Clcn7F318L/+ as a new mouse model of Albers-Schönberg disease.

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Clcn7F318L/+ as a new mouse model of Albers-Schönberg disease.

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2017 nî lūn-bûn

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2017年の論文

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年学术文章

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2017年學術文章

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Clcn7F318L/+ as a new mouse model of Albers-Schönberg disease.

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Clcn7F318L/+ as a new mouse model of Albers-Schönberg disease.

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Clcn7F318L/+ as a new mouse model of Albers-Schönberg disease.

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Clcn7F318L/+ as a new mouse model of Albers-Schönberg disease.

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Clcn7F318L/+ as a new mouse model of Albers-Schönberg disease.

@en

Clcn7F318L/+ as a new mouse model of Albers-Schönberg disease.

@nl

P1476

Clcn7F318L/+ as a new mouse model of Albers-Schönberg disease.

@en

P2093

A G Robling

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D Hu

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D J Horan

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H R Noonan

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K E Lim

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K Espinoza

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K S Kang

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M L Warman

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R Baron

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S G Lessard

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P2860

Lrp5 functions in bone to regulate bone mass

Loss of the ClC-7 chloride channel leads to osteopetrosis in mice and man

Albers-Schönberg disease (autosomal dominant osteopetrosis, type II) results from mutations in the ClCN7 chloride channel gene

The Wnt co-receptor LRP5 is essential for skeletal mechanotransduction but not for the anabolic bone response to parathyroid hormone treatment

The G215R mutation in the Cl-/H+-antiporter ClC-7 found in ADO II osteopetrosis does not abolish function but causes a severe trafficking defect

Targeting the LRP5 pathway improves bone properties in a mouse model of osteogenesis imperfecta.

Evaluation of teriparatide treatment in adults with osteogenesis imperfecta.

Long-term treatment of osteopetrosis with recombinant human interferon gamma.

Osteopetrosis.

Improved reporter strain for monitoring Cre recombinase-mediated DNA excisions in mice.

P304

253-261

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P31

scholarly article

P356

10.1016/J.BONE.2017.09.007

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P407

English

P478

105

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P50

Joana Caetano-Lopes

P577

2017-09-20T00:00:00Z

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P698

28942122

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P921

Albers-Schönberg Disease

P932

5752150

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