Clark D. Wells, Ph.D.



Associate Professor

Department of Biochemistry and Molecular Biology
Indiana University School of Medicine
John D. Van Nuys Medical Science Building
635 Barnhill Drive, Room MS4079A
Indianapolis, Indiana 46202-5126

Phone: (317) 278-1060
Facsimile: (317) 274-4686
Dr. Wells' Lab Website


B.S., 1993, University of Kentucky
Ph.D., 2001, University of Texas Southwestern Medical School at Dallas, Texas
Postdoctoral, 2006 Samuel Lunenfeld Research Inst. at Mount Sinai Hospital, Toronto, CANADA


Area of Study

Causal relationships between differentiation and growth control in Breast Cancer Development; Cross-talk between Cell polarity, HIPPO/YAP dependent transcription and ErbB/MAPK signaling.  More details...


Selected Recent Publications

A Rich1/Amot complex regulates the Cdc42 GTPase and apical-polarity proteins in epithelial cells.  Wells CD, Fawcett JP, Traweger A, Yamanaka Y, Goudreault M, Elder K, Kulkarni S, Gish G, Virag C, Lim C, Colwill K, Starostine A, Metalnikov P Pawson T. Cell. 2006 May 5;125(3):535-48

Amot 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

The 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.

Nguyen HB, Babcock JT, Wells CD, Quilliam LA. LKB1 tumor suppressor regulates AMP kinase/mTOR-independent cell growth and proliferation via the phosphorylation of Yap. Oncogene. 2012 Oct 1. (PMID:  23027127).

Adler JJ, Heller BL, Bringman LR, Ranahan WP, Cocklin RR, Goebl MG, Oh M, Lim HS, Ingham RJ, Wells CD. Amot130 adapts Atrophin-1 Interacting Protein 4 to inhibit Yes-associated Protein signaling and cell growth. J Biol Chem. 2013 Apr 5. (PMID:  23564455)

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)



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Research Interests

My laboratory is interested in the relationship of hyperplastic growth with malignant breast tumor formation. A fundamental GAP in our understanding of the natural history of breast cancer development is the lack of a molecular basis that explains how the loss of cellular differentiation underlies the desensitization of cells to the growth inhibitory influences of the microenvironment. My laboratory has found evidence that such events are strongly influenced by alterations in the signaling pathways that mediate the cross-talk between “polarity” proteins and core pathways involved in cell proliferation. In particular, we are focused on how the differential expression of the Amot family of adaptor proteins mediates the balance between growth arrested and differentiated ductal epithelia with highly proliferative and de-differentiated carcinomas. Our long term goal is to use such information to identify histologically significant markers that indicate whether normal appearing or hyperplastic tissues are likely to develop malignant carcinomas.

635 Barnhill Dr | Indianapolis, IN 46202 | Ph: (317) 274-7151 | Fax: (317) 274-4686