Beta-cell-specific inactivation of the mouse Ipf1/Pdx1 gene results in loss of the beta-cell phenotype and maturity onset diabetes

Article Abstract:

Mice in which the Ipf1/Pdx1 gene was disrupted specifically in beta cells were used for studying late beta-cell-specific action of the homeodomain protein IPF1/PCX1. The mice develop diabetes as they age. IPF1/PDX1 represses expression of glucagon, while positively controlling expression of insulin and islet amyloid polypeptide. It appears that IPF1/PDX1 also regulates the expression of Glut2 in a dosage-dependent way. That indicates that lowered IPF1/PCS1 activity may contribute to development of type II diabetes by bringing on lowered expression of insulin and Glut2.

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Constitutive activation of MEK1 in chondrocytes causes Stat 1-independent achondroplasia-like dwarfism and rescues the Fgfr3-deficient mouse phenotype

Article Abstract:

Studies reveal that mitogen-activated protein kinases (MAPKs) pathway inhibits hypertrophic differentiation of chondrocytes and negatively regulates bone growth without inhibiting chondrocyte proliferation. A model in which Fgfr3 signaling inhibits bone growth by inhibiting chondrocyte differentiation through the MAPK pathway and by inhibiting chondrocyte proliferation through Stat 1 is suggested.

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The Hedgehog-binding proteins Gas 1 and Cdo cooperate to positively regulate Shh signaling during mouse development

Article Abstract:

The signaling of Sonic Hedgehog (Shh) morphogen is promoted by Gas 1 and Cdo proteins. The Shh signaling is crucial for the development of various parts of the central nervous system.

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