Research Topics
Species | Lisa D McDanielSummaryAffiliation: University of Texas Southwestern Medical Center Country: USA Publications
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Publications
TERF2-XPF: caught in the middle; beginnings from the endLisa D McDaniel
Laboratory of Molecular Pathology, Department of Pathology, University of Texas Southwestern Medical Center, Dallas, 75390, USA
DNA Repair (Amst) 5:868-72. 2006..Here, we review these exciting findings that suggest new roles for the TERF2-XPF complex and point out several questions that remain to be addressed...- XPF/ERCC4 and ERCC1: their products and biological rolesLisa D McDaniel
Department of Pathology, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390 9072, USA
Adv Exp Med Biol 637:65-82. 2008..The ERCC1/ERCC4 complex is conserved across most species presenting an opportunity to examine some functions in model organisms where mutants can be more readily generated and phenotypes more quickly assessed... 
Mapping of a single locus capable of complementing the defective heterochromatin phenotype of Roberts syndrome cellsLisa D McDaniel
Department of Pathology, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390 9072, USA
Am J Hum Genet 77:132-9. 2005..The results are consistent with the notion that the single gene defect responsible for heterochromatic splaying and developmental abnormalities maps to chromosome 8p21...- Validation of XP-C pathogenic variations in archival material from a live XP patientLisa D McDaniel
Laboratory of Molecular Pathology, Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390 9072, USA
DNA Repair (Amst) 6:115-20. 2007.... - The role of endogenous and exogenous DNA damage and mutagenesisErrol C Friedberg
Laboratory of Molecular Pathology, Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390 9072, USA
Curr Opin Genet Dev 14:5-10. 2004..This article presents some of the highlights in this area of investigation, with a particular emphasis on DNA repair, the tolerance of DNA damage and its contribution to mutagenesis, and DNA damage checkpoint regulation... - A novel XPC pathogenic variant detected in archival material from a patient diagnosed with Xeroderma Pigmentosum: a case report and review of the genetic variants reported in XPCAmanda Rivera Begeman
Laboratory of Molecular Pathology, Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390 9072, USA
DNA Repair (Amst) 6:100-14. 2007.... - DNA polymerases for translesion DNA synthesis: enzyme purification and mouse models for studying their functionPaula L Fischhaber
Department of Pathology, University of Texas Southwestern Medical Center, Dallas, USA
Methods Enzymol 408:355-78. 2006..It also describes some of the methods employed in the evaluation of mouse strains defective in genes that encode these enzymes... - Polk mutant mice have a spontaneous mutator phenotypeJ Nicole Kosarek Stancel
Laboratory of Molecular Pathology, Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75390 9072, USA
DNA Repair (Amst) 8:1355-62. 2009..These results are consistent with the notion that Pol kappa is required for accurate translesion DNA synthesis past naturally occurring polycyclic guanine adducts, possibly generated by cholesterol and/or its metabolites... - Mutations in the Trp53 gene of UV-irradiated Xpc mutant mice suggest a novel Xpc-dependent DNA repair processDorit Nahari
Laboratory of Molecular Pathology, Department of Pathology, University of Texas, Southwestern Medical Center, Dallas, TX 75390 9072, USA
DNA Repair (Amst) 3:379-86. 2004.... - A Tlr7 translocation accelerates systemic autoimmunity in murine lupusSrividya Subramanian
Center for Immunology and Department of Pathology, University of Texas Southwestern Medical Center, Dallas, TX 75235, USA
Proc Natl Acad Sci U S A 103:9970-5. 2006.... - Chromosome instability and tumor predisposition inversely correlate with BLM protein levelsLisa D McDaniel
Department of Pathology, CY1 107, UT Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390 8840, USA
DNA Repair (Amst) 2:1387-404. 2003.... - Elevated mutation rates in the germline of Polkappa mutant male miceKaren L A Burr
Department of Genetics, University of Leicester, University Road, Leicester LE1 7RH, UK
DNA Repair (Amst) 5:860-2. 2006..We suggest that compromised translesion synthesis in Polkappa(-/-) mice may result in replication fork pausing which, in turn, may affect ESTR mutation rate... - Telomerase-immortalized human fibroblasts retain UV-induced mutagenesis and p53-mediated DNA damage responsesPaul C Porter
Department of Pharmacology and Toxicology, University of Louisville, 570 South Preston Street, Rm221, Louisville, KY 40202, USA
DNA Repair (Amst) 5:61-70. 2006..Furthermore, telomerase immortalization provides permanent cell lines for testing the immediate impact on NER and mutagenesis of selective genetic manipulation without propagation to establish mutant lines... - Transcription-associated breaks in xeroderma pigmentosum group D cells from patients with combined features of xeroderma pigmentosum and Cockayne syndromeTherina Theron
Genome Damage and Stability Centre, University of Sussex, Falmer, Brighton BN1 9RQ, United Kingdom
Mol Cell Biol 25:8368-78. 2005.... 
The molecular mechanism underlying Roberts syndrome involves loss of ESCO2 acetyltransferase activityMiriam Gordillo
McKusick Nathans Institute of Genetic Medicine, Johns Hopkins University, Baltimore, USA
Hum Mol Genet 17:2172-80. 2008..In summary, we provide the first evidence that loss of acetyltransferase activity contributes to the pathogenesis of RBS, underscoring the essential role of the enzymatic activity of the Eco1p family of proteins...- DNA damage responses protect xeroderma pigmentosum variant from UVC-induced clastogenesisMarila Cordeiro-Stone
Department of Pathology and Laboratory Medicine, University of NC at Chapel Hill, Chapel Hill, NC 27599 7525, USA
Carcinogenesis 23:959-65. 2002..These responses protect human cells from chromosomal aberrations, especially when other pathways, such as accurate lesion bypass, are lost...