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L. Henry Goodnough

Researcher at Stanford University

Publications -  46
Citations -  4568

L. Henry Goodnough is an academic researcher from Stanford University. The author has contributed to research in topics: Medicine & Internal fixation. The author has an hindex of 8, co-authored 32 publications receiving 4114 citations. Previous affiliations of L. Henry Goodnough include Case Western Reserve University.

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Functional Demarcation of Active and Silent Chromatin Domains in Human HOX Loci by Noncoding RNAs

TL;DR: The transcriptional landscape of the four human HOX loci is characterized at five base pair resolution in 11 anatomic sites and 231 HOX ncRNAs are identified that extend known transcribed regions by more than 30 kilobases, suggesting transcription of ncRNA may demarcate chromosomal domains of gene silencing at a distance.
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Wnt signaling mediates regional specification in the vertebrate face

TL;DR: The hypothesis that Wnt signaling is an evolutionarily conserved mechanism controlling facial morphogenesis is tested by determining the pattern of Wnt responsiveness in avian faces, and the consequences of WNT inhibition in the chick face are evaluated.
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Twist1 mediates repression of chondrogenesis by β-catenin to promote cranial bone progenitor specification.

TL;DR: It is shown in mice that removal of β-catenin from skull bone progenitors results in the near complete transformation of the skull bones to cartilage, whereas constitutive β- catenin activation inhibits skull bone fate selection.
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Distinct Requirements for Cranial Ectoderm and Mesenchyme-Derived Wnts in Specification and Differentiation of Osteoblast and Dermal Progenitors

TL;DR: Ectoderm Wnt ligands induce osteoblast and dermal fibroblast progenitor specification while initiating expression of a subset of mesenchymal Wnts, and ectoderm-derived Wntligands provide an inductive cue to the cranial mesenchyme for the fate selection of dermal Fibroblast and osteOBlast lineages.
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Stage-dependent craniofacial defects resulting from Sprouty2 overexpression.

TL;DR: It is shown that overexpression of spry2 at the initiation of craniofacial development results in a dramatic arrest in outgrowth of the facial prominences, and this data suggest that Sprouty2 plays a role in the out growth of facial Prominences independent of canonical Fgf signaling.