Dataset Information


Comparison expression data from wild-type and NFATc1-deficient osteoclasts

ABSTRACT: Genetic deletion of Nfatc1 in mice results in profound osteoclast-poor osteopetrosis, a high bone mass state caused by a lack of osteoclast activity. We hypothesized that the family of NFATc1 regulated transcripts in the osteoclast would be enriched for genes associated with osteoclast function. We used microarrays profile gene expression in wild-type and NFATc1-deficient osteoclasts generated in vitro to identify NFATc1-dependent transcripts in osteoclasts. Bone marrow macrophages from wild-type and mice with an induced deficiency of NFATc1 (NFATc1 fl/fl MxCre+ mice where NFATc1 excision was induced by polyIC treatment) were cultured ex vivo in MCSF and RANKL for 3 days. 2 biological replicates were assayed for each genotype.

ORGANISM(S): Mus musculus  

SUBMITTER: Julia F. Charles   Antonios O Aliprantis 

PROVIDER: E-GEOD-37219 | ArrayExpress | 2012-08-18



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NFATc1 in mice represses osteoprotegerin during osteoclastogenesis and dissociates systemic osteopenia from inflammation in cherubism.

Aliprantis Antonios O AO   Ueki Yasuyoshi Y   Sulyanto Rosalyn R   Park Arnold A   Sigrist Kirsten S KS   Sharma Sudarshana M SM   Ostrowski Michael C MC   Olsen Bjorn R BR   Glimcher Laurie H LH  

The Journal of clinical investigation 20081009 11

Osteoporosis results from an imbalance in skeletal remodeling that favors bone resorption over bone formation. Bone matrix is degraded by osteoclasts, which differentiate from myeloid precursors in response to the cytokine RANKL. To gain insight into the transcriptional regulation of bone resorption during growth and disease, we generated a conditional knockout of the transcription factor nuclear factor of activated T cells c1 (Nfatc1). Deletion of Nfatc1 in young mice resulted in osteopetrosis  ...[more]

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