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?7A). Total RNA was isolated from epithelial-enriched cell populations and qPCR was performed. As expected, SmoM2 transgene expression was increased 13-fold (��?4.8) in EGFP-positive SmoM2:Cre MECs compared to the un-recombined Tomato Red-positive population (Fig.?7B). Fig.?7C illustrates the gene expression of the Hh signal pathway components in all three sorted cell populations. An induction of Gli2 (18?��?7.2 fold [http://www.selleckchem.com/screening/epigenetics-compound-library.html check details] change p?=?0.03) expression as well as a marked increase of Gli1 (71?��?24.2 fold change p?=?0.04) and Ptch2 (55?��?20.3 fold change p?=?0.04) was observed in EGFP+ (recombined) SmoM2;Cre MECs as compared to SmoM2;+ cells. An induction (5?��?0.9 fold) in Gli2 was observed in Tomato Red+ (un-recombined) cells. Additionally, and induction of Smo expression was observed in both recombined (EGFP+) and un-recombined (Tomato Red+) cells from SmoM2;Cre mice as compared to cells from Cre negative litter-mates. These data indicate that activation of canonical Hh signaling occurred in the SmoM2 expressing cells. Since SmoM2-expressing cells were stimulating proliferation of wildtype cells adjacent or in-close proximity, we next investigated whether expression of members of the Notch signaling pathway, which is known to function in a juxtacrine manner, was altered. Fig.?7D illustrates the gene expression patterns of several [https://en.wikipedia.org/wiki/Evodiamine Evodiamine] Notch pathway members in all three sorted cell populations. A marked upregulation of the Notch ligands delta-like 1 (Dll-1), (21?��?6.8 fold change p?=?0.02) and Jagged-2 (Jag2) (5?��?1.0 fold change p?[http://www.selleckchem.com/products/BMS-777607.html Selleck BMS-777607] due to aberrant differentiation and organization of distinct mammary epithelial cell subtypes, we examined the luminal and myoepithelial cell layers by immunostaining with antibodies that detect keratin 8 (K8), a luminal cell marker and keratin 14 (K14), a myoepithelial cell marker (Fig.?8). While both of these markers were readily detected in SmoM2;Cre glands, the typical bilayer of ductal epithelium was disrupted as compared to SmoM2;+ controls. Furthermore, K14-expressing cells were rounded as opposed to their characteristic elongated shape (Fig.