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Lisa D. McDaniel
Researcher at University of Texas Southwestern Medical Center
Publications - 34
Citations - 2740
Lisa D. McDaniel is an academic researcher from University of Texas Southwestern Medical Center. The author has contributed to research in topics: Xeroderma pigmentosum & Gene. The author has an hindex of 19, co-authored 34 publications receiving 2602 citations. Previous affiliations of Lisa D. McDaniel include University of Maryland, Baltimore.
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Journal ArticleDOI
A Tlr7 translocation accelerates systemic autoimmunity in murine lupus.
Srividya Subramanian,Katalin Tus,Quan Zhen Li,Andrew Wang,Xiang Hong Tian,Jinchun Zhou,Chaoying Liang,Guy Bartov,Lisa D. McDaniel,Xin J. Zhou,Roger A. Schultz,Edward K. Wakeland +11 more
TL;DR: Transcription profiling of yaa-bearing B cells revealed the overexpression of a cluster of X-linked genes that included Tlr7, and FISH analysis demonstrated the translocation of this segment onto the yaa chromosome, suggesting that Sles1 modulates the activation of adaptive immunity in response to innate immune signaling.
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The Cockayne syndrome group A gene encodes a WD repeat protein that interacts with CSB protein and a subunit of RNA polymerase II TFIIH
Karla A. Henning,Lei Li,Narayan V. Iyer,Lisa D. McDaniel,Michael S. Reagan,Randy J. Legerski,Roger A. Schultz,Miria Stefanini,Alan R. Lehmann,Lynne V. Mayne,Errol C. Friedberg +10 more
TL;DR: The cloned CSB gene encodes a member of a protein family that includes the yeast Snf2 protein, a component of the transcriptional regulator Swi/Snf, which can encode a WD repeat protein.
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Cancer predisposition caused by elevated mitotic recombination in Bloom mice
Guangbin Luo,Irma M. Santoro,Lisa D. McDaniel,Ichiko Nishijima,Michael Mills,Hagop Youssoufian,Hannes Vogel,Roger A. Schultz,Allan Bradley,Allan Bradley +9 more
TL;DR: It is demonstrated that the increased rate of loss of heterozygosity (LOH) resulting from mitotic recombination in vivo constitutes the underlying mechanism causing tumour susceptibility in these mice.
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The establishment of telomerase-immortalized cell lines representing human chromosome instability syndromes
TL;DR: The results show that hTERT efficiently extends the life span of normal human skin fibroblasts derived from patients afflicted with syndromes of genomic instability and/or premature aging, and the ectopic expression of telomerase represents a major improvement over the use of viral oncogenes for the establishment of human cell lines.
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Correction of xeroderma pigmentosum complementation group D mutant cell phenotypes by chromosome and gene transfer: involvement of the human ERCC2 DNA repair gene.
Wendy L. Flejter,Wendy L. Flejter,Lisa D. McDaniel,David Johns,Errol C. Friedberg,Roger A. Schultz +5 more
TL;DR: The phenotypic correction of XP cells from genetic complementation group D (XP-D) by a single human chromosome designated Tneo, which revealed a rearranged structure involving human chromosomes 16 and 19, including the excision repair cross-complementing 2 (ERCC2) gene from the previously described human DNA repair gene cluster at 19q13.3.