As also other Na +-coupled transport systems are influenced, the TPA effect appears to be related to the expression of a general ‘adaptive’ alteration of membrane transport in LLC-PK 1 cells. We conclude that TPA via activation of protein kinase C regulates the number of operating transport systems. Can you ping the APIC-EM server from the 2960. Check the following things: Do you have console access to the 2960 stack. TPA had under the chosen experimental conditions no effect on thymidine incorporation into DNA excluding a general proliferative effect. The stack is even correctly discovered by APIC-EM : But failed health check since device is stuck in non-terminal state DEVICEINFOREQUESTED for more than threshold time: 0 hours, 16 minutes, 0 seconds.

Na +-dependent alanine transport into LLC-PK 1 monolayers was affected by TPA administration in a similar manner. The increased P i transport was retained in isolated apical vesicles.

Kinetic analysis of Na +/P i contransport indicated an increase in the apparent V max without an effect on the apparent K m. Incubation of LLC-PK 1 cells with 10 ng/ml TPA for 8 h led to a 300% increase in Na +/P i cotransport in the presence of cycloheximide the increase amounted only to a 100% and was reached within 2 h. Other phorbol esters which have no potency or a smaller one to activate protein kinase C had no effect on Na +/P i cotransport. The maximal response was reached at a TPA concentration of 10 ng/ml. Incubation of LLC-PK 1 cells with TPA produced an increase in Na +/phosphate (P i) cotransport. We have tested for the effect of the phorbol ester 12- O-tetradecanoylphorbol 13-acetate (TPA) on Na +/phosphate cotransport in an established epithelial cell line of renal origine (LLC-PK 1).

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