Mesenchymal cell-derived Wnt1 signaling regulates subchondral bone remodeling but has no effects on the development of growth plate or articular cartilage in mice.
loss of Lrp5 the co-receptor thought to transmit extracellular WNT signals during bone mass regulation did not reduce the bone-anabolic effect of Wnt1 providing direct evidence that Wnt1 function does not require the LRP5 co-receptor.
Marked elevation of Wnt1 expression in the ventral midbrain is correlated with disruption of the differentiation program of ventral dopaminergic neurons.
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