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WenFang Wang

Researcher at University of Kansas

Publications -  20
Citations -  645

WenFang Wang is an academic researcher from University of Kansas. The author has contributed to research in topics: Gene & Medicine. The author has an hindex of 13, co-authored 17 publications receiving 604 citations. Previous affiliations of WenFang Wang include American Physical Therapy Association & Harvard University.

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Journal ArticleDOI

A Nonsense Mutation in MSX1 Causes Witkop Syndrome

TL;DR: The resemblance between the tooth and nail phenotype in the human family and that ofMsx1-knockout mice strongly supports the conclusions that a nonsense mutation in MSX1 causes TNS and that Msx1 is critical for both Tooth and nail development.
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Groucho homologue Grg5 interacts with the transcription factor Runx2-Cbfa1 and modulates its activity during postnatal growth in mice

TL;DR: In this paper, a yeast two-hybrid system was used to identify a groucho homologue, Grg5, as a Runx2-interacting protein, and by analyses of postnatal growth in mice, it was shown that Grg 5 and Runx 2 interact genetically.
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Commitment to the Osteoblast Lineage Is Not Required for RANKL Gene Expression

TL;DR: It is demonstrated that parathyroid hormone stimulation of RANKL in mice is not affected by a significant reduction in the number of osteoblasts and commitment to the osteoblast lineage is not a requirement for RankL gene transcription in fibroblastic stromal cells, which suggests responsiveness of this gene to specific hormones via control of their receptors may be enhanced.
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Ncb5or Deficiency Increases Fatty Acid Catabolism and Oxidative Stress

TL;DR: Investigating the mechanisms of these phenomena in prediabetic Ncb5or−/− mice suggests that increased FFA accumulation and catabolism and oxidative stress are major consequences of NCB5or deficiency in liver.
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F exclusion of bacteriophage T7 occurs at the cell membrane

TL;DR: The F plasmid PifA protein, known to be the cause of F exclusion of bacteriophage T7, is shown to be a membrane-associated protein and the Escherichia coli FxsAprotein, which, at higher concentrations than found in wild-type cells, protects T7 from exclusion, is shows to interact with PifC.