Title : Role of Akt isoforms in neuronal insulin signaling and resistance.

Pub. Date : 2021 Dec

PMID : 34724097






5 Functional Relationships(s)
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1 By silencing Akt isoforms individually and in pairs, in Neuro-2a and HT22 cells we observed that, in insulin-sensitive condition, Akt isoforms differentially reduced activation of AS160 and glucose uptake with Akt2 playing the major role. Glucose thymoma viral proto-oncogene 1 Mus musculus
2 By silencing Akt isoforms individually and in pairs, in Neuro-2a and HT22 cells we observed that, in insulin-sensitive condition, Akt isoforms differentially reduced activation of AS160 and glucose uptake with Akt2 playing the major role. Glucose thymoma viral proto-oncogene 1 Mus musculus
3 Over-expression of individual isoforms in insulin-sensitive and resistant cells differentially reversed AS160 phosphorylation with concomitant reversal in glucose uptake indicating a compensatory role of Akt isoforms in controlling neuronal insulin signaling. Glucose thymoma viral proto-oncogene 1 Mus musculus
4 Post-insulin stimulation Akt2 translocated to the membrane the most followed by Akt3 and Akt1, decreasing glucose uptake in the similar order in insulin-sensitive cells. Glucose thymoma viral proto-oncogene 1 Mus musculus
5 Thus, isoforms play parallel with predominant role by Akt2, and compensatory yet novel role by Akt1 and Akt3 to regulate neuronal insulin signaling, glucose uptake, and insulin-resistance. Glucose thymoma viral proto-oncogene 1 Mus musculus