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Article

Osteopetrosis in TAK1-deficient mice owing to defective NF-κB and NOTCH signaling.

Proceedings of the National Academy of Sciences of the United States of America - 6 Jan 2015

Swarnkar Gaurav, Karuppaiah Kannan, Mbalaviele Gabriel, Chen Tim Hung-Po, Abu-Amer Yousef

Abstract excerpt

The MAP kinase TGFβ-activated kinase (TAK1) plays a crucial role in physiologic and pathologic cellular functions including cell survival, differentiation, apoptosis, inflammation, and oncogenesis. However, the entire repertoire of its mechanism of action has not been elucidated. Here, we found that ablation of Tak1 in myeloid cells causes osteopetrosis in mice as a result of defective osteoclastogenesis....

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Share to Immunoglobulin J Recombination Signal Sequence-Binding Protein
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Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

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Source

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Identifiers

PMID: 25535389
DOI: 10.1073/pnas.1415213112
PMCID: PMC4291677

Genes

RBPJ
NUMBL
NUMB

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 3 Sept 2026.

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Osteopetrosis in TAK1-deficient mice owing to defective NF-κB and NOTCH signaling.PMID 25535389Read ↗

Ablation of Tak1 in osteoclast progenitor leads to defects in skeletal growth and bone remodeling in mice.Semantic proximity Read ↗

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TAK1-dependent activation of AP-1 and c-Jun N-terminal kinase by receptor activator of NF-kappaB.Semantic proximity Read ↗

Cyld aborts hyperactivation of synovial fibroblasts in inflammatory arthritis by regulating the TAK1/IKK2 signaling axisSemantic proximity Read ↗

TAK1 negatively regulates NF-κB and p38 MAP kinase activation in Gr-1+CD11b+ neutrophils.Semantic proximity Read ↗

Notch4 Negatively Regulates the Inflammatory Response to Mycobacterium tuberculosis Infection by Inhibiting TAK1 ActivationSemantic proximity Read ↗

TAK1 mediates BMP signaling in cartilageSemantic proximity Read ↗

Critical Roles of NF-κB Signaling Molecules in Bone Metabolism Revealed by Genetic Mutations in Osteopetrosis.Semantic proximity Read ↗

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