Location Transport

Postulate the possible hypotheses of the PKC regulation mechanism for the both the hSVCT1 and hSVCT2.?

Phorbol 12-myristate 13-acetate (PMA) activates protein Kinase C (PKC), which in turn phosphorylates other proteins. Experimental data showed that the transport capacity (Vmax) of the cloned human vitamin C transporter 1 (hSVCT1) was reduced to 57% by PMA (from 1150± 28 to 660± 21 pmol per mg protein per min), but the Km was remained almost the same ( 65± 5 and 64± 7µM). Additional experiments revealed that the hSVCT1 protein on the plasma membrane was reduced from 12.1± 1.5 to 5.5 ± 1.6 % by the PMA. For the cloned human vitamin C transporter 2 (hSVCT2), the transport capacity (Vmax) was reduced to about 69% (from 320± 21 to 220 ±16 per mg protein per min by the PMA) with little change in Km (from 29± 7 to 33± 9µM). No reduction in hSVCT2 at the cell surface was observed after the PMA treatment (12.2 ± 2.4 % at the cell surface after the PMA treatment compared with 12.4 ± 1.8%) Use your knowledge on Km and Vmax as well as the membrane transport to interpret the nature of your findings. You should look into: 1)The function of PKC in signal transduction. 2)PKC phophorylation site (motifs) on proteins. 3)The subclass members of PKC. 4)PKC effect on membrane targeting of other transport systems. 5)Address the significance of

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