April 7, 2011Journal of Biological ChemistryOpen Access

Bone Overgrowth-associated Mutations in the LRP4 Gene Impair Sclerostin Facilitator Function

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Population

In vitro models, human and rodent osteoblasts/osteocytes, and patients suffering from bone overgrowth with…

Comparison

LRP4 manipulation and LRP4 mutations vs Wild-type LRP4 or control conditions

Design

Preclinical

Authors

OLOlivier LeupinNovartis (Switzerland)EPElke PitersAZ Delta CHChristine HalleuxWorld Health Organization - Pakistan

Discussion

Member takes

Implication

Preclinical data position LRP4 as sclerostin facilitator in bone; leaves open relevance to human skeletal or vascular disease.

Structured PICO

Population

In vitro models (recombinant proteins, cell lines), human and rodent osteoblasts/osteocytes, and patients suffering from bone overgrowth with LRP4 mutations (R1170W and W1186S).

Intervention

LRP4 manipulation (overexpression, RNAi knockdown, lentivirus shRNA) and LRP4 mutations (R1170W and W1186S)

Comparator

Wild-type LRP4 or control conditions

Outcome

Sclerostin interaction, Wnt1/β-catenin signaling inhibition, and in vitro bone mineralizationsurrogate

Identifies LRP4 as a necessary facilitator for sclerostin's inhibitory function on bone formation, explaining how specific LRP4 mutations lead to bone overgrowth.

Cite This Study

Leupin et al. (2011) studied this question.

synapsesocial.com/papers/6a8665fbfbd12792c9639bbd https://doi.org/10.1074/jbc.m110.190330

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Bone Overgrowth-associated Mutations in the LRP4 Gene Impair Sclerostin Facilitator Function

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Bone Overgrowth-associated Mutations in the LRP4 Gene Impair Sclerostin Facilitator Function

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider