User:Liebermannda/sandbox

Dan Liebermann is a cancer biologist, currently professor of the Fels Institute for Cancer research and Molecular Biology and Professor of the Department of Biochemistry at the Temple University School of Medicine. Dan Liebermann has made seminal discoveries in the fields of Cancer Biology, Leukemia, Hematopoiesis and Molecular Biology. His laboratory, in collaboration with Dr. Barbara Hoffman (Professor of the Fels and Biochemistry Temple University School of Medicine) has pioneered research in Early Growth Response (EGR)[1], Myeloid Differentiation (MyD) and Growth Arrest and DNA Damage (GADD) primary response genes related to genetic changes associated with normal cell development and oncogenesis. He is considered as one of the discoveres of the Gadd45 family of genes, including Gadd45a,Gadd45b (MyD118) and Gadd45g (CR6)[2][3][4][5][6][7], discoverer of the Toll receptor MyD88 gene[8], and the growth arrest pro-apoptotic gadd34/MyD116 gene[9]. He was also among the first to document the finding that the pro-apoptotic protein BAX is a target of the p53 tumor suppressor[10].

References[edit source | editbeta]

^ Gibbs JD, Liebermann DA, Hoffman B. (2008). "Leukemia suppressor function of Egr-1 is dependent on transforming oncogene.Leukemia 22(10):1909-16. ^ Fornace, A.J.; Jackman, J.; Hollander, M.C.; Hoffman-Liebermann, B.; & Liebermann, D.A. (1992). "Genotoxic-stress-response genes and growth-arrest genes: gadd, MyD, and other genes induced by treatments eliciting growth arrest". Annals of the New York Academy of Sciences 663: 139–53. ^ Liebermann, D.A.; Hoffman, B. (2002). "Myeloid differentiation (MyD)/growth arrest DNA damage (GADD) genes in tumor suppression, immunity and inflammation". Leukemia 16 (4): 527–41. ^ Fornace, A.J.; Alamo, I.; and Hollander, M.C. (1988). "DNA damage-inducible transcripts in mammalian cells". Proceedings of the National Academy of Sciences 85 (23): 8800–4. ^ Abdollahi, A.; Lord, K.A.; Hoffman-Liebermann, B.; and Liebermann, D.A. (1991). "Sequence and expression of a cDNA encoding MyD118: a novel myeloid differentiation primary response gene induced by multiple cytokines". Oncogene 6 (1): 165–7. ^ Zhang, W.; Bae, I.; Krishnaraju, K.; Azam, Naiyer et al. (1999). "CR6: A third member in the MyD118 and Gadd45 gene family which functions in negative growth control". Oncogene 18 (35): 4899–907 ^ Beadling, C.; Johnson, K.W.; and Smith, K.A. (1993). "Isolation of interleukin 2-induced immediate-early genes". Proceedings of the National Academy of Sciences 90 (7): 2719–23. ^ Lord KA, Hoffman-Liebermann B, Liebermann DA (1990). "Nucleotide sequence and expression of a cDNA encoding MyD88, a novel myeloid differentiation primary response gene induced by IL6". Oncogene 5 (7): 1095–7 ^ Zhan Q, Lord KA, Alamo I Jr, Hollander MC, Carrier F, Ron D, Kohn KW, Hoffman B, Liebermann DA, Fornace AJ Jr. (1994) "The gadd and MyD genes define a novel set of mammalian genes encoding acidic proteins that synergistically suppress cell growth". Mol Cell Biol.14(4):2361-71 ^ Miyashita T, Krajewski S, Krajewska M, Wang HG, Lin HK, Liebermann DA, Hoffman B, Reed JC. (1994). "Tumor suppressor p53 is a regulator of bcl-2 and bax gene expression in vitro and in vivo".Oncogene. 9(6):1799-1805. Selvakumaran M, Lin HK, Miyashita T, Wang HG, Krajewski S, Reed JC, Hoffman B, Liebermann D. (1994). "Immediate early up-regulation of bax expression by p53 but not TGF beta 1: a paradigm for distinct apoptotic pathways".Oncogene.9(6):1791-1798. Miyashita, Toshiyuki; Reed, John C. (1995). "Tumor Suppressor p53 Is a Direct Transcriptional Activator of the Human bax Gene". Cell 80 (2): 293–299.