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Steve Anderson, Professor

Ph.D. (1981), Rockefeller University
 

 

 

Contact Info:

Molecular Biology
University of Colorado

Steve Anderson, Ph.D. Research One South
(RC1-South), Room 5110Steve.Anderson@ucdenver.eduPhone: 303-724-3742

My lab in interested in signal transduction by tyrosine kinases, with a particular emphasis upon members of the Src family of tyrosine kinases. We primarily work on the receptor for prolactin. Prolactin stimulates the proliferation and differentiation of mammary epithelial cells, and perhaps is best known for stimulating the transcription of milk protein genes. Prolactin also maintains the viability of mammary epithelial cells during lactation by suppressing programmed cell death. We have demonstrated that Src-like kinases are required for activation of mitogenic and anti-apoptotic signaling pathways downstream of both of these receptors. Specifically, Src-like kinases appear to regulate the activation of phosphatidylinositol 3-kinase and the subsequent activation of the anti-apoptotic protein kinase Akt. We are currently determining the mechanism by which Src-like kinases are activated and what intermediates regulate Akt activation. This includes an analysis of mammary gland development in mice that lack expression of specific Src family kinases.

Our interest in Akt has also led us to examine the role of Akt in mammary gland development and tumorigenesis. We have generated transgenic mice that express a constitutively activated mutant of Akt in mammary gland and have demonstrated that Akt significantly delays mammary gland involution, an apoptotic process in which perhaps 80% of mammary epithelial cells die. In addition, it appears that a preneoplatic state is established in these mice which predisposes them to mammary cancer. We are currently characterizing these mice to identify potential substrates for Akt, as well as genes whose transcription maybe regulated by Akt. Future studies will address what oncogenes cooperate with Akt in generating mammary tumors, and whether Akt is activated in human breast cancer.​​​​​​​​​​​

 

Lee RCH, Walters JA, Reyland ME and Anderson SM (1999) " Constitutive activation of the prolactin receptor results in the induction of growth-factor-independent proliferation and constitutive activation of signaling molecules,"  J Biol Chem 274:10024-10034.

Hunter S, Burton EA, Wu SC and Anderson, SM (1999) "Fyn associates with Cbl and phosphorylates tyrosine 731 in Cbl, a binding site for phosphstidylinositol 3-kinase,"  J Biol Chem 274:2097-2106.

Anderson SM, Reyland ME, Hunter S, Diesher LM, Barzen KA, and Quissel DO (1999) Etoposide-induced activation of c-jun N-terminal kinase (JNK) correlates with drug-induced apoptosis in salivary gland acinar cells.  Cell Death and Differentiation 6, 454-462.

Reyland ME, Anderson SM, Matassa AA, Barzen KA, and Quissel DO (1999) Protein kinase C delta is essential for etoposide-induced apoptosis in salivary gland acinar cells.  J. Biol. Chem. 274, 19115-19123.

Gibson S, Tu S, Oyer R, Anderson SM, and Johnson GL (1999) Epidermal growth factor protects epithelial cells against fas induced apoptosis:  Requirement for Akt activation.  J. Biol. Chem. 274, 17612-17618.

Gibson SB, Oyer R, Spalding AC, Anderson SM, and Johnson GL (2000) Increased expression of death receptors 4 and 5 synergizes the apoptosis response to combined treatment with etoposide and TRAIL.  Mol. Cell. Biol. 20, 205-212.

Richert MM, Schwertfeger KL, Ryder JW, and Anderson SM (2000) An atlas of mouse mammary gland development.  J. Mammary Gland Dev. Neoplasia, 5:227-241.

Matassa A, Barzen KA, Anderson SM, Quissell DO, and Reyland ME (2000)  Activation of PKC is sufficient to induce an apoptotic program in salivary gland acinar cells.  Cell Death and Differentiation, 7:1200-1209.

Schwertfeger KL, Hunter S, Heasley LE, Leon RP, DeGregori J, and Anderson SM (2001)  Prolactin stimulates activation of c-jun N-terminal kinase (JNK).  Mol. Endocrinol., 15:867-881.

Schwertfeger KL, Richert MM, and Anderson, SM (2001) Mammary gland involution is delayed by activated Akt in transgenic mice.  Mol. Endocrinol. 15, 867-881.

Boonyaratanakornkit V, Scott MP, Ribon V, Sherman L, Anderson SM, Maller JL, Miller WT, and Edwards, DP (2001) Progesterone receptor contains a proline-rich motif that directly interacts with SH3 domains and activates c-Src family tyrosine kinases.  Mol. Cell 8:269-280.

Kassenbrock CK, Hunter S, Garl PM, Johnson GL, and Anderson SM, 2002.  "Inhibition of Src family kinases blocks EGF-induced activation of Akt, phosphorylation of Cbl, and ubiquitination of the EGF receptor."  Journal of Biological Chemistry 277: 24967-24975.

Limesand, KH, Barzen KA, Quissell DO, and Anderson SM (2003)  Synergistic suppression of apoptosis in salivary acinar cells by IGF1 and EGF: Role of Akt.  Cell Death and Differentation, in press.

Sun W, Wei X, Kesavan K, Garrigton TP, Fan R, Mei J, Anderson SM, Gelfand EW, and Johnson GL (2003) MEKK2 and the adapter protein Lad regulate ERK5 activation by EGF via Src. Molecular and Cellular Biology, in press.