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Article

Osteoblast-specific Notch2 inactivation causes increased trabecular bone mass at specific sites of the appendicular skeleton.

Bone - 1 Jun 2016

Yorgan Timur, Vollersen Nele, Riedel Christoph, Jeschke Anke, Peters Stephanie, Busse Bjoern, Amling Michael, Schinke Thorsten

Abstract excerpt

Notch signaling is a key pathway controlling various cell fate decisions during embryogenesis and adult life. It is activated by binding of specific ligands to four different Notch receptors that are subsequently cleaved by presenilins to release an intracellular domain that enters the nucleus and activates specific transcription factors. While the skeletal analysis of various mouse models with activated or...

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Source

Identifiers

PMID: 27102824
DOI: 10.1016/j.bone.2016.04.012

Genes

NOTCH2

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Osteoblast-specific Notch2 inactivation causes increased trabecular bone mass at specific sites of the appendicular skeleton.PMID 27102824Read ↗

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Sustained Notch2 signaling in osteoblasts, but not in osteoclasts, is linked to osteopenia in a mouse model of Hajdu-Cheney syndrome.Semantic proximity Read ↗

Alteration of Notch signaling in skeletal development and disease.Semantic proximity Read ↗

Aberrant Bone Regulation in Albright Hereditary Osteodystrophy dueto Gnas Inactivation: Mechanisms and Translational Implications.Semantic proximity Read ↗

Loss of Notch signaling in skeletal stem cells enhances bone formation with agingSemantic proximity Read ↗

Jagged1 expression by osteoblast-lineage cells regulates trabecular bone mass and periosteal expansion in miceSemantic proximity Read ↗

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