Intestinal secretory defects and dwarfism in mice lacking cGMP-dependent protein kinase II
Cyclic guanosine 3′, 5′-monophosphate (cGMP)-dependent protein kinases (cGKs)
mediate cellular signaling induced by nitric oxide and cGMP. Mice deficient in the type II cGK
were resistant to Escherichia coli STa, an enterotoxin that stimulates cGMP accumulation
and intestinal fluid secretion. The cGKII-deficient mice also developed dwarfism that was
caused by a severe defect in endochondral ossification at the growth plates. These results
indicate that cGKII plays a central role in diverse physiological processes.
mediate cellular signaling induced by nitric oxide and cGMP. Mice deficient in the type II cGK
were resistant to Escherichia coli STa, an enterotoxin that stimulates cGMP accumulation
and intestinal fluid secretion. The cGKII-deficient mice also developed dwarfism that was
caused by a severe defect in endochondral ossification at the growth plates. These results
indicate that cGKII plays a central role in diverse physiological processes.
Cyclic guanosine 3′,5′-monophosphate (cGMP)-dependent protein kinases (cGKs) mediate cellular signaling induced by nitric oxide and cGMP. Mice deficient in the type II cGK were resistant to Escherichia coli STa, an enterotoxin that stimulates cGMP accumulation and intestinal fluid secretion. The cGKII-deficient mice also developed dwarfism that was caused by a severe defect in endochondral ossification at the growth plates. These results indicate that cGKII plays a central role in diverse physiological processes.
AAAS