Co-localization of the insulin receptor, jun protein and choline acetyltransferase in embryonic chick retina.
Previous work demonstrated that the availability of insulin to the embryonic chick retina at a critical developmental stage stimulated the activity of the acetylcholine synthetic enzyme, choline acetyltransferase (ChAT) and that this increase required the AP-1 transcription factor, c-jun. Here it is shown that immediately following a 2-5 min exposure to insulin there is, in the amacrine and ganglion cells of the chick embryo retina, a transient increase in the level of jun protein followed by a long-lasting increase in ChAT. These and previous results show that insulin receptor activation is necessary for the characteristic retina developmental increase in ChAT protein and that this increase is preceded by a transient increase in the synthesis of the transcription factor c-jun in the same retina cells. The data demonstrate an intracellular signal transduction pathway from the developmentally-activated insulin receptor through c-jun to ChAT and cholinergic differentiation.[1]References
- Co-localization of the insulin receptor, jun protein and choline acetyltransferase in embryonic chick retina. Holdengreber, V., Ren, Y., Ben-Shaul, Y., Hausman, R.E. Exp. Eye Res. (1998) [Pubmed]
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