The research lab of Clark D. Wells, PhD investigates the changes in cell morphology and cell growth that lead to cancer development. The major focus is on the coordination between cell polarity proteins and HIPPO signaling during the early progression of breast and brain cancer. Both pathways have been shown by work from the Wells Laboratory to be coordinated by the Amot family of adaptor proteins. Dysregulation in expression of members of the Amot family have also been shown to promote the malignant potential of cancer cells. These basic science discoveries are being actively pursued for novel avenues for drug development.
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A full list of publications from work in the Wells lab is available on PubMed.
Amot130 adapts atrophin-1 interacting protein 4 to inhibit yes-associated protein signaling and cell growth. Adler JJ, Heller BL, Bringman LR, Ranahan WP, Cocklin RR, Goebl MG, Oh M, Lim HS, Ingham RJ, Wells CD.J Biol Chem. 2013 May 24;288(21):15181-93.
Serum deprivation inhibits the transcriptional co-activator YAP and cell growth via phosphorylation of the 130-kDa isoform of Angiomotin by the LATS1/2 protein kinases. Adler JJ, Johnson DE, Heller BL, Bringman LR, Ranahan WP, Conwell MD, Sun Y, Hudmon A, Wells CD. Proc Natl Acad Sci U S A. 2013 Oct 7. PMID: 24101513
2011The Adaptor Protein AMOT Promotes the Proliferation of Mammary Epithelial Cells via the Prolonged Activation of the Extracellular Signal-regulated Kinases. Ranahan WP, Han Z, Smith-Kinnaman W, Nabinger SC, Heller BD, Herbert BS, Chan RJ, Wells CD. Cancer Res. 2011 Feb 1.
2010Amot recognizes a juxtanuclear endocytic recycling compartment via a novel lipid binding domain. Heller B, Adu-Gyamfi E, Smith-Kinnaman W, Babbey C, Vora M, Xue Y, Bittman R, Stahelin RV, Wells CD. J Biol Chem. 2010 Apr 16;285(16):12308-20.
2006A Rich1/Amot complex regulates the Cdc42 GTPase and apical-polarity proteins in epithelial cells. Wells etal. Cell May 2006
The Wells Lab team includes Kevin Lange, Graduate Student.