Hematological defects in the oc/oc mouse, a model of infantile malignant osteopetrosis (Q80398194)

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31 December 2019

title

Hematological defects in the oc/oc mouse, a model of infantile malignant osteopetrosis (English)

1 reference

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31 December 2019

author

Claudine Blin-Wakkach

1

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31 December 2019

Patrick M. Sexton

3

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31 December 2019

Nathalie Rochet

4

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31 December 2019

Georges F. Carle

5

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31 December 2019

author name string

Wakkach A

2

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31 December 2019

publication date

1 September 2004

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31 December 2019

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31 December 2019

volume

18

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31 December 2019

issue

9

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31 December 2019

page(s)

1505-1511

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https://scigraph.springernature.com/pub.10.1038/sj.leu.2403449

31 December 2019

exact match

0 references

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The gene encoding the mouse homologue of the human osteoclast-specific 116-kDa V-ATPase subunit bears a deletion in osteosclerotic (oc/oc) mutants

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Lack of vacuolar proton ATPase association with the cytoskeleton in osteoclasts of osteosclerotic (oc/oc) mice

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Grey-lethal mutation induces severe malignant autosomal recessive osteopetrosis in mouse and human

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

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Chloride channel ClCN7 mutations are responsible for severe recessive, dominant, and intermediate osteopetrosis

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

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Mutations in the a3 subunit of the vacuolar H(+)-ATPase cause infantile malignant osteopetrosis

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Defects in TCIRG1 subunit of the vacuolar proton pump are responsible for a subset of human autosomal recessive osteopetrosis

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