Burnham Institute for Medical Research - Faculty

MARCIA DAWSON, PH.D.
Professor
Tumor Development

858.646.3100 x3165 (phone)
858.646.3192 (fax)
mdawson@burnham.org

Research Focus

The Dawson laboratory currently has two major research efforts. The first is optimizing the therapeutic index of a new group of compounds that induce cancer cell apoptosis (programmed cell death) and have therapeutic potential in the treatment of leukemia [1�7]. A corollary goal is discerning how these compounds exert their apoptotic effects on cancer cells in collaboration with the molecular biology group of Professor Xiao-kun Zhang at the Institute and the cancer cell biology group of Dr. Joseph A. Fontana at the Wayne State University School of Medicine [8�13]. Thus far, we know that on treatment with these compounds the cancer cells first undergo cell-cycle arrest [14], which is preceded by an increase in the levels of the cyclin kinase inhibitor p21WAF1/CIP1 [15]. Cells then undergo the intrinsic form of apoptosis, which involves the release of cytochrome c and caspase activation. Recently, the Zhang group found that in some cancer cells the expression of the transcription factor TR3 (nur77/NGFI-B) is induced. TR3 then exits the nucleus to interact with mitochondrial membrane-bound Bcl-2 [16]. The interaction between TR3 and Bcl-2 transforms the latter from a cytoprotective protein to one that fosters apoptosis. To facilitate these mechanistic studies we have designed and synthesized the tritiated analog of the parent compound [11], antagonists that prevent apoptosis [17], and other analogs that are only capable of inducing cell-cycle arrest. Recent research with the Fontana group led to identifying the target for these compounds as small heterodimer partner (SHP) [5], a unique orphan nuclear receptor that lacks a DNA-binding domain and modulates the activity of other transcription factors. These compounds are the first ligands identified for this receptor [4]. Apoptosis induced by the interaction of these compounds with SHP requires the activation of the transcription factor NF-kB [7, 18].

Our second area of interest is the design and synthesis of synthetic analogs of retinoic acid that show selectivity for one of the retinoid receptor subtypes [19], of which there are six. Retinoic acid is the carboxylic acid analog of vitamin A and functions as a hormone by regulating such diverse processes as morphogenesis, cell differentiation, and cell proliferation. The retinoid receptors function as dimeric transcription factors that directly interact with responsive elements in gene promoters and in the presence of their retinoid ligands induce gene transcription. They also function indirectly by modulating the activity of other transcription factors. Because of the plethora of these effects, many signaling pathways are impacted. Thus, our objective is the identification of receptor dimer-selective retinoids that target specific signaling pathways. This research is also a collaborative effort with the Zhang group. The Dawson group was the first to report retinoid X receptor-selective agonists [19�22]. We have also identified several RXR antagonists [23] and a new scaffold for RXR agonists [24].

Biography

Marcia I. Dawson earned her Ph.D. from Stanford University in 1968. She received postdoctoral training at California Institute of Technology, Harvard University, and Stanford Research Institute where she was appointed to staff and served in a progressive series of appointments culminating in Director of Drug Discovery, Bio-Organic Chemistry Lab, 1994�1999. She continued as Head of the Medicinal Medical Chemistry Department of the Molecular Medicine Research Institute, 1999�2000. Dr. Dawson was recruited to the Burnham Institute for Medical Research in 2001.

Publications

Y. Zhang, M. I. Dawson, Y. Ning, L. Polin, R. E. Parchment, T. Corbett, A. N. Mohamed, K.-C. Feng, L. Farhana, A. K. Rishi, D. Hogge, M. Leid, V. J. Peterson, X.-K. Zhang, R. Mohammad, J. S. Lu, C. Willman, E. VanBuren, S. Biggar, M. Edelstein, D. Eilender, and J. A. Fontana. Induction of apoptosis in retinoid-refractory acute myelogenous leukemia by a novel AHPN analog. Blood 102, 3743-3752 (2003).
L. Farhana, M. I. Dawson, Y. Huang, Y. Zhang, A. K. Rishi, K. B. Reddy, R. S. Freeman, and J. A. Fontana. Apoptosis signaling by the novel compound 3-Cl-AHPC involves increased EGFR proteolysis and accompanying decreased phosphatidylinositol 3-kinase and AKT kinase activities. Oncogene 23, 1874-1884 (2004).
Y. Zhang, M. I. Dawson, R. Mohammad, A. K. Rishi, L. Farhana, K.-C. Feng, M. Leid, V. Peterson, X.-K. Zhang, M. Edelstein, D. Eilander, S. Biggar, N. Wall, U. Reichert, and J. A. Fontana. Induction of apoptosis of human B-CLL and ALL cells by a novel retinoid and its nonretinoidal analog. Blood 100, 2917-2925 (2002).
M I. Dawson, Z. Xia, G. Liu, J.A. Fontana, L. Farhana, B. Patel, S. Arumugarajah, M. Bhuiyan, X.-K. Zhang, Y.-H. Han, W.B. Stallcup, J. Fukushi, T. Mustelin, L. Tautz, Y. Su, D.L. Harris, N. Waleh, P. D. Hobbs, L. Jong, W. Chao, L. J. Schiff, B.P. Sani. An adamantyl-substituted retinoid-derived molecule that inhibits cancer cell growth and angiogenesis by inducing apoptosis and binds to small heterodimer partner nuclear receptor: Effects of modifying its carboxylate group on apoptosis, proliferation and protein-tyrosine phosphatase activity. J. Med. Chem. 50, 2622-2639 (2007).
L. Farhana, M. I. Dawson, M. Leid, L. Wang, D. D. Moore, G. Liu, Z. Xia, and J. A. Fontana. Adamantyl-substituted retinoid-related molecules bind to short heterodimer partner receptor and modulate the Sin3A repressor. Cancer Res. 67, 318-325 (2007).
M. I. Dawson, Z. Xia, T. Jiang, M. Ye, J. A. Fontana, L. Farhana, B. Patel, L. P. Xue, M. Bhuiyan, R. Pellicciari, A. Macchiarulo, R. Nuti, X.-K. Zhang, Y. H. Han, L. Tautz, P. D. Hobbs, L. Jong, N. Waleh, W. R. Chao, G. S. Feng, Y. Pang, Y. Su. Adamantyl-substituted retinoid-derived molecules that interact with the orphan nuclear receptor small heterodimer partner: effects of replacing the 1-adamantyl or hydroxyl group on inhibition of cancer cell growth, induction of cancer cell apoptosis, and inhibition of SRC homology 2 domain-containing protein tyrosine phosphatase-2 activity. J. Med. Chem. 51, 5650-5652 (2008).
Farhana L, Dawson MI, Xu L, Fontana JA. SHP and Sin3A expression are essential for adamantyl-substituted retinoid-related molecule-mediated nuclear factor-{kappa}B activation, c-Fos/c-Jun expression, and cellular apoptosis. Mol. Cancer Ther. 8, 1625-1635 (2009).
C. K. A. Hsu, A. K. Rishi, X.-S. Li, T. M. Gerald, M. I. Dawson, C. Schiffer, U. Reichert, B. Shroot, G. C. Poirer, and J. A. Fontana. Retinoid induced apoptosis in leukemia cells through a retinoic acid nuclear receptor-independent pathway. Blood 89, 4470-4479 (1997).
Y. Li, B. Lin, A. Agadir, R. Liu, M. I. Dawson, J. C. Reed, J. A. Fontana, F. Bost, P. D. Hobbs, Y. Zheng, G.-Q. Chen, B. Shroot, D. Mercola, and X.-K. Zhang. Molecular determinants of AHPN (CD437)-induced growth arrest and apoptosis in human lung cancer cell lines. Mol. Cell. Biol. 18, 4719-4731 (1998).
Y. Zhang, Y. Huang, A. K. Rishi, M. S. Sheikh, B. Shroot, U. Reichert, M. I. Dawson, G. Poirer, and J. A. Fontana. Activation of the p38 and JNK/SAPK mitogen-activated protein kinase pathways during apoptosis is mediated by a novel retinoid. Exp. Cell Res. 247, 233-240 (1999).
J. A. Fontana, M. I. Dawson, M. Leid, A. K. Rishi, Y. Zhang, C. A. Hsu, J. S. Lu, V. J. Peterson, L. Jong, P. Hobbs, W.-R. Chao, B. Shroot, and U. Reichert. Identification of a unique binding protein specific for a novel retinoid inducing cellular apoptosis. Int. J. Cancer 86, 474-479 (2000).
H. Li, S. K. Kolluri, J. Gu, M. I. Dawson, X. Cao, P. D. Hobbs, B. Lin, G. Chen, J. Lu, F. Lin, Z. Xie, J. A. Fontana, J. C. Reed, and X. Zhang. Cytochrome c release and apoptosis induced by mitochondrial targeting of nuclear orphan receptor TR3. Science 289, 1159-1164 (2000).
M. I. Dawson, P. D. Hobbs, V. J. Peterson, M. Leid, C. W. Lange, K. C. Feng, G. Chen, J. Gu, H. Li, S. K. Kolluri, X. Zhang, Y. Zhang, and J. A. Fontana. Apoptosis induction in cancer cells by a novel analogue of 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid lacking retinoid receptor transcriptional activation activity. Cancer Res. 61, 4723-4730 (2001).
Z.-M. Shao, M. I. Dawson, X.-S. Li, A. K. Rishi, M. S. Sheikh, Q. X. Han, J. V. Ordonez, B. Shroot, and J. A. Fontana. p53 independent G₀/G₁ arrest and apoptosis induced by a novel retinoid in human breast cancer cells. Oncogene 11, 493-504 (1995).
X.-S. Li, A. K. Rishi, Z.-M. Shao, M. I. Dawson, L. Jong, B. Shroot, U. Reichert, J. Ordonez, and J. A. Fontana. Posttranscriptional regulation of p21^WAF1/CIP1 expression in human breast carcinoma cells. Cancer Res. 56, 5055-5062 (1996).
B. Lin, S. K. Kolluri, F. Lin, W. Liu, Y. H. Han, X. Cao, M. I. Dawson, J. C. Reed, and X.-K. Zhang. Conversion of Bcl-2 from protector to killer by interaction with nuclear orphan receptor Nur77/TR3. Cell 116, 527-540 (2004).
M. I. Dawson, D. L. Harris, G. Liu, P. D. Hobbs, C. W. Lange, L. Jong, N. Bruey-Sedano, S. Y. James, X. Zhang, V. J. Peterson, M. Leid, L. Farhana, A. K. Rishi, and J. A. Fontana. Antagonist analogue of 6-[3�-(1-adamantyl)-4�-hydroxyphenyl]-2-naphthalenecarboxylic acid (AHPN) family of apoptosis inducers that effectively blocks AHPN-induced apoptosis but not cell-cycle arrest. J. Med. Chem. 47, 3518-3536 (2004).
L. Farhana, M. I. Dawson, and J. A. Fontana. Apoptosis induction by a novel retinoid-related molecule requires nuclear factor-kappaB activation. Cancer Res. 65, 4909-4917 (2005).
M. I. Dawson. Synthetic retinoids and their nuclear receptors. Curr. Med. Chem. Anti-Cancer Drugs 4, 199-230 (2004).
J. M. Lehmann, L. Jong, A. Fanjul, J. F. Cameron, X. P. Liu, P. Haefner, M. I. Dawson, and M. Pfahl. A novel class of retinoids, selective for retinoid X receptor response pathways. Science 258, 1944-1946 (1992).
M. I. Dawson, P. D. Hobbs, L. Jong, D. Xiao, W.-R. Chao, C. Pan, and X.-K. Zhang. sp2-bridged diaryl retinoids: Effects of bridge-region substitution on retinoid X receptor (RXR) selectivity. Bioorg. Med. Chem. Lett. 10, 1307-1310 (2000).
M. I. Dawson and X.-K. Zhang. Discovery and design of retinoic acid receptor and retinoid X receptor class- and subtype-selective synthetic analogs of all-trans-retinoic acid and 9-cis-retinoic acid. Curr. Med. Chem. 9, 623-637 (2002).
C. N. Cavasotto, G. Liu, S. Y. James, P. D. Hobbs, V. J. Peterson, A. A. Bhattacharya, S. K. Kolluri, R. A. Abagyan, X. Zhang, M. Leid, R. C. Liddington, and M. I. Dawson. Determinants of retinoid X receptor transcriptional antagonism. J. Med. Chem. 47, 4360-4372 (2004).
M. I. Dawson, M. Ye, X. Cao, L. Farhana, Q. Y. Hu, Y. Zhao, L. P. Xu, A. Kiselyuk, R. G. Correa, L. Yang, T. Hou, J. C. Reed, P. Itkin-Ansari, F. Levine, M. F. Sanner, J. A. Fontana, X.-K. Zhang. Derivation of a retinoid X receptor scaffold from peroxisome proliferator-activated receptor γ ligand 1-Di(1H-indol-3-yl)methyl-4-trifluoromethylbenzene. ChemMedChem 4, 116-119 (2009).

List of Publications via PubMed
(NIH National Library of Medicine)

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	Print Version MARCIA DAWSON, PH.D. Professor Tumor Development 858.646.3100 x3165 (phone) 858.646.3192 (fax) mdawson@burnham.org Research Focus The Dawson laboratory currently has two major research efforts. The first is optimizing the therapeutic index of a new group of compounds that induce cancer cell apoptosis (programmed cell death) and have therapeutic potential in the treatment of leukemia [1�7]. A corollary goal is discerning how these compounds exert their apoptotic effects on cancer cells in collaboration with the molecular biology group of Professor Xiao-kun Zhang at the Institute and the cancer cell biology group of Dr. Joseph A. Fontana at the Wayne State University School of Medicine [8�13]. Thus far, we know that on treatment with these compounds the cancer cells first undergo cell-cycle arrest [14], which is preceded by an increase in the levels of the cyclin kinase inhibitor p21WAF1/CIP1 [15]. Cells then undergo the intrinsic form of apoptosis, which involves the release of cytochrome c and caspase activation. Recently, the Zhang group found that in some cancer cells the expression of the transcription factor TR3 (nur77/NGFI-B) is induced. TR3 then exits the nucleus to interact with mitochondrial membrane-bound Bcl-2 [16]. The interaction between TR3 and Bcl-2 transforms the latter from a cytoprotective protein to one that fosters apoptosis. To facilitate these mechanistic studies we have designed and synthesized the tritiated analog of the parent compound [11], antagonists that prevent apoptosis [17], and other analogs that are only capable of inducing cell-cycle arrest. Recent research with the Fontana group led to identifying the target for these compounds as small heterodimer partner (SHP) [5], a unique orphan nuclear receptor that lacks a DNA-binding domain and modulates the activity of other transcription factors. These compounds are the first ligands identified for this receptor [4]. Apoptosis induced by the interaction of these compounds with SHP requires the activation of the transcription factor NF-kB [7, 18]. Our second area of interest is the design and synthesis of synthetic analogs of retinoic acid that show selectivity for one of the retinoid receptor subtypes [19], of which there are six. Retinoic acid is the carboxylic acid analog of vitamin A and functions as a hormone by regulating such diverse processes as morphogenesis, cell differentiation, and cell proliferation. The retinoid receptors function as dimeric transcription factors that directly interact with responsive elements in gene promoters and in the presence of their retinoid ligands induce gene transcription. They also function indirectly by modulating the activity of other transcription factors. Because of the plethora of these effects, many signaling pathways are impacted. Thus, our objective is the identification of receptor dimer-selective retinoids that target specific signaling pathways. This research is also a collaborative effort with the Zhang group. The Dawson group was the first to report retinoid X receptor-selective agonists [19�22]. We have also identified several RXR antagonists [23] and a new scaffold for RXR agonists [24]. Biography Marcia I. Dawson earned her Ph.D. from Stanford University in 1968. She received postdoctoral training at California Institute of Technology, Harvard University, and Stanford Research Institute where she was appointed to staff and served in a progressive series of appointments culminating in Director of Drug Discovery, Bio-Organic Chemistry Lab, 1994�1999. She continued as Head of the Medicinal Medical Chemistry Department of the Molecular Medicine Research Institute, 1999�2000. Dr. Dawson was recruited to the Burnham Institute for Medical Research in 2001. Publications Y. Zhang, M. I. Dawson, Y. Ning, L. Polin, R. E. Parchment, T. Corbett, A. N. Mohamed, K.-C. Feng, L. Farhana, A. K. Rishi, D. Hogge, M. Leid, V. J. Peterson, X.-K. Zhang, R. Mohammad, J. S. Lu, C. Willman, E. VanBuren, S. Biggar, M. Edelstein, D. Eilender, and J. A. Fontana. Induction of apoptosis in retinoid-refractory acute myelogenous leukemia by a novel AHPN analog. Blood 102, 3743-3752 (2003). L. Farhana, M. I. Dawson, Y. Huang, Y. Zhang, A. K. Rishi, K. B. Reddy, R. S. Freeman, and J. A. Fontana. Apoptosis signaling by the novel compound 3-Cl-AHPC involves increased EGFR proteolysis and accompanying decreased phosphatidylinositol 3-kinase and AKT kinase activities. Oncogene 23, 1874-1884 (2004). Y. Zhang, M. I. Dawson, R. Mohammad, A. K. Rishi, L. Farhana, K.-C. Feng, M. Leid, V. Peterson, X.-K. Zhang, M. Edelstein, D. Eilander, S. Biggar, N. Wall, U. Reichert, and J. A. Fontana. Induction of apoptosis of human B-CLL and ALL cells by a novel retinoid and its nonretinoidal analog. Blood 100, 2917-2925 (2002). M I. Dawson, Z. Xia, G. Liu, J.A. Fontana, L. Farhana, B. Patel, S. Arumugarajah, M. Bhuiyan, X.-K. Zhang, Y.-H. Han, W.B. Stallcup, J. Fukushi, T. Mustelin, L. Tautz, Y. Su, D.L. Harris, N. Waleh, P. D. Hobbs, L. Jong, W. Chao, L. J. Schiff, B.P. Sani. An adamantyl-substituted retinoid-derived molecule that inhibits cancer cell growth and angiogenesis by inducing apoptosis and binds to small heterodimer partner nuclear receptor: Effects of modifying its carboxylate group on apoptosis, proliferation and protein-tyrosine phosphatase activity. J. Med. Chem. 50, 2622-2639 (2007). L. Farhana, M. I. Dawson, M. Leid, L. Wang, D. D. Moore, G. Liu, Z. Xia, and J. A. Fontana. Adamantyl-substituted retinoid-related molecules bind to short heterodimer partner receptor and modulate the Sin3A repressor. Cancer Res. 67, 318-325 (2007). M. I. Dawson, Z. Xia, T. Jiang, M. Ye, J. A. Fontana, L. Farhana, B. Patel, L. P. Xue, M. Bhuiyan, R. Pellicciari, A. Macchiarulo, R. Nuti, X.-K. Zhang, Y. H. Han, L. Tautz, P. D. Hobbs, L. Jong, N. Waleh, W. R. Chao, G. S. Feng, Y. Pang, Y. Su. Adamantyl-substituted retinoid-derived molecules that interact with the orphan nuclear receptor small heterodimer partner: effects of replacing the 1-adamantyl or hydroxyl group on inhibition of cancer cell growth, induction of cancer cell apoptosis, and inhibition of SRC homology 2 domain-containing protein tyrosine phosphatase-2 activity. J. Med. Chem. 51, 5650-5652 (2008). Farhana L, Dawson MI, Xu L, Fontana JA. SHP and Sin3A expression are essential for adamantyl-substituted retinoid-related molecule-mediated nuclear factor-{kappa}B activation, c-Fos/c-Jun expression, and cellular apoptosis. Mol. Cancer Ther. 8, 1625-1635 (2009). C. K. A. Hsu, A. K. Rishi, X.-S. Li, T. M. Gerald, M. I. Dawson, C. Schiffer, U. Reichert, B. Shroot, G. C. Poirer, and J. A. Fontana. Retinoid induced apoptosis in leukemia cells through a retinoic acid nuclear receptor-independent pathway. Blood 89, 4470-4479 (1997). Y. Li, B. Lin, A. Agadir, R. Liu, M. I. Dawson, J. C. Reed, J. A. Fontana, F. Bost, P. D. Hobbs, Y. Zheng, G.-Q. Chen, B. Shroot, D. Mercola, and X.-K. Zhang. Molecular determinants of AHPN (CD437)-induced growth arrest and apoptosis in human lung cancer cell lines. Mol. Cell. Biol. 18, 4719-4731 (1998). Y. Zhang, Y. Huang, A. K. Rishi, M. S. Sheikh, B. Shroot, U. Reichert, M. I. Dawson, G. Poirer, and J. A. Fontana. Activation of the p38 and JNK/SAPK mitogen-activated protein kinase pathways during apoptosis is mediated by a novel retinoid. Exp. Cell Res. 247, 233-240 (1999). J. A. Fontana, M. I. Dawson, M. Leid, A. K. Rishi, Y. Zhang, C. A. Hsu, J. S. Lu, V. J. Peterson, L. Jong, P. Hobbs, W.-R. Chao, B. Shroot, and U. Reichert. Identification of a unique binding protein specific for a novel retinoid inducing cellular apoptosis. Int. J. Cancer 86, 474-479 (2000). H. Li, S. K. Kolluri, J. Gu, M. I. Dawson, X. Cao, P. D. Hobbs, B. Lin, G. Chen, J. Lu, F. Lin, Z. Xie, J. A. Fontana, J. C. Reed, and X. Zhang. Cytochrome c release and apoptosis induced by mitochondrial targeting of nuclear orphan receptor TR3. Science 289, 1159-1164 (2000). M. I. Dawson, P. D. Hobbs, V. J. Peterson, M. Leid, C. W. Lange, K. C. Feng, G. Chen, J. Gu, H. Li, S. K. Kolluri, X. Zhang, Y. Zhang, and J. A. Fontana. Apoptosis induction in cancer cells by a novel analogue of 6-[3-(1-adamantyl)-4-hydroxyphenyl]-2-naphthalene carboxylic acid lacking retinoid receptor transcriptional activation activity. Cancer Res. 61, 4723-4730 (2001). Z.-M. Shao, M. I. Dawson, X.-S. Li, A. K. Rishi, M. S. Sheikh, Q. X. Han, J. V. Ordonez, B. Shroot, and J. A. Fontana. p53 independent G₀/G₁ arrest and apoptosis induced by a novel retinoid in human breast cancer cells. Oncogene 11, 493-504 (1995). X.-S. Li, A. K. Rishi, Z.-M. Shao, M. I. Dawson, L. Jong, B. Shroot, U. Reichert, J. Ordonez, and J. A. Fontana. Posttranscriptional regulation of p21^WAF1/CIP1 expression in human breast carcinoma cells. Cancer Res. 56, 5055-5062 (1996). B. Lin, S. K. Kolluri, F. Lin, W. Liu, Y. H. Han, X. Cao, M. I. Dawson, J. C. Reed, and X.-K. Zhang. Conversion of Bcl-2 from protector to killer by interaction with nuclear orphan receptor Nur77/TR3. Cell 116, 527-540 (2004). M. I. Dawson, D. L. Harris, G. Liu, P. D. Hobbs, C. W. Lange, L. Jong, N. Bruey-Sedano, S. Y. James, X. Zhang, V. J. Peterson, M. Leid, L. Farhana, A. K. Rishi, and J. A. Fontana. Antagonist analogue of 6-[3�-(1-adamantyl)-4�-hydroxyphenyl]-2-naphthalenecarboxylic acid (AHPN) family of apoptosis inducers that effectively blocks AHPN-induced apoptosis but not cell-cycle arrest. J. Med. Chem. 47, 3518-3536 (2004). L. Farhana, M. I. Dawson, and J. A. Fontana. Apoptosis induction by a novel retinoid-related molecule requires nuclear factor-kappaB activation. Cancer Res. 65, 4909-4917 (2005). M. I. Dawson. Synthetic retinoids and their nuclear receptors. Curr. Med. Chem. Anti-Cancer Drugs 4, 199-230 (2004). J. M. Lehmann, L. Jong, A. Fanjul, J. F. Cameron, X. P. Liu, P. Haefner, M. I. Dawson, and M. Pfahl. A novel class of retinoids, selective for retinoid X receptor response pathways. Science 258, 1944-1946 (1992). M. I. Dawson, P. D. Hobbs, L. Jong, D. Xiao, W.-R. Chao, C. Pan, and X.-K. Zhang. sp2-bridged diaryl retinoids: Effects of bridge-region substitution on retinoid X receptor (RXR) selectivity. Bioorg. Med. Chem. Lett. 10, 1307-1310 (2000). M. I. Dawson and X.-K. Zhang. Discovery and design of retinoic acid receptor and retinoid X receptor class- and subtype-selective synthetic analogs of all-trans-retinoic acid and 9-cis-retinoic acid. Curr. Med. Chem. 9, 623-637 (2002). C. N. Cavasotto, G. Liu, S. Y. James, P. D. Hobbs, V. J. Peterson, A. A. Bhattacharya, S. K. Kolluri, R. A. Abagyan, X. Zhang, M. Leid, R. C. Liddington, and M. I. Dawson. Determinants of retinoid X receptor transcriptional antagonism. J. Med. Chem. 47, 4360-4372 (2004). M. I. Dawson, M. Ye, X. Cao, L. Farhana, Q. Y. Hu, Y. Zhao, L. P. Xu, A. Kiselyuk, R. G. Correa, L. Yang, T. Hou, J. C. Reed, P. Itkin-Ansari, F. Levine, M. F. Sanner, J. A. Fontana, X.-K. Zhang. Derivation of a retinoid X receptor scaffold from peroxisome proliferator-activated receptor γ ligand 1-Di(1H-indol-3-yl)methyl-4-trifluoromethylbenzene. ChemMedChem 4, 116-119 (2009). List of Publications via PubMed (NIH National Library of Medicine)
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