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Dale Frank

Researcher at University of Pennsylvania

Publications -  49
Citations -  2244

Dale Frank is an academic researcher from University of Pennsylvania. The author has contributed to research in topics: Gene & Genomic imprinting. The author has an hindex of 21, co-authored 44 publications receiving 1980 citations. Previous affiliations of Dale Frank include Columbia University & Columbia University Medical Center.

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International, evidence-based consensus diagnostic criteria for HHV-8–negative/idiopathic multicentric Castleman disease

TL;DR: The proposed consensus criteria will facilitate consistent diagnosis, appropriate treatment, and collaborative research and exclude infectious, malignant, and autoimmune disorders that can mimic iMCD.
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Placental overgrowth in mice lacking the imprinted gene Ipl.

TL;DR: Results show a nonredundant function for Ipl in restraining placental growth and indicate that Ipl can act, at least in part, independently of insulin-like growth factor-2 signaling, which regulates multiple pathways to control placental size.
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Competition between noggin and bone morphogenetic protein 4 activities may regulate dorsalization during Xenopus development.

TL;DR: Competition between these two molecules may determine the final degree of muscle formation in the marginal zone, thus defining the border between dorsolateral and ventral mesoderm.
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The IPL Gene on Chromosome 11p15.5 is Imprinted in Humans and Mice and is Similar to TDAG51, Implicated in Fas Expression and Apoptosis

TL;DR: The cloning and characterization of the IPL gene is described, which shows tissue-specific expression and functional imprinting, with the maternal allele active and the paternal allele relatively inactive, in many human and mouse tissues.
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Placental growth retardation due to loss of imprinting of Phlda2

TL;DR: Phlda2 acts as a true rheostat for placental growth, with overgrowth after gene deletion and growth retardation after loss of imprinting, as well as significant placental stunting in BAC-transgenic mice that over-expressed Phlda2 and one flanking gene, Slc22a1l, but did not over-express Cdkn1c.