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Janet E. Henderson

Researcher at McGill University

Publications -  93
Citations -  5741

Janet E. Henderson is an academic researcher from McGill University. The author has contributed to research in topics: Parathyroid hormone & Bone remodeling. The author has an hindex of 41, co-authored 93 publications receiving 5477 citations. Previous affiliations of Janet E. Henderson include McGill University Health Centre & Jewish General Hospital.

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Parathyroid hormone-related peptide-depleted mice show abnormal epiphyseal cartilage development and altered endochondral bone formation.

TL;DR: P appears to modulate both the proliferation and differentiation of chondrocytes and its absence alters the temporal and spatial sequence of epiphyseal cartilage development and of subsequent endochondral bone formation necessary for normal elongation of long bones.
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Nucleolar Localization of Parathyroid Hormone-Related Peptide Enhances Survival of Chondrocytes under Conditions That Promote Apoptotic Cell Death

TL;DR: Evidence is presented that PTHrP promotes some of its cellular effects by translocating to the nucleolus and a novel mechanism by which this peptide growth factor may modulate programmed cell death.
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Osteoblast differentiation and skeletal development are regulated by Mdm2–p53 signaling

TL;DR: In this paper, Mdm2 is required to negatively regulate p53 activity at the peri-implantation stage of early mouse development, and the absolute requirement for MDM2 throughout embryogenesis and in organogenesis is unknown.
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Fibroblast growth factor (FGF) 18 signals through FGF receptor 3 to promote chondrogenesis.

TL;DR: FGF18 and FGFR3 are identified as potential molecular targets for intervention in tissue engineering aimed at cartilage repair and regeneration of damaged cartilage.
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Haploinsufficiency of Parathyroid Hormone-Related Peptide (PTHrP) Results in Abnormal Postnatal Bone Development

TL;DR: Observation that identification of both the ligand and its N-terminal receptor in metaphyseal osteoblasts and their progenitors suggests an autocrine/paracrine role for the protein in osteoblast differentiation and/or function indicates that the skeletal effects of PTH are influenced by locally produced PTHrP.