Fig. 4. Immunolocalization of protein kinase C (PKC)-α. In untreated cells, PKC-α was detected in the cytoplasm (  A ). Treatment with phorbol 12-myristate 13-acetate caused translocation of PKC-α from cytoplasm to membrane (  B ). Treatment with acetylcholine also induced translocation of PKC-α to membrane (  C ). The muscarinic receptor antagonist, atropine, alone had no effect on the subcellular distribution of PKC-α compared with unstimulated cells (  D ). However, pretreatment of pulmonary venous smooth muscle cells with atropine before acetylcholine treatment abolished the acetylcholine-induced translocation of PKC-α (  E ). 

Fig. 4. Immunolocalization of protein kinase C (PKC)-α. In untreated cells, PKC-α was detected in the cytoplasm (  A ). Treatment with phorbol 12-myristate 13-acetate caused translocation of PKC-α from cytoplasm to membrane (  B ). Treatment with acetylcholine also induced translocation of PKC-α to membrane (  C ). The muscarinic receptor antagonist, atropine, alone had no effect on the subcellular distribution of PKC-α compared with unstimulated cells (  D ). However, pretreatment of pulmonary venous smooth muscle cells with atropine before acetylcholine treatment abolished the acetylcholine-induced translocation of PKC-α (  E ). 

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