Dental Hygiene Laboratory, Coleman Bldg., Westbrook College, 1970s

Four Westbrook College dental hygiene students work in the dental hygiene laboratory in Coleman in this 1970s photograph by Ellis Herwig Photography of Cambridge, Mass.https://dune.une.edu/wchc_photos_labs/1028/thumbnail.jp

Additional file 2: of MASTL inhibition promotes mitotic catastrophe through PP2A activation to inhibit cancer growth and radioresistance in breast cancer cells

Figure S2. MASTL depletion increases G2 arrest and the accumulation of pH 3. a The quantification of the relative percentage of cells expressing red fluorescence (pH 3). b Representative images of a normal mitotic cells (left panel) and MASTL-depleted mitotic defect cells stained with anti-acetyl-tubulin antibody (green), anti-phospho-Histone H3 antibody (red), and DAPI (blue). Scale bar = 10 μm. (TIF 763 kb

Multipotent neurogenic fate of mesenchymal stem cell is determined by Cdk4-mediated hypophosphorylation of Smad-STAT3

<p>Cyclin-dependent kinase (Cdk) in complex with a corresponding cyclin plays a pivotal role in neurogenic differentiation. In particular, Cdk4 activity acts as a signaling switch to direct human mesenchymal stem cells (MSCs) to neural transdifferentiation. However, the molecular evidence of how Cdk4 activity converts MSCs to neurogenic lineage remains unknown. Here, we found that Cdk4 inhibition in human MSCs enriches the populations of neural stem and progenitor pools rather than differentiated glial and neuronal cell pools. Interestingly, Cdk4 inhibition directly inactivates Smads and subsequently STAT3 signaling by hypophosphorylation, and both Cdk4 and Smads levels are linked during the processes of neural transdifferentiation and differentiation. In summary, our results provide novel molecular evidence in which Cdk4 inhibition leads to directing human MSCs to a multipotent neurogenic fate by inactivating Smads-STAT3 signaling.</p