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Targeted ablation of the vitamin D receptor: an animal model of vitamin D-dependent rickets type II with alopecia.
  • Y. Li, A. Pirro, M. Demay
  • Medicine, Biology
    Proceedings of the National Academy of Sciences…
  • 2 September 1997
TLDR
A mouse model of VDDR II is generated by targeted ablation of the second zinc finger of the VDR DNA-binding domain and homozygous mice are phenotypically normal at birth and demonstrate normal survival at least until 6 months, compared to animals made vitamin D deficient by dietary means.
A Cbfa1-dependent genetic pathway controls bone formation beyond embryonic development.
TLDR
This study demonstrates that beyond its differentiation function Cbfa1 is the first transcriptional activator of bone formation identified to date and illustrates that developmentally important genes control physiological processes postnatally.
Targeted overexpression of parathyroid hormone-related peptide in chondrocytes causes chondrodysplasia and delayed endochondral bone formation.
TLDR
It is reported that overexpression of PTHrP in chondrocytes using the mouse type II collagen promoter induces a novel form of chondrodysplasia characterized by short-limbed dwarfism and a delay in endochondral ossification that is sufficiently marked that the mice are born with a cartilaginousendochondral skeleton.
Genetic ablation of parathyroid glands reveals another source of parathyroid hormone
TLDR
Gcm2 deletion uncovers an auxiliary mechanism for the regulation of calcium homeostasis in the absence of parathyroid glands, and it is proposed that this backup mechanism may be a general feature of endocrine regulation.
Bcl-2 Lies Downstream of Parathyroid Hormone–related Peptide in a Signaling Pathway That Regulates Chondrocyte Maturation during Skeletal Development
TLDR
It is reported here that PTHrP increases the expression of Bcl-2, a protein that controls programmed cell death in several cell types, in growth plate chondrocytes both in vitro and in vivo, leading to delays in their maturation towards hypertrophy and apoptotic cell death.
Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice.
TLDR
It is demonstrated that normalization of mineral ion homeostasis can prevent the development of hyperparathyroidism, osteomalacia, and rickets in the absence of the genomic actions of 1,25-dihydroxyvitamin D3.
Rescue of the skeletal phenotype of vitamin D receptor-ablated mice in the setting of normal mineral ion homeostasis: formal histomorphometric and biomechanical analyses.
TLDR
The principle action of the VDR in skeletal growth, maturation, and remodeling is its role in intestinal calcium absorption, and the skeletal consequences of VDR ablation are a result of impairedestinal calcium absorption and/or the resultant secondary hyperparathyroidism and hypophosphatemia.
Overexpression of ΔFosB transcription factor(s) increases bone formation and inhibits adipogenesis
TLDR
Because osteoblasts and adipocytes are thought to share a common precursor, it is concluded that ΔFosB transcriptionally regulates osteoblastogenesis, possibly at the expense of adipogenesis.
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