Lack of HIF-2α in limb bud mesenchyme causes a modest and transient delay of endochondral bone development.
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HIF-1α and growth plate development: what we really knowEffects of exposure to a DNA damaging agent on the hypoxia inducible factors in organogenesis stage mouse limbsFlavonoid Compound Icariin Activates Hypoxia Inducible Factor-1α in Chondrocytes and Promotes Articular Cartilage RepairA novel loss-of-function mutation in Npr2 clarifies primary role in female reproduction and reveals a potential therapy for acromesomelic dysplasia, Maroteaux typeA central role for hypoxic signaling in cartilage, bone, and hematopoiesis.HIF targets in bone remodeling and metastatic disease.A Qualitative Model of the Differentiation Network in Chondrocyte Maturation: A Holistic View of Chondrocyte Hypertrophy.Hypoxia-inducible factor-1 (HIF-1) but not HIF-2 is essential for hypoxic induction of collagen prolyl 4-hydroxylases in primary newborn mouse epiphyseal growth plate chondrocytes.Conditional Deletion of Prolyl Hydroxylase Domain-Containing Protein 2 (Phd2) Gene Reveals Its Essential Role in Chondrocyte Function and Endochondral Bone Formation.Vascular tissues are a primary source of BMP2 expression during bone formation induced by distraction osteogenesisHypoxia promotes redifferentiation and suppresses markers of hypertrophy and degeneration in both healthy and osteoarthritic chondrocytes.Hypoxia-driven pathways in bone development, regeneration and disease.Osteoblast recruitment to sites of bone formation in skeletal development, homeostasis, and regeneration.The chondrocytic journey in endochondral bone growth and skeletal dysplasia.Chondrocyte hypertrophy in skeletal development, growth, and disease.Hypoxia signalling manipulation for bone regeneration.Regulation of Cartilage Development and Diseases by Transcription Factors.Loss of VHL in mesenchymal progenitors of the limb bud alters multiple steps of endochondral bone development.Fibrosis and hypoxia-inducible factor-1α-dependent tumors of the soft tissue on loss of von Hippel-Lindau in mesenchymal progenitors.Transcriptional network systems in cartilage development and disease.A large-scale replication study for the association of rs17039192 in HIF-2α with knee osteoarthritis
P2860
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P2860
Lack of HIF-2α in limb bud mesenchyme causes a modest and transient delay of endochondral bone development.
description
2011 nî lūn-bûn
@nan
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
2011年论文
@zh
2011年论文
@zh-cn
name
Lack of HIF-2α in limb bud mes ...... endochondral bone development.
@en
Lack of HIF-2α in limb bud mes ...... endochondral bone development.
@nl
type
label
Lack of HIF-2α in limb bud mes ...... endochondral bone development.
@en
Lack of HIF-2α in limb bud mes ...... endochondral bone development.
@nl
prefLabel
Lack of HIF-2α in limb bud mes ...... endochondral bone development.
@en
Lack of HIF-2α in limb bud mes ...... endochondral bone development.
@nl
P2093
P2860
P356
P1433
P1476
Lack of HIF-2α in limb bud mes ...... endochondral bone development.
@en
P2093
Amato J Giaccia
Ernestina Schipani
M Celeste Simon
Richa Khatri
P2860
P2888
P304
25-6; author reply 27-9
P356
10.1038/NM0111-25
P407
P50
P577
2011-01-01T00:00:00Z