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W B Huttner

Publications and source records attributed to W B Huttner.

148 records · Page 9Linked to original sources

Stimulation by 6-N,2'-O-dibutyryladenosine 3' :5'-cyclic monophosphate and glucocorticoids of phosphoenolpyruvate carboxykinase in the isolated perfused rat liver.

Dibutyryl cyclic AMP stimulated the activity of phosphoenolpyruvate carboxykinase in perfused livers of rats, fed on a low-protein diet, linearly over a 6h period. The enzyme activity was also significantly elevated by dexamethasone, the effect being considerably lower than that of the cyclic nucleotide. Since the time-course of phosphoenolpyruvate carboxykinase activity in response to dibutyryl cyclic AMP resembled that observed after dibutyryl cyclic AMP injection into intact animals, it is suggested that induction of the enzyme in vivo is due to a direct action of the cyclic nucleotide on the liver. Combined administration of dibutyryl cyclic AMP and glucocorticoids did not lead to an additive increase of liver phosphoenolpyruvate carboxykinase activity, either in vivo or in the perfused organ.

Animals↗

XL alpha s is a new type of G protein.

The GTP-binding proteins are well-known regulators of cellular functions, including vesicular transport. Cholera toxin, which is known to catalyse ADP-ribosylation of the alpha s subunit of heterotrimeric G proteins, stimulates secretory vesicle formation from the trans-Golgi network. Here we describe a new cholera toxin target, an 'extra large' G protein (XL alpha s; M(r) 92K) which consists of a new 51K XL-portion linked to a G alpha s truncated at the amino terminus. XL alpha s is specifically associated with the trans-Golgi network and occurs selectively in cells containing both the regulated and the constitutive pathway of protein secretion. Hence, XL alpha s may mediate the effects of cholera toxin on secretory vesicle formation.

Adenosine Diphosphate Ribose↗