Figure 1

The Akt1m transcript is upregulated during lactation and in mouse mammary tumors. (A) Quantitative real-time RT-PCR analysis to assess the relative transcriptional activation of the Akt1m transcript at various stages of normal mammary gland development (nulliparous/virgin, lactation, involution, and non-pregnant multiparous) as well as 12 mammary tumors from Brca1 conditional knockout mice (MMTV-Cre Brca1 ^fl/fl, tumors 1–3), a model for Cowden Syndrome (Pten ^G129E, tumors 4–6), and transgenic females expressing wildtype ErbB2 (MMTV-neu, tumors 7–9) or prolactin (NRL-PRL, tumors 10–12). Each sample was examined in triplicate and normalized to Gapdh expression. The relative expression levels of Akt1m were compared to the virgin control female, and statistical analysis was performed for each sample relative to the virgin control; t test, *P < 0.05, **P < 0.01. (B) Western blot analysis to determine the levels of phosphorylated AKT1 (pAKT, Ser473) and total AKT1 in selected mammary tumors (corresponding to tumors 1, 4, 7, and 10 in panel A) in comparison to a normal mammary gland of a multiparous female (control). Beta-actin (ACTB) was used as a loading control.