P
Peter G. Schultz
Researcher at Scripps Research Institute
Publications - 901
Citations - 96321
Peter G. Schultz is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Amino acid & Transfer RNA. The author has an hindex of 156, co-authored 893 publications receiving 89716 citations. Previous affiliations of Peter G. Schultz include Novartis Foundation & University of California, Berkeley.
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Journal ArticleDOI
Alternate protein frameworks for molecular recognition.
Jung Ku,Peter G. Schultz +1 more
TL;DR: The individual mutants, which fold into native-like structure, bind selectively to the BSA-1 conjugate with micromolar dissociation constants (Kd), in comparison to a monoclonal antibody that binds selectively to 1 with a Kd of 290 nM.
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Unnatural amino acid mutagenesis of green fluorescent protein.
TL;DR: The spectral properties of the mutant GFPs, including the absorbance and fluorescence maxima and quantum yields, correlate with the structural and electronic properties ofThe substituents on the amino acids.
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A Genome-Wide Overexpression Screen in Yeast for Small-Molecule Target Identification
Hendrik Luesch,Tom Y.-H. Wu,Pingda Ren,Nathanael S. Gray,Peter G. Schultz,Peter G. Schultz,Frantisek Supek +6 more
TL;DR: A multicopy gene suppression screen of drug sensitivity in Saccharomyces cerevisiae that facilitates the identification of cellular targets of small molecules demonstrates the utility of this approach for the rapid deconvolution of small-molecule targets.
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Searching for Interferon-Induced Genes That Inhibit Hepatitis B Virus Replication in Transgenic Mouse Hepatocytes
Stefan Wieland,Raquel Vega,Rolf Müller,Claire F. Evans,Brian S. Hilbush,Luca G. Guidotti,J. Gregor Sutcliffe,Peter G. Schultz,Francis V. Chisari +8 more
TL;DR: The present study was designed to identify transcriptionally controlled hepatocellular genes that are tightly associated with the inhibition of HBV replication and that might, therefore, mediate the antiviral effect of these cytokines.
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CXCR4 activation maintains a stem cell population in tamoxifen-resistant breast cancer cells through AhR signalling
Anna Dubrovska,Anna Dubrovska,A Hartung,A Hartung,L C Bouchez,L C Bouchez,John R. Walker,V A Reddy,V A Reddy,Charles Y. Cho,Peter G. Schultz +10 more
TL;DR: The chemokine receptor CXCR4 maintains a cancer progenitor population in tamoxifen-resistant MCF7 cells through AhR signalling and could be a putative target for the treatment of tamoxIFen- resistant breast cancers.