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Classification of Intrinsically Disordered Regions and Proteins

Chemical reviews, 2014-07, Vol.114 (13), p.6589-6631

2014

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Interaction between p53 N terminus and core domain regulates specific and nonspecific DNA binding

Proceedings of the National Academy of Sciences - PNAS, 2019-04, Vol.116 (18), p.8859-8868

2019

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Disorder for Dummies: Functional Mutagenesis of Transient Helical Segments in Disordered Proteins

Methods in molecular biology (Clifton, N.J.), 2020, Vol.2141, p.3

Daughdrill, Gary W

2020

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Conformational buffering underlies functional selection in intrinsically disordered protein regions

Nature structural & molecular biology, 2022-08, Vol.29 (8), p.781

2022

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Disorder and residual helicity alter p53-Mdm2 binding affinity and signaling in cells

Nature chemical biology, 2014-12, Vol.10 (12), p.1000

2014

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Evolution and disorder

Current opinion in structural biology, 2011-06, Vol.21 (3), p.441-446

2011

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Sequence Properties of An Intramolecular Interaction That Inhibits p53 DNA Binding

Biomolecules (Basel, Switzerland), 2022-10, Vol.12 (11), p.1558

2022

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Conserved Helix-Flanking Prolines Modulate Intrinsically Disordered Protein:Target Affinity by Altering the Lifetime of the Bound Complex

Biochemistry (Easton), 2017-05, Vol.56 (18), p.2379-2384

2017

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Secondary interaction between MDMX and p53 core domain inhibits p53 DNA binding

Proceedings of the National Academy of Sciences - PNAS, 2016-05, Vol.113 (19), p.E2558-E2563

2016

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Comparing Models of Evolution for Ordered and Disordered Proteins

Molecular biology and evolution, 2010-03, Vol.27 (3), p.609-621

2010

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Uncoupling the Folding and Binding of an Intrinsically Disordered Protein

Journal of molecular biology, 2018-08, Vol.430 (16), p.2389-2402

2018

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Autoinhibition of MDMX by intramolecular p53 mimicry

Proceedings of the National Academy of Sciences - PNAS, 2015-04, Vol.112 (15), p.4624-4629

2015

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Using NMR Chemical Shifts to Determine Residue-Specific Secondary Structure Populations for Intrinsically Disordered Proteins

Methods in enzymology, 2018, Vol.611, p.101-136

2018

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Optimal Affinity Enhancement by a Conserved Flexible Linker Controls p53 Mimicry in MdmX

Biophysical journal, 2017-05, Vol.112 (10), p.2038-2042

2017

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Conserved Glycines Control Disorder and Function in the Cold-Regulated Protein, COR15A

Biomolecules (Basel, Switzerland), 2019-03, Vol.9 (3), p.84

2019

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Inhibition of p53 DNA binding by a small molecule protects mice from radiation toxicity

Oncogene, 2020-07, Vol.39 (29), p.5187-5200

2020

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Shifts in the host range of a promiscuous plasmid through parallel evolution of its replication initiation protein

The ISME Journal, 2010-12, Vol.4 (12), p.1568-1580

2010

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Disorder predictors also predict backbone dynamics for a family of disordered proteins

PloS one, 2011-12, Vol.6 (12), p.e29207-e29207

2011

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A transient α-helical molecular recognition element in the disordered N-terminus of the Sgs1 helicase is critical for chromosome stability and binding of Top3/Rmi1

Nucleic acids research, 2013-12, Vol.41 (22), p.10215

2013

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Contribution of proline to the pre-structuring tendency of transient helical secondary structure elements in intrinsically disordered proteins

Biochimica et biophysica acta, 2014-03, Vol.1840 (3), p.993-1003

2014

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Structural divergence is more extensive than sequence divergence for a family of intrinsically disordered proteins

Proteins, structure, function, and bioinformatics, 2013-10, Vol.81 (10), p.1686-1698

2013

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p53 Phosphomimetics Preserve Transient Secondary Structure but Reduce Binding to Mdm2 and MdmX

Biomolecules (Basel, Switzerland), 2019-03, Vol.9 (3), p.83

2019

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Protein dynamics: bridging the gap

Nature chemical biology, 2011-04, Vol.7 (4), p.193

Daughdrill, Gary W

2011

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Impact of the K24N mutation on the transactivation domain of p53 and its binding to murine double-minute clone 2

Proteins, structure, function, and bioinformatics, 2013-10, Vol.81 (10), p.1738-1747

2013

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Modeling the accessible conformations of the intrinsically unstructured transactivation domain of p53

Proteins, structure, function, and bioinformatics, 2008-05, Vol.71 (2), p.587-598

2008

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Tumor Suppressor Protein P53 - Chemistry
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Classification of Intrinsically Disordered Regions and Proteins

Interaction between p53 N terminus and core domain regulates specific and nonspecific DNA binding

Disorder for Dummies: Functional Mutagenesis of Transient Helical Segments in Disordered Proteins

Conformational buffering underlies functional selection in intrinsically disordered protein regions

Disorder and residual helicity alter p53-Mdm2 binding affinity and signaling in cells

Evolution and disorder

Sequence Properties of An Intramolecular Interaction That Inhibits p53 DNA Binding

Conserved Helix-Flanking Prolines Modulate Intrinsically Disordered Protein:Target Affinity by Altering the Lifetime of the Bound Complex

Secondary interaction between MDMX and p53 core domain inhibits p53 DNA binding

Comparing Models of Evolution for Ordered and Disordered Proteins

Uncoupling the Folding and Binding of an Intrinsically Disordered Protein

Autoinhibition of MDMX by intramolecular p53 mimicry

Using NMR Chemical Shifts to Determine Residue-Specific Secondary Structure Populations for Intrinsically Disordered Proteins

Optimal Affinity Enhancement by a Conserved Flexible Linker Controls p53 Mimicry in MdmX

Conserved Glycines Control Disorder and Function in the Cold-Regulated Protein, COR15A

Inhibition of p53 DNA binding by a small molecule protects mice from radiation toxicity

Shifts in the host range of a promiscuous plasmid through parallel evolution of its replication initiation protein

Disorder predictors also predict backbone dynamics for a family of disordered proteins

A transient α-helical molecular recognition element in the disordered N-terminus of the Sgs1 helicase is critical for chromosome stability and binding of Top3/Rmi1

Contribution of proline to the pre-structuring tendency of transient helical secondary structure elements in intrinsically disordered proteins

Structural divergence is more extensive than sequence divergence for a family of intrinsically disordered proteins

p53 Phosphomimetics Preserve Transient Secondary Structure but Reduce Binding to Mdm2 and MdmX

Protein dynamics: bridging the gap

Impact of the K24N mutation on the transactivation domain of p53 and its binding to murine double-minute clone 2

Modeling the accessible conformations of the intrinsically unstructured transactivation domain of p53

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