Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0700208 (
scoliosis
)
8,574
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Parathyroid hormone (PTH)-related peptide (
PTHrP
) was determined to be a factor inducing malignancy-associated hypercalcemia by activating a common receptor (PTH/PTHrP receptor) with PTH.
PTHrP
gene "knock out" mice showed a form of dyschondroplasia due to reduced proliferation of chondrocytes. In addition, heterogenous populations of variously-differentiated chondrocytes were present in the hypertrophic zone of the mutant epiphyseal plate. Although the homozygotes die within several hours after birth, the adult mice, heterozygous for
PTHrP
gene deletion, showed a delayed skeletal abnormality at 3 month old, with a reduced amount of
PTHrP
transcript, therefore,
PTHrP
appears to modulate cell proliferation and differentiation at both fetal and adult stages. The co-localization of
PTHrP
and its receptor in osteoblastic cells and chondrocytes suggested a paracrine/autocine mode of action manner of these molecules. Recently, fibroblast growth factor receptor 3 (FGFR3) deficient mice demonstrated skeletal defects including kyphosis,
scoliosis
, crooked tails and curvature and overgrowth of long bones and vertebrae, which are caused by an increase in proliferation. Therefore, it seems that
PTHrP
and FGFR3 serve as positive and negative regulators on the chondrocyte proliferation, respectively. In this paper, we review our recent studies on the histological abnormality of long bone seen in
PTHrP
gene deficient- and FGFR3 gene deficient-mice.
...
PMID:The biological action of parathyroid hormone-related peptide (PTHrP) and fibroblast growth factor receptor 3 (FGFR3) on bone and cartilage. 1115 87