U
Uta Francke
Researcher at Stanford University
Publications - 475
Citations - 49980
Uta Francke is an academic researcher from Stanford University. The author has contributed to research in topics: Gene & Gene mapping. The author has an hindex of 108, co-authored 475 publications receiving 48481 citations. Previous affiliations of Uta Francke include McGill University & University of North Carolina at Chapel Hill.
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Neonatal Maternal Deprivation Response and Developmental Changes in Gene Expression Revealed by Hypothalamic Gene Expression Profiling in Mice
TL;DR: Genes that are affected by adult starvation showed no expression change in the hypothalamus of 5 day-old pups after 6 hours of maternal deprivation, and expression levels of Nanos2 and Pdk4 were increased, and those of Pgpep1, Ndp, Brms1l, Mett10d, and Snx1 were decreased after neonatal deprivation.
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The involvement of 6p in melanoma
TL;DR: Karyotype analysis of first passage cells from a melanoma, occurring in a patient with a giant congenital nevus, revealed monosomy of chromosomes #6 and #11, and trisomy of chromosome #8 and #22, and five marker chromosomes were present, including two ring chromosomes.
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Dystrophin immunocytochemistry in muscle culture: detection of a carrier of Duchenne muscular dystrophy.
Armand F. Miranda,Uta Francke,Eduardo Bonilla,G. Martucci,B Schmidt,Giovanni Salviati,M Rubin +6 more
TL;DR: Immunocytochemical analysis of clonal muscle cultures may be a useful method to determine whether mothers of DMD patients are carriers of the DMD mutation, especially in the absence of demonstrable gene defects.
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A single mutation that results in an Asp to His substitution and partial exon skipping in a family with congenital contractural arachnodactyly
TL;DR: Analysis of FBN2 allele expression in cultured dermal fibroblasts derived from the proband has shown that the mutant allele is preferentially expressed, contributing about 84% of the total transcript, indicating that an overabundance of mutant transcript does not necessarily correlate with a more severe CCA phenotype.