Mark Wallert

Photo of  Mark Wallert


Office/Department: Biology, Department of

Location: Sattgast Hall 218 H

Phone: (218) 755-2925

Box #: 27



Mark joined the Biology Department as Associate Professor Fall Semester 2015. Prior to coming to BSU, he was a Professor in the Biosciences Department at Minnesota State University for 25 years. Mark’s research focuses on the regulation of tumor development and metastasis in non-small cell lung cancer (NSCLC) and ovarian cancer. The Wallert Cancer Research Team currently has projects in four specific areas (see Research Interests below).  Mark is the Northwest Regional Director for the American Society of Biochemistry and Molecular Biology Student Chapters Steering Committee where he has helped organize the Undergraduate Research in the Molecular Sciences annual meeting held in Moorhead, Minnesota for the past 11 years. In 2005, Mark was recognized as the Council for Advancement and Support of Education / Carnegie Foundation for the Advancement of Teaching Minnesota College Professor of the Year.


Postdoctoral Fellow, Pharmacology, Mayo Clinic

Ph.D. Physiology, Emory University

Bachelor of Arts, Biology and Chemistry, Southwest Minnesota State University



Fall Semester 2016

  • Biol 1930: Nursing Anatomy and Physiology I
  • Biol 1930: Nursing Anatomy and Physiology I Laboratory
  • Biol 3590/5590: Cell Biology and Laboratory
  • Biol 4894: Advanced Research Project I
  • Biol 6894: Advanced Laboratory Projects

Spring Semester 2017

  • Biol 1930: Nursing Anatomy and Physiology II
  • Biol 1930: Nursing Anatomy and Physiology II Laboratory
  • Biol 4360/5360: Developmental and Tumor Biology
  • Biol 4895: Advanced Research Projects II
  • Biology 4930/5930: Stem Cells and Regenerative Medicine

Research Interests

The Wallert Cancer Research Team investigates the function of a transmembrane, transport protein, the sodium-hydrogen exchanger isoform 1 (NHE1), as a potential therapeutic target for the treatment of invasive and metastatic tumors.  This investigation has four distinct avenues:

  1. The role of Calcineurin B Homologous Protein Isoform 2 (CHP2) in the development and progression of NSCLC. CHP2 is an NHE1 binding partner that is predominantly expressed during cancer development and progression. This project focuses on the characterization of the function of CHP2 in cancer development and identifying a mechanism to block CHP2 binding to NHE1.
  2. The Regulation of NHE1 Function by Phosphorylation. NHE1 has a series of seven amino acid phosphorylation sites on the cytoplasmic regulatory domain of the protein. These phosphorylation events are catalyzed by five different protein kinases activated by distinct signaling pathways. This project focuses on identifying the role of each of these phosphorylation sites in the regulation of cancer progression and development.
  3. The Regulation of Cell Migration and Invasion by the Palmitoylation of NHE1. Palmitoylation is the reversible, covalent addition of a palmitic acid to a protein. When cells migrate NHE1 moves to the leading edge of the cell and coordinates the events that allow the cells to move and invade surrounding tissues, two key attributes of metastasis. This project focuses on the role of palmitoylation in regulating cell migration and invasion.
  4. The role of Lysophosphatidic Acid (LPA) and Urokinase-type Plasminogen Activator (uPA) signaling to NHE1 in the development and progression of ovarian cancer. LPA and uPA signaling enhance ovarian cancer invasion and metastasis especially in hypoxic microenvironments.  This project investigates the role of NHE1 activation by LPA and uPA in this process.


Team Members:

Front Row (Left to Right)
Emily Halberg – Freshman Undergraduate Biology Major
Anna Corradi – Bemidji High School Senior
Clarice Wallert – Biology Graduate Student

Middle Row (Left to Right)
Ashley Stiglich – Sophomore Undergraduate Biology Major
Stephanie Hanowski – Sophomore Undergraduate Biology Major
Taylor Manzella – Junior Undergraduate Biology Major

Back Row (Left to Right)
Mark Wallert – Associate Professor of Biology
Amanda Kooiker – Junior Undergraduate Biology Major
Kyle Bagnell – Biology Graduate Student
Tayler Smith – Sophomore Undergraduate Biology Major

Recent Work

Mark A. Wallert, Dan Hastle*, Clarice H. Wallert, Wayne Taylor Cottle*, and Joseph J. Provost.  You can never have too many kinases: The sodium hydrogen exchanger isoform 1 regulation by phosphorylation.  J. Cell Signal. 2016: 1:121

Wallert M.A, Hammes D.*, Nguyen T.*, Kiefer L.*, Berthelsen N.*, Kern A.*, Anderson-Tiege K.*, Shabb J.B., Muhonen W.W., Grove B.D., Provost J.J.
RhoA Kinase (Rock) and p90 Ribosomal S6 Kinase (p90Rsk) phosphorylation of the sodium hydrogen exchanger (NHE1) is required for lysophosphatidic acid-inducedtransport, cytoskeletal organization and migration. Cell Signaling 2015. 27(3):498-509.

Provost J.J. and Wallert M.A. Inside Out: Targeting NHE1 as an Intracellular and Extracellular Regulator of Cancer Progression. Chemical Biology and Drug Design 2013. 81(1): 85 – 101.

Provost J.J., Rastedt D*., Canine J*., Ngyuen T*., Haak A*., Kutz C. *, Berthelsen N. *, Slusser A*., Anderson K*., Dorsam G., Wallert, M. Urokinase plasminogen activator receptor induced non-small cell lung cancer invasion and metastasis requires NHE1 transporter expression and transport activity. Cellular Oncology 2012 35(2): 95-110

Wallert, M., McCoy, A*, Voog, J*, Rastedt, D*., Taves, J*,, Korpi-Steiner, N*., Canine, J. *, Ngyuen T*., Ngyuen C*., and Provost J.J.. alpha-1 adrenergic receptor-induced cytoskeletal organization and cell motility in CCL39 fibroblasts requires Phospholipase D1. J Cell Biochem. 2011 Oct;112(10):3025-34

Taves* J., Rastedt*, D., Canine* J., Mork D., Wallert, MA. and Provost, J.J. Sodium hydrogen exchanger and phospholipase D are required for alpha(1)-adrenergic receptor stimulation of metalloproteinase-9 and cellular invasion in CCL39 fibroblasts. Arch Biochem Biophys 2008: 477, 60-66.
Sang*, R.S., Johnson*, J.F., Taves*, J., Nyguen*, C., Wallert, M.A., and Provost, J.J.. alpha1-adrenergic receptor stimulation of cell motility requires phospholipase D mediated extracellular signal-regulated kinase activation. Chem Biol Drug Des 2007; 69: 240–250

Provost, J.J., Korp*i N.L. ,. Olmschenk* S.M , Funfar* M, McCoy* A., and Wallert M.A.. Protein Kinase C and Phospholipase Cß Mediate the alpha1-Adrenergic Activation of NHE1 in Chinese Hamster Lung Fibroblasts. Biochemistry and Cell Biology 2005 2. 123-132.

Wallert, M.A., H.L. Thronson*, N.L. Korpi*, S.M. Olmschenk*, A. McCoy*, M. Funfar*, and J.J. Provost. Two G-Protein Coupled Receptors Activate NHE1 in Chinese Hamster Lung Fibroblasts Through an ERK-dependent Pathway. Cellular Signaling 2004. 12: p. 231-242

* Undergraduate Student Authors