Joshua H. Cook, Norikiyo Ueno, Melissa B. Lodoen

The motility of blood monocytes is orchestrated by the activity of cell surface integrins, which translate extracellular signals into cytoskeletal changes to mediate adhesion and migration. Toxoplasma gondii is an intracellular parasite that infects migratory cells and enhances their motility, but the mechanisms underlying T. gondii-induced hypermotility are incompletely understood. We have investigated the molecular basis for the hypermotility of primary human peripheral blood monocytes and THP-1 cells infected with T. gondii. Compared to uninfected monocytes, T. gondii infection of monocytes reduced cell spreading and the number of activated β1 integrin clusters in contact with fibronectin during settling, an effect not observed in monocytes treated with LPS or E. coli. Furthermore, T. gondii infection disrupted the phosphorylation of focal adhesion kinase (FAK) at tyrosine 397 (Y397) and Y925 and of the related protein proline-rich tyrosine kinase (Pyk2) at Y402. The localization of paxillin, FAK, and vinculin to focal adhesions and the colocalization of these proteins with activated β1 integrins were also impaired in T. gondii-infected monocytes. Using time-lapse confocal microscopy of THP-1 cells expressing eGFP-FAK during settling on fibronectin, we found that T. gondii-induced monocyte hypermotility was characterized by a reduced number of eGFP-FAK-containing clusters over time compared to uninfected cells. This study demonstrates an integrin conformation-independent regulation of the β1 integrin adhesion pathway, providing further insight into the molecular mechanism of T. gondii- induced monocyte hypermotility.