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Bryce Chackerian, Ph.D.
Vojo Deretic, Ph.D.
Jeremy S. Edwards, Ph.D.
Hattie Gresham, Ph.D.
Carolyn Mold, Ph.D.
Scott A. Ness, Ph.D.
Jac A. Nickoloff, Ph.D.
Mary Ann Osley, Ph.D.
Michelle A. Ozbun, Ph.D.
Antonito Panganiban, Ph.D.
David Peabody, Ph.D.
Roger Radloff, Ph.D.
Robert L. Rubin, Ph.D.
Stephanie Ruby, Ph.D.
Cosette Wheeler, Ph.D.
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John P. O'Rourke Jr., Ph.D.
Isabelle Vergne, Ph.D.
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Albuquerque
New Mexico
UNM Health Sciences Cntr
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Department of Molecular Genetics and Microbiology
Ness Lab Homepage
Scott A. Ness, Ph.D.
Molecular Genetics and Microbiology
University of New Mexico
School of Medicine
Albuquerque, NM 87131
Lab: Cancer Research Facility 121
Tel: (505) 272-9883 (office)
Tel: (505) 272-3464 (lab)
Fax: (505) 272-3463
e-mail: ness@unm.edu
Lab Phone: (505) 272-3464
Scott A. Ness received his B.A. in biology at the University of California, San Diego in La Jolla, CA in 1980 and his Ph.D. in biochemistry from the Department of Chemistry and Biochemistry at the University of California, Los Angeles in 1985. He did post-doctoral research at the European Molecular Biology Laboratory in Heidelberg, Germany, in the laboratory of Dr. Thomas Graf, studying oncogenes, transcription and leukemia. Dr. Ness started his own laboratory at Northwestern University in Evanston, IL in 1991 and moved to UNM in 1998.
Dr. Ness is a member of AAAS, AACR and serves on the Editorial Board of the journal Oncogene, part of the Nature Publishing Group and serves on the Medical Advisory Board for the Leukemia Research Foundation. He is also a member of the UNM Cancer Research and Treatment Center (CRTC) and serves as Director of the Keck-UNM Genomics Resource, the microarray and genomics facility supported by the CRTC and the NIEHS Center. Dr. Ness has been continuously funded by the National Cancer Institute, the American Cancer Society and other agencies for over 16 years and is currently supported by two research grants from the National Cancer Institute.
The Ness laboratory studies cancer cell biology, the relationship between oncogenes and transcriptional regulation, hematopoietic stem cells and the control of cell fate. Our work focuses on the c-Myb and v-Myb transcription factors, and regulatory proteins that control their activity.
Ness Lab Downloads Page
Short narrative description of research:
How does a stem cell become a differentiated, specialized cell? How does a normal cell become transformed into a tumor cell? These are the basic questions that the Ness laboratory is addressing. We use a variety of genetic, molecular biology, cell biology and biochemical methods to study how gene regulation changes as cells differentiate from an immature stem cell precursor to a mature, specialized cell. We also study how gene regulation changes when normal cells become tumor cells. By understanding the mechanisms controlling gene expression and the regulation of specific genes in different cell types, during differentiation and during tumorigenesis, we hope to identify novel targets and techniques that could be used for developing new therapeutic or diagnostic approaches to treating leukemias, solid tumors and stem cell diseases.

Find out more about our laboratory:
Find out more about our RESEARCH
See the MEMBERS OF OUR LABORATORY
See a list of our PUBLICATIONS
See our favorite VIEWS OF ALBUQUERQUE AND UNM
For information about our graduate program, see the Biomedical Sciences Graduate Program web page.
Our laboratory is in the Cancer Research Facility, part of the Health Sciences Center on the North Campus of the University of New Mexico, in Albuquerque, NM.
Current Members of the Ness Laboratory (2006):
Post-Doctoral Researchers:
John O'Rourke (Research Assistant Professor)
Graduate Students:
Anita Quintana
Ye Zhou
Research Technicians:
Julie Torres
Undergraduate Students:
Chris Contreras
Lab phone number: (505) 272-3464
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Ness Lab Publications
Research Publications:
Bremnes, B., Rode, M., Gedde-Dahl, M., Nordeng, T. W., Jacobsen, J., Ness, S. A., and Bakke, O. (2000). The MHC class II-associated chicken invariant chain shares functional properties with its mammalian homologs. Exp Cell Res 259, 360-9.
Dash, A. B., Orrico, F. C., and Ness, S. A. (1996). The EVES motif mediates both intermolecular and intramolecular regulation of c-Myb. Genes Dev. 10, 1858-1869.
Frampton, J., Gibson, T., Lim, F., McNagny, K., Metz, T., Ness, S., and Graf, T. (1992). Mechanisms for the Transformation of Myeloid and Erythroid Cells by the Nuclear Oncogene V-myb. Leukemia 6, 1265-1295.
Frampton, J., Gibson, T. J., Ness, S. A., Döderlein, G., and Graf, T. (1991). Proposed structure for the DNA-binding domain of the Myb oncoprotein based on model building and mutational analysis. Protein Eng. 4, 891-901.
Fuerstenberg, S., Beug, H., Introna, M., Khazaie, K., Muñoz, A., Ness, S., Nordström, K., Sap, J., Stanley, I., Zenke, M., and Vennström, B. (1990). Ectopic Expression of the Erythrocyte Band 3 Anion Exchange Protein, Using a New Avian Retrovirus Vector. J. Virol. 64, 5891-5902.
Introna, M., Golay, J., Frampton, J., Nakano, T., Ness, S. A., and Graf, T. (1990). Mutations in v-myb alter the differentiation of myelomonocytic cells transformed by the oncogene. Cell 63, 1287-1297.
Katz, S., Kowenz-Leutz, E., Müller, C., Meese, K., Ness, S. A., and Leutz, A. (1993). The NF-M transcription factor is related to C/EBPß and plays a role in signal transduction, differentiation and leukemogenesis of avian myelomonocytic cells. EMBO J. 12, 1321-1332.
Kowenz-Leutz, E., Ansieau, S., Twamley, G., Ness, S. A., and Leutz, A. (1995). Gene regulation by NF-M and Myb during differentiation and leukemic transformation. Immunobiol. 193, 356-62.
Leutz, A., Damm., K., Sterneck, E., Kowenz, E., Ness, S., Frank, R., Gausepohl, H., Pan, A.-C. E., Smart, J., Hayman, M. J., and Graf, T. (1989). Molecular cloning of the chicken myelomonocytic growth factor (cMGF) reveals relationship to interleukin 6 and granulocyte colony stimulating factor. EMBO J. 8, 175-181.
Leverson, J. D., Koskinen, P. J., Orrico, F. C., Rainio, E.-M., Jalkanen, K. J., Dash, A. B., Eisenman, R. N., and Ness, S. A. (1998). Pim-1 Kinase and p100 Cooperate to Enhance c-Myb Activity. Molec. Cell 2, 417-425.
Leverson, J. D., and Ness, S. A. (1998). Point Mutations in v-Myb Disrupt a Cyclophilin-Catalyzed Negative Regulatory Mechanism. Molec. Cell 1, 203-211.
Ness, S. A. (1999). Myb Binding Proteins: Regulators and Cohorts in Transformation. Oncogene 18, 3039-3046.
Ness, S. A. (1996). The myb oncoprotein: regulating a regulator. BBA Rev. Cancer 1288, F123-F139.
Ness, S. A., Beug, H., and Graf, T. (1987). v-myb dominance over v-myc in doubly transformed chick myelomonocytic cells. Cell 51, 41-50.
Ness, S. A., and Engel, J. D. (1994). Vintage Reds and Whites: Combinatorial Transcription Factor Utilization in Hematopoietic Differentiation. Curr Opin Genet & Devel. 4, 718-724.
Ness, S. A., Kowenz-Leutz, E., Casini, T., Graf, T., and Leutz, A. (1993). Myb and NF-M: Combinatorial activators of myeloid genes in heterologous cell types. Genes Dev. 7, 749-759.
Ness, S. A., Marknell, Å., and Graf, T. (1989). The v-myb oncogene product binds to and activates the promyelocyte-specific mim-1 gene. Cell 59, 1115-1125.
Ness, S. A., and Weiss, R. L. (1985). Carbamoyl-phosphate synthetases from Neurospora crassa: Immunological relatedness of the enzymes from Neurospora, bacteria, yeast and mammals. J. Biol. Chem. 260, 14355-14362.
Ness, S. A., and Weiss, R. L. (1987). Carboxyl-terminal sequences influence the import of mitochondrial protein precursors in vivo. Proc. Natl. Acad. Sci. USA 84, 6692-6696.
Pope, R. M., Leutz, A., and Ness, S. A. (1994). C/EBPb Regulation of the Tumor Necrosis Factor a Gene. J. Clin. Invest. 94, 1449-1455.
Queva, C., Ness, S. A., Grässer, F. A., Graf, T., Vandenbunder, B., and Stéhelin, D. (1992). Expression patterns of c-myb and of v-myb induced myeloid (mim-1) gene during the development of the chick embryo. Development 114, 125-133.
Rushton, J. J., and Ness, S. A. (2001). The Conserved DNA Binding Domain Mediates Similar Regulatory Interactions for A-Myb, B-Myb, and c-Myb Transcription Factors. Blood Cells Mol Dis 27, 459-63.
Wandinger-Ness, A. U., Ness, S. A., and Weiss, R. L. (1986). Simultaneous Purification of Three Mitochondrial Enzymes. J. Biol. Chem. 261, 4820-4827.
Zagariya, A., Mungre, S., Lovis, R., Birrer, M., Ness, S., Thimmapaya, B., and Pope, R. (1998). Tumor necrosis factor alpha gene regulation: enhancement of C/EBPbeta- induced activation by c-Jun. Mol Cell Biol 18, 2815-24.
Rushton JJ, Davis LM, Lei W, Mo X, Leutz A and Ness SA. Distinct changes in gene expression induced by a-myb, b-myb and c-myb proteins. Oncogene 2003; 22: 308-13.
Ness, S. A. (2003). Myb Protein Specificity: Evidence of a Context-Specific Transcription Factor Code. Blood Cells Mol Dis 31, 192-200.
Rushton, J. J., Davis, L. M., Lei, W., Mo, X., Leutz, A., and Ness, S. A. (2003). Distinct changes in gene expression induced by A-Myb, B-Myb and c-Myb proteins. Oncogene 22, 308-313.
Winn, L. M., Lei, W., and Ness, S. A. (2003). Pim-1 Phosphorylates the DNA Binding Domain of c-Myb. Cell Cycle 2, 258-262.
Roitbak, T., Ward, C. J., Harris, P. C., Bacallao, R., Ness, S. A., and Wandinger-Ness, A. (2004). A Polycystin-1 Multiprotein Complex is Disrupted in Polycystic Kidney Disease Cells. Mol Biol Cell 15, 1334-1346.
Lei, W., Rushton, J. J., Davis, L. M., Liu, F., and Ness, S. A. (2004). Positive and negative determinants of target gene specificity in Myb transcription factors. J Biol Chem 279, 29519-29527.
Lei, W., Liu, F., and Ness, S. A. (2005). Positive and Negative Regulation of c-Myb by Cyclin D1, Cyclin-Dependent Kinases and p27 Kip1. Blood 105, 3855-3861.
Liu, F., Lei, W., O'Rourke, J. P., and Ness, S. A. (2006). Oncogenic mutations cause dramatic, qualitative changes in the transcriptional activity of c-Myb. Oncogene 25, 795-805.
Shah, VO, Dominic, EA, Moseley, P, Pickett, G, Fleet, M, Ness, S and Raj, DSC. (2006) “Hemodialysis Modulates Gene Expression Profile in Skeletal Muscle.” American Journal of Kidney Disease. 48, 816-828
Pilkinton, M, Sandoval, R, Song, J, Ness, SA and Colamonici, OR (2006) “Mip/LIN-9 regulates the expression of B-Myb, and the induction of cyclin A, cyclin B and CDK1.” J. Biol. Chem. In press
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