J. Sommers

发表

Biochemical and Kinetic Characterization of the DNA Helicase and Exonuclease Activities of Werner Syndrome Protein*

R. Brosh, Saba Choudhary, J. Sommers, 2004, Journal of Biological Chemistry.

Analysis of the DNA Substrate Specificity of the Human BACH1 Helicase Associated with Breast Cancer*

S. Cantor, R. Brosh, J. Sommers, 2005, Journal of Biological Chemistry.

Specialization among Iron-Sulfur Cluster Helicases to Resolve G-quadruplex DNA Structures That Threaten Genomic Stability*

K. Shin‐ya, C. Kisker, S. Bharti, 2013, The Journal of Biological Chemistry.

Biochemical Characterization of Warsaw Breakage Syndrome Helicase*

J. D. de Winter, Yuliang Wu, R. Brosh, 2011, The Journal of Biological Chemistry.

Werner syndrome helicase has a critical role in DNA damage responses in the absence of a functional fanconi anemia pathway.

R. Shoemaker, R. Brosh, J. Sommers, 2013, Cancer research.

Targeting an Achilles’ heel of cancer with a WRN helicase inhibitor

J. Sommers, M. Aggarwal, Robert M. Brosh Jr., 2013, Cell cycle.

p53 modulates RPA-dependent and RPA-independent WRN helicase activity.

C. Harris, P. Karmakar, Qin Yang, 2005, Cancer research.

p53 Modulates the Exonuclease Activity of Werner Syndrome Protein*

X. Wang, C. Harris, X. W. Wang, 2001, The Journal of Biological Chemistry.

Repeat expansions confer WRN dependence in microsatellite-unstable cancers

K. Garimella, S. West, P. Meltzer, 2020, Nature.

Biochemical and cell biological assays to identify and characterize DNA helicase inhibitors.

R. Brosh, J. Sommers, M. Aggarwal, 2016, Methods.

WRN helicase safeguards deprotected replication forks in BRCA2-mutated cancer cells

R. Shoemaker, Tanay Thakar, George-Lucian Moldovan, 2021, Nature Communications.

In vivo function of the conserved non-catalytic domain of Werner syndrome helicase in DNA replication.

R. Brosh, J. Sommers, Sudha Sharma, 2004, Human molecular genetics.

Werner syndrome protein: biochemical properties and functional interactions

V. Bohr, D. Orren, R. Brosh, 2000, Experimental Gerontology.

Impact of Age-Associated Cyclopurine Lesions on DNA Repair Helicases

C. Kisker, D. Kaplan, R. Brosh, 2014, PloS one.

RECON syndrome is a genome instability disorder caused by mutations in the DNA helicase RECQL1

S. Smerdon, G. Stewart, T. Harel, 2022, The Journal of clinical investigation.

Catalytic Strand Separation by RECQ1 Is Required for RPA-Mediated Response to Replication Stress

Jing Huang, M. Seidman, R. Brosh, 2015, Current Biology.

Biochemical analysis of DNA synthesis blockage by G-quadruplex structure and bypass facilitated by a G4-resolving helicase.

R. Maul, R. Brosh, J. Sommers, 2021, Methods.

Molecular functions and cellular roles of the ChlR1 (DDX11) helicase defective in the rare cohesinopathy Warsaw breakage syndrome

S. Bharti, Yuliang Wu, R. Brosh, 2014, Cellular and Molecular Life Sciences.

Cellular Assays to Study the Functional Importance of Human DNA Repair Helicases.

Srijita Dhar, R. Brosh, J. Sommers, 2019, Methods in molecular biology.

Molecular analyses of DNA helicases involved in the replicational stress response.

Yuliang Wu, R. Brosh, J. Sommers, 2010, Methods.

Delineation of WRN helicase function with EXO1 in the replicational stress response.

R. Brosh, J. Sommers, M. Aggarwal, 2010, DNA repair.

Biochemical Analysis of the DNA Unwinding and Strand Annealing Activities Catalyzed by Human RECQ1*[boxs]

A. Vindigni, R. Brosh, Saba Choudhary, 2005, Journal of Biological Chemistry.

A minimal threshold of FANCJ helicase activity is required for its response to replication stress or double-strand break repair

K. Shin‐ya, K. Neuman, H. Kitao, 2018, Nucleic acids research.

Identification and Biochemical Characterization of a Novel Mutation in DDX11 Causing Warsaw Breakage Syndrome

E. Chouery, A. Mégarbané, G. Rouleau, 2013, Human mutation.

Repeat Expansions Confers WRN Dependence in Microsatellite Unstable 1 Cancers

Anthony, Tubbs, K. Garimella, 2020 .

Close encounters for the first time: Helicase interactions with DNA damage.

R. Brosh, J. Sommers, I. Khan, 2015, DNA repair.

FANCJ Uses Its Motor ATPase to Destabilize Protein-DNA Complexes, Unwind Triplexes, and Inhibit RAD51 Strand Exchange*

Robert M Brosh, S. Cantor, R. Brosh, 2009, Journal of Biological Chemistry.

Human RECQ1 Interacts with Ku70/80 and Modulates DNA End-Joining of Double-Strand Breaks

A. Stortchevoi, R. Brosh, J. Sommers, 2013, PloS one.

Repeat expansions confer WRN dependence in microsatellite-unstable cancers

K. Garimella, S. West, P. Meltzer, 2020, Nature.

Mitochondrial genetic variation is enriched in G-quadruplex regions that stall DNA synthesis in vitro.

Thomas J. Butler, A. Moore, S. Bandinelli, 2020, Human molecular genetics.

Biochemical Characterization of the Human Mitochondrial Replicative Twinkle Helicase

Sean M. Carney, M. García-Díaz, S. Bharti, 2016, The Journal of Biological Chemistry.

Stimulation of Flap Endonuclease-1 by the Bloom's Syndrome Protein*

I. Hickson, V. Bohr, R. Brosh, 2004, Journal of Biological Chemistry.

The Exonucleolytic and Endonucleolytic Cleavage Activities of Human Exonuclease 1 Are Stimulated by an Interaction with the Carboxyl-terminal Region of the Werner Syndrome Protein*

R. Brosh, J. Sommers, Sudha Sharma, 2003, Journal of Biological Chemistry.

Inhibition of helicase activity by a small molecule impairs Werner syndrome helicase (WRN) function in the cellular response to DNA damage or replication stress

Monika Aggarwal, Robert M Brosh, R. Shoemaker, 2011, Proceedings of the National Academy of Sciences.

Novel Function of the Fanconi Anemia Group J or RECQ1 Helicase to Disrupt Protein-DNA Complexes in a Replication Protein A-stimulated Manner*

M. Lei, M. Wold, R. Brosh, 2014, The Journal of Biological Chemistry.

The Q Motif of Fanconi Anemia Group J Protein (FANCJ) DNA Helicase Regulates Its Dimerization, DNA Binding, and DNA Repair Function*

H. Kitao, C. Kisker, Yuliang Wu, 2012, The Journal of Biological Chemistry.

Discovery of a new hereditary RECQ helicase disorder RECON syndrome positions the replication stress response and genome homeostasis as centrally important processes in aging and age-related disease

G. Stewart, T. Harel, J. Sommers, 2023, Ageing Research Reviews.

CDK1 phosphorylates WRN at collapsed replication forks

L. Zolla, R. Brosh, J. Sommers, 2016, Nature Communications.

Biochemical Characterization of the DNA Substrate Specificity of Werner Syndrome Helicase*

R. Brosh, J. Sommers, Juwaria F. Waheed, 2002, The Journal of Biological Chemistry.

A high-throughput screen to identify novel small molecule inhibitors of the Werner Syndrome Helicase-Nuclease (WRN)

A. Jadhav, A. Simeonov, V. Bohr, 2019, PloS one.

Biochemical analysis of SARS-CoV-2 Nsp13 helicase implicated in COVID-19 and factors that regulate its catalytic functions

J. Sommers, Rebecca A. Lee, Robert Michael Brosh, 2023, Journal of Biological Chemistry.

Werner syndrome protein interacts with human flap endonuclease 1 and stimulates its cleavage activity

G. Dianov, P. Karmakar, V. Bohr, 2001, The EMBO journal.

DNA Sequences Proximal to Human Mitochondrial DNA Deletion Breakpoints Prevalent in Human Disease Form G-quadruplexes, a Class of DNA Structures Inefficiently Unwound by the Mitochondrial Replicative Twinkle Helicase*

J. Mergny, S. Bharti, J. N. Spelbrink, 2014, The Journal of Biological Chemistry.

WRN helicase and FEN-1 form a complex upon replication arrest and together process branchmigrating DNA structures associated with the replication fork.

G. Dianov, R. Bambara, M. Otterlei, 2003, Molecular biology of the cell.

Werner Protein Is a Target of DNA-dependent Protein Kinase in Vivo and in Vitro, and Its Catalytic Activities Are Regulated by Phosphorylation*

D. Ramsden, P. Karmakar, V. Bohr, 2002, The Journal of Biological Chemistry.

Biochemical characterization of the WRN-FEN-1 functional interaction.

G. Dianov, R. Brosh, J. Sommers, 2002, Biochemistry.

The interaction site of Flap Endonuclease-1 with WRN helicase suggests a coordination of WRN and PCNA

R. Gary, U. Hübscher, R. Brosh, 2005, Nucleic acids research.

Molecular functions and cellular roles of the ChlR1 (DDX11) helicase defective in the rare cohesinopathy Warsaw breakage syndrome

S. Bharti, Yuliang Wu, R. Brosh, 2014, Cellular and Molecular Life Sciences.

Fanconi anemia group J mutation abolishes its DNA repair function by uncoupling DNA translocation from helicase activity or disruption of protein-DNA complexes.

K. Shin‐ya, T. Leonard, H. Kitao, 2010, Blood.

DNA Repair and Replication Fork Helicases Are Differentially Affected by Alkyl Phosphotriester Lesion*

Z. Kelman, Yuliang Wu, D. Kaplan, 2012, The Journal of Biological Chemistry.

Interaction between the helicases genetically linked to Fanconi anemia group J and Bloom's syndrome

S. Cantor, I. Hickson, Yuliang Wu, 2011, The EMBO journal.

FANCJ (BACH1) helicase forms DNA damage inducible foci with replication protein A and interacts physically and functionally with the single-stranded DNA-binding protein.

S. Cantor, M. Kenny, R. Brosh, 2007, Blood.

DNA polymerase β outperforms DNA polymerase γ in key mitochondrial base excision repair activities.

V. Bohr, B. A. Baptiste, T. Kulikowicz, 2021, DNA repair.

FANCJ Helicase Uniquely Senses Oxidative Base Damage in Either Strand of Duplex DNA and Is Stimulated by Replication Protein A to Unwind the Damaged DNA Substrate in a Strand-specific Manner*

R. Camerini-Otero, A. Mason, M. Wold, 2009, The Journal of Biological Chemistry.

single-stranded DNA-binding protein replication protein A and interacts physically and functionally with the FANCJ (BACH1) helicase forms DNA damage inducible foci with

S. Cantor, M. Kenny, J. Sommers, 2013 .

FANCJ ( BACH 1 ) helicase forms DNA damage inducible foci with replication protein A and interacts physically and functionally with the single-stranded DNA-binding protein

S. Cantor, M. Kenny, R. Brosh, 2007 .

Physical and Functional Mapping of the Replication Protein A Interaction Domain of the Werner and Bloom Syndrome Helicases*

M. Gray, K. Doherty, M. Kenny, 2005, Journal of Biological Chemistry.

Inhibition of BACH1 (FANCJ) helicase by backbone discontinuity is overcome by increased motor ATPase or length of loading strand

S. Cantor, K. Doherty, R. Brosh, 2006, Nucleic acids research.

FANCJ compensates for RAP80 deficiency and suppresses genomic instability induced by interstrand cross-links.

S. Cantor, M. Bellani, M. Seidman, 2020, Nucleic acids research.

Protein Degradation Pathways Regulate the Functions of Helicases in the DNA Damage Response and Maintenance of Genomic Stability

R. Brosh, J. Sommers, A. Suhasini, 2015, Biomolecules.

Fanconi Anemia Group J Helicase and MRE11 Nuclease Interact To Facilitate the DNA Damage Response

S. Cantor, J. Masson, P. Muniandy, 2013, Molecular and Cellular Biology.

PHOSPHORYLATION-DEPENDENT ASSOCIATION OF WRN WITH RPA IS REQUIRED FOR RECOVERY OF REPLICATION FORKS STALLED AT SECONDARY DNA STRUCTURES

M. Crescenzi, T. Kulikowicz, J. Sommers, 2023, bioRxiv.

Biochemical Characterization of the DNA Substrate Specificity of Werner Syndrome Helicase*

R. Brosh, J. Sommers, Juwaria F. Waheed, 2002, The Journal of Biological Chemistry.

Interaction between the helicases genetically linked to Fanconi anemia group J and Bloom's syndrome

I. Hickson, Yuliang Wu, P. North, 2011, The EMBO journal.

FANCJ compensates for RAP80 deﬁciency and suppresses genomic instability induced by interstrand cross-links

M. Bellani, George-Lucian Moldovan, J. Sommers, 2022 .