Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
about
TGF-β/Smad3 stimulates stem cell/developmental gene expression and vascular smooth muscle cell de-differentiationNephroblastoma overexpressed (Nov) inactivation sensitizes osteoblasts to bone morphogenetic protein-2, but nov is dispensable for skeletal homeostasisStrategic applications of gene expression: from drug discovery/development to bedsideFollistatin-like protein 1 regulates chondrocyte proliferation and chondrogenic differentiation of mesenchymal stem cellsNephroblastoma overexpressed (Nov) inhibits osteoblastogenesis and causes osteopeniaOsteoporosis: the current status of mesenchymal stem cell-based therapy.Transgenic overexpression of gremlin results in developmental defects in enamel and dentin in miceUpdate in new anabolic therapies for osteoporosisBone morphogenetic proteins and their antagonists: current and emerging clinical uses.Col3.6-HSD2 transgenic mice: a glucocorticoid loss-of-function model spanning early and late osteoblast differentiation.Caloric restriction leads to high marrow adiposity and low bone mass in growing miceConnective tissue growth factor is required for skeletal development and postnatal skeletal homeostasis in male mice.Early-onset type 2 diabetes impairs skeletal acquisition in the male TALLYHO/JngJ mouseGrowth factor control of bone mass.The transcriptional profile of mesenchymal stem cell populations in primary osteoporosis is distinct and shows overexpression of osteogenic inhibitorsConnective tissue growth factor (CTGF) transactivates nuclear factor of activated T-cells (NFAT) in cells of the osteoblastic lineageRapidly polymerizing injectable click hydrogel therapy to delay bone growth in a murine re-synostosis model.SMAD signaling regulates CXCL12 expression in the bone marrow niche, affecting homing and mobilization of hematopoietic progenitorsHES1 (hairy and enhancer of split 1) is a determinant of bone massFunctional comparison of chronological and in vitro aging: differential role of the cytoskeleton and mitochondria in mesenchymal stromal cellsReciprocal regulation of Notch and nuclear factor of activated T-cells (NFAT) c1 transactivation in osteoblastsConditional deletion of gremlin causes a transient increase in bone formation and bone mass.Nephroblastoma overexpressed (Nov) induces gremlin in ST-2 stromal cell lines by post-transcriptional mechanismsOsteoblast maturation on microtextured titanium involves paracrine regulation of bone morphogenetic protein signaling.Gremlin1 is required for skeletal development and postnatal skeletal homeostasisGremlin, a bone morphogenetic protein antagonist, is a crucial angiogenic factor in pituitary adenoma.BMD regulation on mouse distal chromosome 1, candidate genes, and response to ovariectomy or dietary fat.Activation of Nfatc2 in osteoblasts causes osteopenia.Lack of noggin expression by cancer cells is a determinant of the osteoblast response in bone metastases.Nemo-like kinase inhibits osteoblastogenesis by suppressing bone morphogenetic protein and WNT canonical signaling.CCAAT/Enhancer-binding protein homologous protein (CHOP) decreases bone formation and causes osteopenia.Chronic inhibition of ERK1/2 signaling improves disordered bone and mineral metabolism in hypophosphatemic (Hyp) mice.Conditional inactivation of noggin in the postnatal skeleton causes osteopeniaThe Role of Parathyroid Hormone-Related Protein (PTHrP) in Osteoblast Response to Microgravity: Mechanistic Implications for Osteoporosis Development.A soluble activin type IIA receptor induces bone formation and improves skeletal integrity.Notch inhibits osteoblast differentiation and causes osteopenia.TSG-6 regulates bone remodeling through inhibition of osteoblastogenesis and osteoclast activationSkeletal overexpression of connective tissue growth factor impairs bone formation and causes osteopeniaThe expression patterns of gremlin 1 and noggin in normal adult and tumor tissuesAccentuated osteoclastic response to parathyroid hormone undermines bone mass acquisition in osteonectin-null mice.
P2860
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P2860
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
description
2005 nî lūn-bûn
@nan
2005 թուականի Փետրուարին հրատարակուած գիտական յօդուած
@hyw
2005 թվականի փետրվարին հրատարակված գիտական հոդված
@hy
2005年の論文
@ja
2005年論文
@yue
2005年論文
@zh-hant
2005年論文
@zh-hk
2005年論文
@zh-mo
2005年論文
@zh-tw
2005年论文
@wuu
name
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@ast
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@en
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@en-gb
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@nl
type
label
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@ast
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@en
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@en-gb
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@nl
prefLabel
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@ast
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@en
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@en-gb
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@nl
P2093
P921
P3181
P356
P1433
P1476
Skeletal overexpression of gremlin impairs bone formation and causes osteopenia
@en
P2093
Elisabetta Gazzerro
Ernesto Canalis
Renata C Pereira
Sarah Olson
P304
P3181
P356
10.1210/EN.2004-0766
P407
P577
2004-11-11T00:00:00Z