Biomedical Research Education & Training
Faculty Member

Hiebert, Scott W., Ph.D.
Professor of Biochemistry
Hortense B. Ingram Chair in Cancer Research
Associate Professor of Medicine

Lab Url:

Phone Number: 615-936-3582

Email Address:

Hiebert, Scott's picture
Academic history
B.S., Bethel College, N. Newton, KS
Ph.D., Northwestern Univ., Evanston, IL

Office Address   Mailing Address

512 Preston Research Building

512 PRB 0146

Research Keywords
Acute leukemia, tumor suppressors, cell cycle, transcriptional repression, co-repressors,Cell cycle,Chromatin,Chromosome,Gene regulation,Malignancy,Mouse,Signal transduction,Stem cells,Transcription,Transcription factor

Research Specialty
Molecular Mechanisms of Acute Leukemia, cell cycle control, and the action of tumor suppressors.

Research Description
The work in my laboratory focuses on determining the normal function of the AML1/RUNX1 transcription factor in the regulation of hematopoietic gene expression and the mechanism by which the t(8;21), inv(16), and the t(12;21) chromosomal translocations disrupt normal AML-1 function to promote acute leukemia. We have defined AML-1 as a transcription factor that binds the "enhancer core" motif, which regulates the expression of a large number of tissue specific genes. Transcriptional studies demonstrated that AML1 both activates and represses transcription, and that the translocation fusion proteins inhibit expression of AML1-dependent target genes. We have determined that the t(8;21) fusion protein, AML1/ETO, interacts with the mSin3 and nuclear hormone co-repressors that recruit histone deacetylases to repress transcription. This initial observation led us to demonstrate that the t(12;21) and inv(16) proteins also associate with co-repressors and histone deacetylases. Thus, we have identified a common mechanism for transcriptional repression for these three translocations. Given that these fusion proteins repress transcription and cause cancer, we asked whether they inhibit the expression of known tumor suppressor genes. We have identified 2 tumor suppressors that are regulated by these translocation fusion proteins (p19ARF and Neurofibromatosis-1), which regulate the p53 tumor suppressor and the Ras oncogene, respectively. We continue to use mouse models to dissect the molecular mechanisms by which these chromosomal translocation fusion proteins trigger acute leukemia.

In addition, we are examining the function of the ETO/MTG family of transcriptional co-repressors using gene ablation in the mouse. Both ETO (also known as MTG8) and MTG16 (a closely related family member) are disrupted by chromosomal translocations in acute myeloid leukemia (the t(8;21) and t(16;21), respectively). Moreover, MTG16 is commonly deleted in Breast cancer and ETO/MTG8 is mutated in colon cancer. Disruption of ETO caused perinatal lethality with some defects in gut development and we are still exploring the cause(s) of death. Disruption of MTG16 caused defects in stem cell functions and disruptions in cell fate decisions. Deletion of the third family member, Mtgr1, affected cell fate decisions in the small intestine. Global gene expression analysis is being used to dissect the transcriptional changes upon deletion of these master regulators and to relate the inactivation phenotypes to tumorigenesis. These studies have also linked the ETO family to the regulation of Wnt signaling and suggest that these factors function as tumor suppressors in Breast and Colon cancer.

Finally, we are extending our analysis of transcriptional control to the enzymes that are recruited by MTG family members and AML1/RUNX1. Specifically, we have inactivated Histone Deacetylase 3 in the mouse. We are currently dissecting the phenotypes associated with inactivation of this key regulator of chromatin structure and function. These phenotypes include cell cycle disruption, and wide spread changes in gene expression.

Bhaskara, S, Chyla, BJ, Amann, JM, Knutson, SK, Cortez, D, Sun, ZW, Hiebert, SW. Deletion of histone deacetylase 3 reveals critical roles in S phase progression and DNA damage control. Mol Cell, 30(1), 61-72, 2008 PMCID:2373760

Farmer, TE, Williams, CS, Washington, MK, Hiebert, SW. Inactivation of the p19(ARF) tumor suppressor affects intestinal epithelial cell proliferation and integrity. J Cell Biochem, 104(6), 2228-40, 2008

Knutson, SK, Chyla, BJ, Amann, JM, Bhaskara, S, Huppert, SS, Hiebert, SW. Liver-specific deletion of histone deacetylase 3 disrupts metabolic transcriptional networks. EMBO J, 27(7), 1017-28, 2008 PMCID:2323257

Hanson, CA, Wood, LD, Hiebert, SW. Cellular stress triggers TEL nuclear export via two genetically separable pathways. J Cell Biochem, 2007

Moore, AC, Amann, JM, Williams, CS, Tahinci, E, Farmer, TE, Martinez, JA, Yang, G, Luce, KS, Lee, E, Hiebert, SW. Myeloid Translocation Gene Family Members Associate with TCFs and Influence TCF-Dependent Transcription. Mol Cell Biol, 2007 PMCID:2223385

Yang, G, Thompson, MA, Brandt, SJ, Hiebert, SW. Histone deacetylase inhibitors induce the degradation of the t(8;21) fusion oncoprotein. Oncogene, 26(1), 91-101, 2007

Martinez, JA, Williams, CS, Amann, JM, Ellis, TC, Moreno-Miralles, I, Washington, MK, Gregoli, P, Hiebert, SW. Deletion of Mtgr1 sensitizes the colonic epithelium to dextran sodium sulfate-induced colitis. Gastroenterology, 131(2), 579-88, 2006

Reed-Inderbitzin, E, Moreno-Miralles, I, Vanden-Eynden, SK, Xie, J, Lutterbach, B, Durst-Goodwin, KL, Luce, KS, Irvin, BJ, Cleary, ML, Brandt, SJ, Hiebert, SW. RUNX1 associates with histone deacetylases and SUV39H1 to repress transcription. Oncogene, 25(42), 5777-86, 2006

Amann, JM, Chyla, BJ, Ellis, TC, Martinez, A, Moore, AC, Franklin, JL, McGhee, L, Meyers, S, Ohm, JE, Luce, KS, Ouelette, AJ, Washington, MK, Thompson, MA, King, D, Gautam, S, Coffey, RJ, Whitehead, RH, Hiebert, SW. Mtgr1 is a transcriptional corepressor that is required for maintenance of the secretory cell lineage in the small intestine. Mol Cell Biol, 25(21), 9576-85, 2005 PMCID:1265807

Ice, RJ, Wildonger, J, Mann, RS, Hiebert, SW. Comment on "Nervy links protein kinase A to plexin-mediated semaphorin repulsion". Science, 309(5734), 558; author reply 558, 2005

Linggi, BE, Brandt, SJ, Sun, ZW, Hiebert, SW. Translating the histone code into leukemia. J Cell Biochem, 96(5), 938-50, 2005

Moreno-Miralles, I, Pan, L, Keates-Baleeiro, J, Durst-Goodwin, K, Yang, C, Kim, HG, Thompson, MA, Klug, CA, Cleveland, JL, Hiebert, SW. The inv(16) cooperates with ARF haploinsufficiency to induce acute myeloid leukemia. J Biol Chem, 280(48), 40097-103, 2005

Yang, G, Khalaf, W, van de Locht, L, Jansen, JH, Gao, M, Thompson, MA, van der Reijden, BA, Gutmann, DH, Delwel, R, Clapp, DW, Hiebert, SW. Transcriptional repression of the Neurofibromatosis-1 tumor suppressor by the t(8;21) fusion protein. Mol Cell Biol, 25(14), 5869-79, 2005 PMCID:1168824

Durst, KL, Hiebert, SW. Role of RUNX family members in transcriptional repression and gene silencing. Oncogene, 23(24), 4220-4, 2004

Irvin, Brenda J, Hiebert, Scott W. AML-1 steps up to the platelets. Nat Med, 10(3), 238-9, 2004

M??ller-Tidow, Carsten, Steffen, Bj??rn, Cauvet, Thomas, Tickenbrock, Lara, Ji, Ping, Diederichs, Sven, Sargin, B??lent, K??hler, Gabriele, Stelljes, Matthias, Puccetti, Elena, Ruthardt, Martin, DeVos, Sven, Hiebert, Scott W., Koeffler, H. Phillip, Berdel, Wolfgang E., Serve, Hubert. Translocation Products in Acute Myeloid Leukemia Activate the Wnt Signaling Pathway in Hematopoietic Cells. Mol Cell Biol, 24(7), 2890-2904, 2004 PMCID:371102

Yang, G, Khalaf, W, van de Locht, L, Jansen, JH, van der Reijden, BA, M??ller-Tidow, C, Delwel, HR, Serve, H, Clapp, DW, Hiebert, SW. Epigenetic regulation of tumor suppressors in t(8:21)-containing AML. Ann Hematol, 83(6), 329-30, 2004

Yang, G, Khalaf, W, van de Locht, L, Jansen, JH, van der Reijden, BA, M??ller-Tidow, C, Delwel, HR, Serve, H, Clapp, DW, Hiebert, SW. Epigenetic regulation of tumor suppressors in t(8:21)-containing AML. Ann Hematol, 83 Suppl 1, S83, 2004

Durst, Kristie L, Lutterbach, Bart, Kummalue, Tanawan, Friedman, Alan D, Hiebert, Scott W. The inv(16) fusion protein associates with corepressors via a smooth muscle myosin heavy-chain domain.. Mol Cell Biol, 23(2), 607-19, 2003 PMCID:151524

Hiebert, Scott W, Reed-Inderbitzin, Edward F, Amann, Joseph, Irvin, Brenda, Durst, Kristie, Linggi, Bryan. The t(8;21) fusion protein contacts co-repressors and histone deacetylases to repress the transcription of the p14(ARF) tumor suppressor.. Blood Cells Mol Dis, 30(2), 177-83, 2003

Irvin, Brenda J, Wood, Lauren D, Wang, Lilin, Fenrick, Randy, Sansam, Courtney G, Packham, Graham, Kinch, Michael, Yang, Elizabeth, Hiebert, Scott W. TEL, a putative tumor suppressor, induces apoptosis and represses transcription of Bcl-XL. J Biol Chem, 278(47), 46378-86, 2003

Wood, Lauren D, Irvin, Brenda J, Nucifora, Giuseppina, Luce, K Scott, Hiebert, Scott W. Small ubiquitin-like modifier conjugation regulates nuclear export of TEL, a putative tumor suppressor.. Proc Natl Acad Sci U S A, 100(6), 3257-62, 2003 PMCID:152279

Barseguian, Karina, Lutterbach, Bart, Hiebert, Scott W, Nickerson, Jeffrey, Lian, Jane B, Stein, Janet L, van Wijnen, Andre J, Stein, Gary S. Multiple subnuclear targeting signals of the leukemia-related AML1/ETO and ETO repressor proteins.. Proc Natl Acad Sci U S A, 99(24), 15434-9, 2002 PMCID:137734

King, Dana, Yang, Genyan, Thompson, Mary Ann, Hiebert, Scott W. Loss of neurofibromatosis-1 and p19(ARF) cooperate to induce a multiple tumor phenotype.. Oncogene, 21(32), 4978-82, 2002

Linggi, Bryan, M??ller-Tidow, Carsten, van de Locht, Louis, Hu, Ming, Nip, John, Serve, Hubert, Berdel, Wolfgang E, van der Reijden, Bert, Quelle, Dawn E, Rowley, Janet D, Cleveland, John, Jansen, Joop H, Pandolfi, Pier Paolo, Hiebert, Scott W. The t(8;21) fusion protein, AML1 ETO, specifically represses the transcription of the p14(ARF) tumor suppressor in acute myeloid leukemia.. Nat Med, 8(7), 743-50, 2002

de Guzman, Cristina G, Warren, Alan J, Zhang, Zheng, Gartland, Larry, Erickson, Paul, Drabkin, Harry, Hiebert, Scott W, Klug, Christopher A. Hematopoietic stem cell expansion and distinct myeloid developmental abnormalities in a murine model of the AML1-ETO translocation.. Mol Cell Biol, 22(15), 5506-17, 2002 PMCID:133929

Amann, J M, Nip, J, Strom, D K, Lutterbach, B, Harada, H, Lenny, N, Downing, J R, Meyers, S, Hiebert, S W. ETO, a target of t(8;21) in acute leukemia, makes distinct contacts with multiple histone deacetylases and binds mSin3A through its oligomerization domain. Mol Cell Biol, 21(19), 6470-83, 2001 PMCID:99794

Eischen, C M, Packham, G, Nip, J, Fee, B E, Hiebert, S W, Zambetti, G P, Cleveland, J L. Bcl-2 is an apoptotic target suppressed by both c-Myc and E2F-1.. Oncogene, 20(48), 6983-93, 2001

Hiebert, S W, Lutterbach, B, Amann, J. Role of co-repressors in transcriptional repression mediated by the t(8;21), t(16;21), t(12;21), and inv(16) fusion proteins.. Curr Opin Hematol, 8(4), 197-200, 2001

Nip, J, Strom, D K, Eischen, C M, Cleveland, J L, Zambetti, G P, Hiebert, S W. E2F-1 induces the stabilization of p53 but blocks p53-mediated transactivation.. Oncogene, 20(8), 910-20, 2001

Wang, L, Hiebert, S W. TEL contacts multiple co-repressors and specifically associates with histone deacetylase-3.. Oncogene, 20(28), 3716-25, 2001

Fenrick, R, Wang, L, Nip, J, Amann, J M, Rooney, R J, Walker-Daniels, J, Crawford, H C, Hulboy, D L, Kinch, M S, Matrisian, L M, Hiebert, S W. TEL, a putative tumor suppressor, modulates cell growth and cell morphology of ras-transformed cells while repressing the transcription of stromelysin-1.. Mol Cell Biol, 20(16), 5828-39, 2000 PMCID:86060

Lutterbach, B, Hiebert, S W. Role of the transcription factor AML-1 in acute leukemia and hematopoietic differentiation.. Gene, 245(2), 223-35, 2000

Lutterbach, B, Westendorf, J J, Linggi, B, Isaac, S, Seto, E, Hiebert, S W. A mechanism of repression by acute myeloid leukemia-1, the target of multiple chromosomal translocations in acute leukemia.. J Biol Chem, 275(1), 651-6, 2000

Melnick, A M, Westendorf, J J, Polinger, A, Carlile, G W, Arai, S, Ball, H J, Lutterbach, B, Hiebert, S W, Licht, J D. The ETO protein disrupted in t(8;21)-associated acute myeloid leukemia is a corepressor for the promyelocytic leukemia zinc finger protein.. Mol Cell Biol, 20(6), 2075-86, 2000 PMCID:110824

Melnick, A, Carlile, G W, McConnell, M J, Polinger, A, Hiebert, S W, Licht, J D. AML-1/ETO fusion protein is a dominant negative inhibitor of transcriptional repression by the promyelocytic leukemia zinc finger protein.. Blood, 96(12), 3939-47, 2000

Meyers, S, Hiebert, S W. Alterations in subnuclear trafficking of nuclear regulatory factors in acute leukemia.. J Cell Biochem Suppl, Suppl 35, 93-8, 2000

Nip, J, Hiebert, S W. Topoisomerase IIalpha mediates E2F-1-induced chemosensitivity and is a target for p53-mediated transcriptional repression.. Cell Biochem Biophys, 33(2), 199-207, 2000

Strom, D K, Nip, J, Westendorf, J J, Linggi, B, Lutterbach, B, Downing, J R, Lenny, N, Hiebert, S W. Expression of the AML-1 oncogene shortens the G(1) phase of the cell cycle.. J Biol Chem, 275(5), 3438-45, 2000

Fenrick, R, Amann, J M, Lutterbach, B, Wang, L, Westendorf, J J, Downing, J R, Hiebert, S W. Both TEL and AML-1 contribute repression domains to the t(12;21) fusion protein.. Mol Cell Biol, 19(10), 6566-74, 1999 PMCID:84626

Lutterbach, B, Hou, Y, Durst, K L, Hiebert, S W. The inv(16) encodes an acute myeloid leukemia 1 transcriptional corepressor.. Proc Natl Acad Sci U S A, 96(22), 12822-7, 1999 PMCID:23113

Westendorf, J J, Hiebert, S W. Mammalian runt-domain proteins and their roles in hematopoiesis, osteogenesis, and leukemia.. J Cell Biochem, Suppl 32-33, 51-8, 1999

Westendorf, J J, Mernaugh, R, Hiebert, S W. Identification and characterization of a protein containing formin homology (FH1/FH2) domains.. Gene, 232(2), 173-82, 1999

Fenrick, R, Hiebert, S W. Role of histone deacetylases in acute leukemia.. J Cell Biochem Suppl, 30-31, 194-202, 1998

Ji, C, Casinghino, S, Chang, D J, Chen, Y, Javed, A, Ito, Y, Hiebert, S W, Lian, J B, Stein, G S, McCarthy, T L, Centrella, M. CBFa(AML/PEBP2)-related elements in the TGF-beta type I receptor promoter and expression with osteoblast differentiation.. J Cell Biochem, 69(3), 353-63, 1998

Lutterbach, B, Sun, D, Schuetz, J, Hiebert, S W. The MYND motif is required for repression of basal transcription from the multidrug resistance 1 promoter by the t(8;21) fusion protein.. Mol Cell Biol, 18(6), 3604-11, 1998 PMCID:108942

Lutterbach, B, Westendorf, J J, Linggi, B, Patten, A, Moniwa, M, Davie, J R, Huynh, K D, Bardwell, V J, Lavinsky, R M, Rosenfeld, M G, Glass, C, Seto, E, Hiebert, S W. ETO, a target of t(8;21) in acute leukemia, interacts with the N-CoR and mSin3 corepressors.. Mol Cell Biol, 18(12), 7176-84, 1998 PMCID:109299

Petrovick, M S, Hiebert, S W, Friedman, A D, Hetherington, C J, Tenen, D G, Zhang, D E. Multiple functional domains of AML1: PU.1 and C/EBPalpha synergize with different regions of AML1.. Mol Cell Biol, 18(7), 3915-25, 1998 PMCID:108976

Strom, D K, Cleveland, J L, Chellappan, S, Nip, J, Hiebert, S W. E2F-1 and E2F-3 are functionally distinct in their ability to promote myeloid cell cycle progression and block granulocyte differentiation.. Cell Growth Differ, 9(1), 59-69, 1998

Westendorf, J J, Yamamoto, C M, Lenny, N, Downing, J R, Selsted, M E, Hiebert, S W. The t(8;21) fusion product, AML-1-ETO, associates with C/EBP-alpha, inhibits C/EBP-alpha-dependent transcription, and blocks granulocytic differentiation.. Mol Cell Biol, 18(1), 322-33, 1998 PMCID:121499

Westendorf, J. J., Yamamoto, C. M., Lenny, N., Downing, J. R., Selsted, M.E., Hiebert, S. W. The t(8;21) fusion product, AML-1ETO, associates with C/EBP-a inhibits C/EBP-a dependent transcription, and blocks granulocytic differentiation. Mol. Cell. Biol., 18, 322-333, 1998

Zeng, C, van Wijnen AJ, Stein JL, Meyers, S, Sun, W, Shopland, L, Lawrence, JB, Penman, S, Lian, JB, Stein, GS, Hiebert, SW. Identification of a Nuclear Matrix Targeting Signal in the Leukemia and Bone-Related Transcription Factor AML-1B. Proc. Natl. Acad. Sci., 94, 6746-51, 1997

Banerjee, C, McCabe, L R, Choi, J Y, Hiebert, S W, Stein, J L, Stein, G S, Lian, J B. Runt homology domain proteins in osteoblast differentiation: AML3/CBFA1 is a major component of a bone-specific complex.. J Cell Biochem, 66(1), 1-8, 1997

Lenny, N, Westendorf, J J, Hiebert, S W. Transcriptional regulation during myelopoiesis.. Mol Biol Rep, 24(3), 157-68, 1997

Nip, J, Strom, D K, Fee, B E, Zambetti, G, Cleveland, J L, Hiebert, S W. E2F-1 cooperates with topoisomerase II inhibition and DNA damage to selectively augment p53-independent apoptosis.. Mol Cell Biol, 17(3), 1049-56, 1997 PMCID:231829

Zeng, C, van Wijnen, A J, Stein, J L, Meyers, S, Sun, W, Shopland, L, Lawrence, J B, Penman, S, Lian, J B, Stein, G S, Hiebert, S W. Identification of a nuclear matrix targeting signal in the leukemia and bone-related AML/CBF-alpha transcription factors.. Proc Natl Acad Sci U S A, 94(13), 6746-51, 1997 PMCID:21229

Banerjee, C, Hiebert, S W, Stein, J L, Lian, J B, Stein, G S. An AML-1 consensus sequence binds an osteoblast-specific complex and transcriptionally activates the osteocalcin gene.. Proc Natl Acad Sci U S A, 93(10), 4968-73, 1996 PMCID:39389

Hiebert, S W, Downing, J R, Lenny, N, Meyers, S. Transcriptional regulation by the t(8;21) fusion protein, AML-1/ETO.. Curr Top Microbiol Immunol, 211, 253-8, 1996

Hiebert, S W, Sun, W, Davis, J N, Golub, T, Shurtleff, S, Buijs, A, Downing, J R, Grosveld, G, Roussell, M F, Gilliland, D G, Lenny, N, Meyers, S. The t(12;21) translocation converts AML-1B from an activator to a repressor of transcription.. Mol Cell Biol, 16(4), 1349-55, 1996 PMCID:231119

Hitomi, M, Shu, J, Strom, D, Hiebert, S W, Harter, M L, Stacey, D W. Prostaglandin A2 blocks the activation of G1 phase cyclin-dependent kinase without altering mitogen-activated protein kinase stimulation.. J Biol Chem, 271(16), 9376-83, 1996

Meyers, S, Lenny, N, Sun, W, Hiebert, S W. AML-2 is a potential target for transcriptional regulation by the t(8;21) and t(12;21) fusion proteins in acute leukemia.. Oncogene, 13(2), 303-12, 1996

Okuda, T, van Deursen, J, Hiebert, S W, Grosveld, G, Downing, J R. AML1, the target of multiple chromosomal translocations in human leukemia, is essential for normal fetal liver hematopoiesis.. Cell, 84(2), 321-30, 1996

Rhoades, K L, Hetherington, C J, Rowley, J D, Hiebert, S W, Nucifora, G, Tenen, D G, Zhang, D E. Synergistic up-regulation of the myeloid-specific promoter for the macrophage colony-stimulating factor receptor by AML1 and the t(8;21) fusion protein may contribute to leukemogenesis.. Proc Natl Acad Sci U S A, 93(21), 11895-900, 1996 PMCID:38155

Zhang, D E, Hetherington, C J, Meyers, S, Rhoades, K L, Larson, C J, Chen, H M, Hiebert, S W, Tenen, D G. CCAAT enhancer-binding protein (C/EBP) and AML1 (CBF alpha2) synergistically activate the macrophage colony-stimulating factor receptor promoter.. Mol Cell Biol, 16(3), 1231-40, 1996 PMCID:231105

Frank, R, Zhang, J, Uchida, H, Meyers, S, Hiebert, S W, Nimer, S D. The AML1/ETO fusion protein blocks transactivation of the GM-CSF promoter by AML1B.. Oncogene, 11(12), 2667-74, 1995

Golub, T R, Barker, G F, Bohlander, S K, Hiebert, S W, Ward, D C, Bray-Ward, P, Morgan, E, Raimondi, S C, Rowley, J D, Gilliland, D G. Fusion of the TEL gene on 12p13 to the AML1 gene on 21q22 in acute lymphoblastic leukemia.. Proc Natl Acad Sci U S A, 92(11), 4917-21, 1995 PMCID:41818

Hiebert, S W, Packham, G, Strom, D K, Haffner, R, Oren, M, Zambetti, G, Cleveland, J L. E2F-1:DP-1 induces p53 and overrides survival factors to trigger apoptosis.. Mol Cell Biol, 15(12), 6864-74, 1995 PMCID:230941

Lenny, N, Meyers, S, Hiebert, S W. Functional domains of the t(8;21) fusion protein, AML-1/ETO.. Oncogene, 11(9), 1761-9, 1995

Meyers, S, Hiebert, S W. Indirect and direct disruption of transcriptional regulation in cancer: E2F and AML-1.. Crit Rev Eukaryot Gene Expr, 5(3-4), 365-83, 1995

Meyers, S, Lenny, N, Hiebert, S W. The t(8;21) fusion protein interferes with AML-1B-dependent transcriptional activation.. Mol Cell Biol, 15(4), 1974-82, 1995 PMCID:230424

Shurtleff, S A, Meyers, S, Hiebert, S W, Raimondi, S C, Head, D R, Willman, C L, Wolman, S, Slovak, M L, Carroll, A J, Behm, F. Heterogeneity in CBF beta/MYH11 fusion messages encoded by the inv(16)(p13q22) and the t(16;16)(p13;q22) in acute myelogenous leukemia.. Blood, 85(12), 3695-703, 1995

Dobrowolski, S F, Stacey, D W, Harter, M L, Stine, J T, Hiebert, S W. An E2F dominant negative mutant blocks E1A induced cell cycle progression.. Oncogene, 9(9), 2605-12, 1994

Roussel, M F, Davis, J N, Cleveland, J L, Ghysdael, J, Hiebert, S W. Dual control of myc expression through a single DNA binding site targeted by ets family proteins and E2F-1.. Oncogene, 9(2), 405-15, 1994

Hiebert, S W. Regions of the retinoblastoma gene product required for its interaction with the E2F transcription factor are necessary for E2 promoter repression and pRb-mediated growth suppression.. Mol Cell Biol, 13(6), 3384-91, 1993 PMCID:359800

Kato, J, Matsushime, H, Hiebert, S W, Ewen, M E, Sherr, C J. Direct binding of cyclin D to the retinoblastoma gene product (pRb) and pRb phosphorylation by the cyclin D-dependent kinase CDK4.. Genes Dev, 7(3), 331-42, 1993

Meyers, S, Downing, J R, Hiebert, S W. Identification of AML-1 and the (8;21) translocation protein (AML-1/ETO) as sequence-specific DNA-binding proteins: the runt homology domain is required for DNA binding and protein-protein interactions.. Mol Cell Biol, 13(10), 6336-45, 1993 PMCID:364692

Roussel MF, Davis JN, Cleveland JL, Hiebert SW. Duel Control of myc Expression Through a Single DNA Binding Site targeted by ets Family Proteins and E2F-1. Oncogene, 9, 405-415, 1993

Hiebert, S W, Chellappan, S P, Horowitz, J M, Nevins, J R. The interaction of RB with E2F coincides with an inhibition of the transcriptional activity of E2F.. Genes Dev, 6(2), 177-85, 1992

Hiebert, S W, Blake, M, Azizkhan, J, Nevins, J R. Role of E2F transcription factor in E1A-mediated trans activation of cellular genes.. J Virol, 65(7), 3547-52, 1991 PMCID:241350

Mudryj, M, Devoto, S H, Hiebert, S W, Hunter, T, Pines, J, Nevins, J R. Cell cycle regulation of the E2F transcription factor involves an interaction with cyclin A.. Cell, 65(7), 1243-53, 1991

Mudryj, M, Hiebert, S W, Nevins, J R. A role for the adenovirus inducible E2F transcription factor in a proliferation dependent signal transduction pathway.. EMBO J, 9(7), 2179-84, 1990 PMCID:551940

Ng, D T, Hiebert, S W, Lamb, R A. Different roles of individual N-linked oligosaccharide chains in folding, assembly, and transport of the simian virus 5 hemagglutinin-neuraminidase.. Mol Cell Biol, 10(5), 1989-2001, 1990 PMCID:360545

Hiebert, S W, Lipp, M, Nevins, J R. E1A-dependent trans-activation of the human MYC promoter is mediated by the E2F factor.. Proc Natl Acad Sci U S A, 86(10), 3594-8, 1989 PMCID:287184

Hiebert, S W, Lamb, R A. Cell surface expression of glycosylated, nonglycosylated, and truncated forms of a cytoplasmic protein pyruvate kinase.. J Cell Biol, 107(3), 865-76, 1988 PMCID:2115283

Hiebert, S W, Richardson, C D, Lamb, R A. Cell surface expression and orientation in membranes of the 44-amino-acid SH protein of simian virus 5.. J Virol, 62(7), 2347-57, 1988 PMCID:253391

Hiebert, S W, Williams, M A, Lamb, R A. Nucleotide sequence of RNA segment 7 of influenza B/Singapore/222/79: maintenance of a second large open reading frame.. Virology, 155(2), 747-51, 1986

Hiebert, S W, Paterson, R G, Lamb, R A. Identification and predicted sequence of a previously unrecognized small hydrophobic protein, SH, of the paramyxovirus simian virus 5.. J Virol, 55(3), 744-51, 1985 PMCID:255058

Hiebert, S W, Paterson, R G, Lamb, R A. Hemagglutinin-neuraminidase protein of the paramyxovirus simian virus 5: nucleotide sequence of the mRNA predicts an N-terminal membrane anchor.. J Virol, 54(1), 1-6, 1985 PMCID:254752

Paterson, R G, Hiebert, S W, Lamb, R A. Expression at the cell surface of biologically active fusion and hemagglutinin/neuraminidase proteins of the paramyxovirus simian virus 5 from cloned cDNA.. Proc Natl Acad Sci U S A, 82(22), 7520-4, 1985 PMCID:390848

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