Moshe Oren

Summary

Affiliation: Weizmann Institute of Science
Country: Israel

Publications

  1. pmc The p53-inducible TSAP6 gene product regulates apoptosis and the cell cycle and interacts with Nix and the Myt1 kinase
    Brent J Passer
    Molecular Engines Laboratories, 20 Rue Bouvier, 75011 Paris, France
    Proc Natl Acad Sci U S A 100:2284-9. 2003
  2. ncbi request reprint NFκB and p53: A life and death affair
    Moshe Oren
    Weizmann Institute of Science, Rehovot, Israel
    Cell Cycle 9:1027. 2010
  3. ncbi request reprint Regulation of p53: intricate loops and delicate balances
    Moshe Oren
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Ann N Y Acad Sci 973:374-83. 2002
  4. pmc Mutant p53 gain-of-function in cancer
    Moshe Oren
    Department of Molecular Cell Biology, The Weizmann Institute, Rehovot 76100, Israel
    Cold Spring Harb Perspect Biol 2:a001107. 2010
  5. ncbi request reprint Regulation of p53: intricate loops and delicate balances
    Moshe Oren
    Department of Molecular Cell Biology, The Weizmann Institute of Science, P O Box 26, Rehovot, Israel
    Biochem Pharmacol 64:865-71. 2002
  6. pmc The Lats2 tumor suppressor augments p53-mediated apoptosis by promoting the nuclear proapoptotic function of ASPP1
    Yael Aylon
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Genes Dev 24:2420-9. 2010
  7. pmc The histone H2B-specific ubiquitin ligase RNF20/hBRE1 acts as a putative tumor suppressor through selective regulation of gene expression
    Efrat Shema
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Genes Dev 22:2664-76. 2008
  8. ncbi request reprint Downregulation of beta-catenin by p53 involves changes in the rate of beta-catenin phosphorylation and Axin dynamics
    Elina Levina
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Oncogene 23:4444-53. 2004
  9. ncbi request reprint Inhibition of p53 degradation by Mdm2 acetylation
    Xinjiang Wang
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    FEBS Lett 561:195-201. 2004
  10. pmc A positive feedback loop between the p53 and Lats2 tumor suppressors prevents tetraploidization
    Yael Aylon
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Genes Dev 20:2687-700. 2006

Research Grants

Detail Information

Publications82

  1. pmc The p53-inducible TSAP6 gene product regulates apoptosis and the cell cycle and interacts with Nix and the Myt1 kinase
    Brent J Passer
    Molecular Engines Laboratories, 20 Rue Bouvier, 75011 Paris, France
    Proc Natl Acad Sci U S A 100:2284-9. 2003
    ..Cell-cycle studies indicated that TSAP6 could augment Myt1 activity. Overall, these data suggest that TSAP6 may act downstream to p53 to interface apoptosis and cell-cycle progression...
  2. ncbi request reprint NFκB and p53: A life and death affair
    Moshe Oren
    Weizmann Institute of Science, Rehovot, Israel
    Cell Cycle 9:1027. 2010
  3. ncbi request reprint Regulation of p53: intricate loops and delicate balances
    Moshe Oren
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Ann N Y Acad Sci 973:374-83. 2002
    ..Genetic alterations characteristic of cancer are capable of severely distorting this balance, thereby overriding the tumor suppressor effects of p53 in a manner that facilitates neoplastic conversion...
  4. pmc Mutant p53 gain-of-function in cancer
    Moshe Oren
    Department of Molecular Cell Biology, The Weizmann Institute, Rehovot 76100, Israel
    Cold Spring Harb Perspect Biol 2:a001107. 2010
    ..This article addresses the biological manifestations of mutant p53 gain-of-function, the underlying molecular mechanisms, and their possible clinical implications...
  5. ncbi request reprint Regulation of p53: intricate loops and delicate balances
    Moshe Oren
    Department of Molecular Cell Biology, The Weizmann Institute of Science, P O Box 26, Rehovot, Israel
    Biochem Pharmacol 64:865-71. 2002
    ..Genetic alterations characteristic of cancer are capable of severely distorting this balance, thereby overriding the tumor suppressor effects of p53 in a manner that facilitates neoplastic conversion...
  6. pmc The Lats2 tumor suppressor augments p53-mediated apoptosis by promoting the nuclear proapoptotic function of ASPP1
    Yael Aylon
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Genes Dev 24:2420-9. 2010
    ..These effects are overridden by the Yap1 (Yes-associated protein 1) oncoprotein, which disrupts Lats2-ASPP1 binding and antagonizes the tumor-suppressing function of the Lats2/ASPP1/p53 axis...
  7. pmc The histone H2B-specific ubiquitin ligase RNF20/hBRE1 acts as a putative tumor suppressor through selective regulation of gene expression
    Efrat Shema
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Genes Dev 22:2664-76. 2008
    ..Furthermore, frequent RNF20 promoter hypermethylation was observed in tumors. RNF20 may thus be a putative tumor suppressor, acting through selective regulation of a distinct subset of genes...
  8. ncbi request reprint Downregulation of beta-catenin by p53 involves changes in the rate of beta-catenin phosphorylation and Axin dynamics
    Elina Levina
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Oncogene 23:4444-53. 2004
    ..These results suggest that p53 induces a faster mobilization of Axin into the degradation complex thereby enhancing beta-catenin turnover as part of a protective mechanism against the development of cancer...
  9. ncbi request reprint Inhibition of p53 degradation by Mdm2 acetylation
    Xinjiang Wang
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    FEBS Lett 561:195-201. 2004
    ..Moreover, K466/467Q is defective in promoting p53 degradation in living cells. We thus suggest that acetyltransferases may modulate cellular p53 activity not only by modifying p53, but also by inactivating Mdm2...
  10. pmc A positive feedback loop between the p53 and Lats2 tumor suppressors prevents tetraploidization
    Yael Aylon
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Genes Dev 20:2687-700. 2006
    ..The Lats2-Mdm2-p53 axis thus constitutes a novel checkpoint pathway critical for the maintenance of proper chromosome number...
  11. pmc Modulation of the vitamin D3 response by cancer-associated mutant p53
    Perry Stambolsky
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Cancer Cell 17:273-85. 2010
    ..Furthermore, mutp53 increases the nuclear accumulation of VDR. Importantly, mutp53 converts vitamin D into an antiapoptotic agent. Thus, p53 status can determine the biological impact of vitamin D on tumor cells...
  12. pmc Coupling transcriptional and post-transcriptional miRNA regulation in the control of cell fate
    Reut Shalgi
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Aging (Albany NY) 1:762-70. 2009
    ..We propose that examining miRNAs in the context of the regulatory transcriptional and post-transcriptional networks they are embedded in may provide a broader view of their role in controlling cell fate...
  13. ncbi request reprint Transactivation of the EGR1 gene contributes to mutant p53 gain of function
    Lilach Weisz
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel
    Cancer Res 64:8318-27. 2004
    ..Functional assays indicate that induction of EGR1 by mutant p53 contributes to enhanced transformed properties and resistance to apoptosis. We propose that EGR1 is a significant contributor to mutant p53 gain of function...
  14. pmc Discovery of novel proteasome inhibitors using a high-content cell-based screening system
    Irena Lavelin
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    PLoS ONE 4:e8503. 2009
    ..The special features of the current screen, compared to those of other approaches are discussed...
  15. pmc p53-dependent regulation of autophagy protein LC3 supports cancer cell survival under prolonged starvation
    Ruth Scherz-Shouval
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Proc Natl Acad Sci U S A 107:18511-6. 2010
    ..We propose that some cancer cells retain wt p53 to benefit from the resultant increased fitness under limited nutrient supply...
  16. ncbi request reprint Regulation of p53 by Mdm2: fate is in the numbers
    Ayelet Shmueli
    Department of Molecular Cell Biology, The Weizmann Institute of Science, POB 26, 76100 Rehovot, Israel
    Mol Cell 13:4-5. 2004
    ....
  17. pmc Mutant p53 prolongs NF-κB activation and promotes chronic inflammation and inflammation-associated colorectal cancer
    Tomer Cooks
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Cancer Cell 23:634-46. 2013
    ..These findings might explain the early appearance of p53 mutations in human CAC...
  18. pmc Detection and characterization of ubiquitylated H2B in mammalian cells
    Efrat Shema
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Methods 54:326-30. 2011
    ..Here we describe several techniques to detect ubiquitylated H2B in mammalian cells and to dissect its genomic localization...
  19. doi request reprint Repression of transposable-elements - a microRNA anti-cancer defense mechanism?
    Reut Shalgi
    Molecular Genetics Department, Weizmann Institute of Science, Rehovot, Israel
    Trends Genet 26:253-9. 2010
    ..This hypothesis calls into consideration the need to study the role of miRNAs and the RNAi machinery in the nucleus, and specifically their impact on the maintenance of genomic integrity in the context of cancer...
  20. ncbi request reprint Cross-talk between Akt, p53 and Mdm2: possible implications for the regulation of apoptosis
    Tanya M Gottlieb
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Oncogene 21:1299-303. 2002
    ....
  21. ncbi request reprint Living with p53, dying of p53
    Yael Aylon
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Cell 130:597-600. 2007
    ..In this issue of Cell, Das et al. (2007) and Tanaka et al. (2007) provide new insights into the mechanisms that dictate the life and death decisions of p53...
  22. pmc RNF20 inhibits TFIIS-facilitated transcriptional elongation to suppress pro-oncogenic gene expression
    Efrat Shema
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Mol Cell 42:477-88. 2011
    ..Our findings provide a molecular mechanism for selective gene repression by RNF20 and position TFIIS as a key target of RNF20's tumor suppressor activity...
  23. ncbi request reprint CD74 induces TAp63 expression leading to B-cell survival
    Frida Lantner
    Departments of Immunology, Weizmann Institute of Science, Rehovot, Israel
    Blood 110:4303-11. 2007
    ..Thus, the CD74/NF-kappaB/TAp63 axis defines a novel antiapoptotic pathway in mature B cells, resulting in the shaping of both the B-cell repertoire and the immune response...
  24. doi request reprint Systematic identification of proteins binding to chromatin-embedded ubiquitylated H2B reveals recruitment of SWI/SNF to regulate transcription
    Efrat Shema-Yaacoby
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Cell Rep 4:601-8. 2013
    ..Our findings substantially expand the known H2Bub1 interactome and provide insights into the functions of this PTM in mammalian gene regulation...
  25. pmc Mdm2 regulates p53 mRNA translation through inhibitory interactions with ribosomal protein L26
    Yaara Ofir-Rosenfeld
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Mol Cell 32:180-9. 2008
    ..The Mdm2-L26 interaction thus represents an additional important component of the autoregulatory feedback loop that dictates cellular p53 levels and activity...
  26. ncbi request reprint p53 and p21 regulate error-prone DNA repair to yield a lower mutation load
    Sharon Avkin
    Department of Biological Chemistry, Weizmann Institute of Science, Rehovot 76100, Israel
    Mol Cell 22:407-13. 2006
    ..Loss of this regulation by inactivation of p53 or p21 causes an out of control lesion-bypass activity, which increases the mutational load and might therefore play a role in pathogenic processes caused by genetic instability...
  27. pmc p53 binds preferentially to genomic regions with high DNA-encoded nucleosome occupancy
    Efrat Lidor Nili
    Department of Molecular Cell Biology, The Weizmann Institute, Rehovot 76100, Israel
    Genome Res 20:1361-8. 2010
    ....
  28. pmc p53 status in stromal fibroblasts modulates tumor growth in an SDF1-dependent manner
    Yoseph Addadi
    Department of Biological Regulation, The Weizmann Institute, Rehovot, Israel
    Cancer Res 70:9650-8. 2010
    ..Moreover, expression of mutant p53 by tumor stroma fibroblasts might exert a gain of function effect, further accelerating tumor development...
  29. ncbi request reprint The RING domain of Mdm2 mediates histone ubiquitylation and transcriptional repression
    Neri Minsky
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Mol Cell 16:631-9. 2004
    ..Histone ubiquitylation may thus constitute a novel mechanism of transcriptional repression by Mdm2, possibly underlying some of its oncogenic activities...
  30. ncbi request reprint The p53-Mdm2 module and the ubiquitin system
    Dan Michael
    Department of Molecular Cell Biology, Weizmann Institute of Science, PO Box 26, Rehovot 76100, Israel
    Semin Cancer Biol 13:49-58. 2003
    ..p53 may be targeted by other E3 ligases besides Mdm2, as well as by non-proteasomal mechanisms. Despite extensive information about p53 degradation, many important aspects remain unresolved...
  31. doi request reprint Monoubiquitinated H2B is associated with the transcribed region of highly expressed genes in human cells
    Neri Minsky
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Nat Cell Biol 10:483-8. 2008
    ....
  32. pmc Two phases of mitogenic signaling unveil roles for p53 and EGR1 in elimination of inconsistent growth signals
    Yaara Zwang
    Department of Biological Regulation, The Weizmann Institute of Science, Rehovot 76100, Israel
    Mol Cell 42:524-35. 2011
    ..Together, our findings uncover two gating mechanisms, which ensure that cells ignore fortuitous growth factors and undergo proliferation only in response to consistent mitogenic signals...
  33. ncbi request reprint p53 Activation by nitric oxide involves down-regulation of Mdm2
    Xinjiang Wang
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    J Biol Chem 277:15697-702. 2002
    ..The drop in endogenous Mdm2 levels following NO treatment is accompanied by a corresponding reduction in the rate of p53 ubiquitination. Thus, the down-regulation of Mdm2 by NO is likely to contribute to the activation of p53...
  34. ncbi request reprint Mutant p53 enhances nuclear factor kappaB activation by tumor necrosis factor alpha in cancer cells
    Lilach Weisz
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Cancer Res 67:2396-401. 2007
    ..Together, these findings suggest that p53 mutations may promote cancer progression by augmenting NFkappaB activation in the context of chronic inflammation...
  35. doi request reprint The majority of endogenous microRNA targets within Alu elements avoid the microRNA machinery
    Yonit Hoffman
    Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel
    Bioinformatics 29:894-902. 2013
    ..Here, we examine the functionality of miRNA targets within Alu elements in 3'UTRs in the human genome...
  36. pmc Noise-mean relationship in mutated promoters
    Gil Hornung
    Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel
    Genome Res 22:2409-17. 2012
    ..Our results suggest that burst size is a promoter-specific property that is relatively robust to sequence mutations but is strongly dependent on the interaction between the TATA box and promoter nucleosomes...
  37. ncbi request reprint A short mitochondrial form of p19ARF induces autophagy and caspase-independent cell death
    Sharon Reef
    Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel
    Mol Cell 22:463-75. 2006
    ..smARF induces massive autophagy and caspase-independent cell death that can be partially rescued by knocking down ATG5 or Beclin-1, suggesting a different prodeath function for this short isoform...
  38. pmc Consistency test of the cell cycle: roles for p53 and EGR1
    Yaara Zwang
    Department of Biological Regulation, Weizmann Institute of Science, Rehovot, Israel
    Cancer Res 72:1051-4. 2012
    ..We propose that this "consistency test" prevents repeated division cycles of normal cells but might become defective in most cancer cells...
  39. ncbi request reprint Tiny actors, great roles: microRNAs in p53's service
    Nina Raver-Shapira
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel
    Cell Cycle 6:2656-61. 2007
    ..This review will discuss the recent studies and their implications...
  40. ncbi request reprint p53 Attenuates cancer cell migration and invasion through repression of SDF-1/CXCL12 expression in stromal fibroblasts
    Neta Moskovits
    Departments of Molecular Cell Biology and Immunology, The Weizmann Institute of Science, Rehovot, Israel and Department of Oncology, Sheba Medical Center, Tel Hashomer, Israel
    Cancer Res 66:10671-6. 2006
    ....
  41. pmc Global and local architecture of the mammalian microRNA-transcription factor regulatory network
    Reut Shalgi
    Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel
    PLoS Comput Biol 3:e131. 2007
    ..Together these findings provide new insights on the architecture of the combined transcriptional-post transcriptional regulatory network...
  42. ncbi request reprint Transcriptional activation of miR-34a contributes to p53-mediated apoptosis
    Nina Raver-Shapira
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Mol Cell 26:731-43. 2007
    ..Perturbation of miR-34a expression, as occurs in some human cancers, may thus contribute to tumorigenesis by attenuating p53-dependent apoptosis...
  43. ncbi request reprint The p53 and Mdm2 families in cancer
    Dan Michael
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Curr Opin Genet Dev 12:53-9. 2002
    ..Work over the past year has provided better understanding of the p53-Mdm2 module that lies in the heart of this regulatory network, and of the intricate interplay between the various members of the network...
  44. ncbi request reprint Mdm2: p53's lifesaver?
    Ayelet Shmueli
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Mol Cell 25:794-6. 2007
    ..In a recent issue of Molecular Cell, Taira et al. (2007) and Rinaldo et al. (2007) provide insight into the involvement of the DYRK2 kinase and a surprising role of MDM2 in regulation of DNA damage-induced apoptosis via p53 phosphorylation...
  45. ncbi request reprint PML is a target gene of beta-catenin and plakoglobin, and coactivates beta-catenin-mediated transcription
    Michael Shtutman
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Cancer Res 62:5947-54. 2002
    ....
  46. ncbi request reprint Life, death, and ubiquitin: taming the mule
    Ayelet Shmueli
    Department of Molecular Cell Biology, The Weizmann Institute, Rehovot, Israel
    Cell 121:963-5. 2005
    ..A key player in this process is the E3 ubiquitin ligase. In this issue of Cell, and describe a new E3 ligase, ARF-BP1/Mule, which targets two very different substrates, p53 and Mcl-1, with completely different cellular outcomes...
  47. ncbi request reprint hTERT-immortalized prostate epithelial and stromal-derived cells: an authentic in vitro model for differentiation and carcinogenesis
    Ira Kogan
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Cancer Res 66:3531-40. 2006
    ....
  48. pmc RNF20 and USP44 regulate stem cell differentiation by modulating H2B monoubiquitylation
    Gilad Fuchs
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Mol Cell 46:662-73. 2012
    ..Our findings suggest that optimal ESC differentiation requires dynamic changes in H2B ubiquitylation patterns, which must occur in a timely and well-coordinated manner...
  49. pmc Nucleosome organization affects the sensitivity of gene expression to promoter mutations
    Gil Hornung
    Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel
    Mol Cell 46:362-8. 2012
    ..Our study suggests an important role for chromatin structure in the evolution of gene expression...
  50. pmc p53-Repressed miRNAs are involved with E2F in a feed-forward loop promoting proliferation
    Ran Brosh
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Mol Syst Biol 4:229. 2008
    ..Taken together, these findings position miRNAs as novel key players in the mammalian cellular proliferation network...
  51. pmc Regulatory module involving FGF13, miR-504, and p53 regulates ribosomal biogenesis and supports cancer cell survival
    Debora R Bublik
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Proc Natl Acad Sci U S A . 2016
    ..Thus, FGF13 may serve as an enabler, allowing cancer cells to evade proteostasis stress triggered by oncogene activation...
  52. pmc RNF20 Links Histone H2B Ubiquitylation with Inflammation and Inflammation-Associated Cancer
    Ohad Tarcic
    Department of Molecular Cell Biology, The Weizmann Institute, Rehovot 7610001, Israel
    Cell Rep 14:1462-76. 2016
    ....
  53. pmc 3'UTR Shortening Potentiates MicroRNA-Based Repression of Pro-differentiation Genes in Proliferating Human Cells
    Yonit Hoffman
    Department of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel
    PLoS Genet 12:e1005879. 2016
    ..Thus 3'UTR shortening appears not only to enable escape from inhibition of growth promoting genes but also to potentiate repression of anti-proliferative genes. ..
  54. doi request reprint p53 and ribosome biogenesis stress: the essentials
    Lior Golomb
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    FEBS Lett 588:2571-9. 2014
    ..In this review we discuss when, how and why p53 is activated upon ribosomal biogenesis stress, and how perturbation of this critical regulatory interplay may impact human disease. ..
  55. ncbi request reprint DNA damage-induced translocation of the Werner helicase is regulated by acetylation
    Gil Blander
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    J Biol Chem 277:50934-40. 2002
    ....
  56. pmc p53: guardian of ploidy
    Yael Aylon
    Department of Molecular Cell Biology, The Weizmann Institute of Science, PO Box 26, Rechovot 76100, Israel
    Mol Oncol 5:315-23. 2011
    ..Not surprisingly, these proteins are frequently inactivated or downregulated in tumors, synergizing with p53 inactivation to establish an atmosphere of "tolerance" for a non-diploid state...
  57. ncbi request reprint Attenuation of the p53 response to DNA damage by high cell density
    Jair Bar
    Department of Molecular Cell Biology, Weizmann Institute of Science, POB26, Rehovot 76100, Israel
    Oncogene 23:2128-37. 2004
    ..The impact of cell density on p53 activation may have important bearings on the involvement of p53 in tumor suppression and the cellular response to anticancer therapy...
  58. ncbi request reprint The sunny side of p53
    Moshe Oren
    Department of Molecular Cell Biology, Weizmann Institute, Rehovot, Israel
    Cell 128:826-8. 2007
    ..A report by Cui et al. (2007) in this issue of Cell explains how the tumor suppressor p53 protects the skin by stimulating the suntan response...
  59. pmc Cancer therapeutic approach based on conformational stabilization of mutant p53 protein by small peptides
    Perry Tal
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot, Israel
    Oncotarget 7:11817-37. 2016
    ..Importantly, lead peptides elicited dramatic regression of aggressive tumors in mouse xenograft models. Such peptides might serve as novel agents for human cancer therapy. ..
  60. pmc TM7SF3, a novel p53-regulated homeostatic factor, attenuates cellular stress and the subsequent induction of the unfolded protein response
    Roi Isaac
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Cell Death Differ . 2016
    ..Cell Death and Differentiation advance online publication, 14 October 2016; doi:10.1038/cdd.2016.108...
  61. pmc Down-regulation of LATS kinases alters p53 to promote cell migration
    Noa Furth
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Genes Dev 29:2325-30. 2015
    ..Notably, LATS1 and LATS2 are frequently down-regulated in breast cancer; we propose that such down-regulation might benefit cancer by converting p53 from a tumor suppressor into a tumor facilitator. ..
  62. pmc The LATS2 tumor suppressor inhibits SREBP and suppresses hepatic cholesterol accumulation
    Yael Aylon
    Department of Molecular Cell Biology, The Weizmann Institute of Science, Rehovot 76100, Israel
    Genes Dev 30:786-97. 2016
    ..Together, these findings further highlight the tight links between tumor suppressors and metabolic homeostasis...
  63. doi request reprint Simultaneous measurement of genome-wide transcription elongation speeds and rates of RNA polymerase II transition into active elongation with 4sUDRB-seq
    Gilad Fuchs
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Nat Protoc 10:605-18. 2015
    ..The experimental protocol requires basic molecular biology skills, whereas data analysis requires knowledge in bioinformatics, particularly MATLAB and the Linux environment. ..
  64. pmc Cotranscriptional histone H2B monoubiquitylation is tightly coupled with RNA polymerase II elongation rate
    Gilad Fuchs
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Genome Res 24:1572-83. 2014
    ..Overall, our data shed light on the organization of H2Bub1 within transcribed genes and single out H2Bub1 as a reliable marker for ongoing transcription elongation...
  65. pmc microRNAs and Alu elements in the p53-Mdm2-Mdm4 regulatory network
    Yonit Hoffman
    Department of Molecular Genetics, Weizmann Institute of Science, Rehovot 76100, Israel Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    J Mol Cell Biol 6:192-7. 2014
    ..We review the possible influence of Alu sequences on miRNA functionality in general and specifically within the p53 network. ..
  66. pmc Importin 7 and exportin 1 link c-Myc and p53 to regulation of ribosomal biogenesis
    Lior Golomb
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel
    Mol Cell 45:222-32. 2012
    ..Perturbation of this balance may play a significant role in promoting cancer...
  67. pmc Mutations in the p53 Tumor Suppressor Gene: Important Milestones at the Various Steps of Tumorigenesis
    Noa Rivlin
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, Israel
    Genes Cancer 2:466-74. 2011
    ..Here, the authors review the different studies on the involvement of p53 inactivation at various stages of tumorigenesis and highlight the specific contribution of p53 mutations at each phase of cancer progression...
  68. ncbi request reprint Overexpression of mouse Mdm2 induces developmental phenotypes in Drosophila
    Adriana Folberg-Blum
    Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot, 76100, Israel
    Oncogene 21:2413-7. 2002
    ..These transgenic flies may provide a unique experimental model for exploring the molecular interactions of Mdm2 in a developmental context...
  69. ncbi request reprint Mutant p53 gain of function: repression of CD95(Fas/APO-1) gene expression by tumor-associated p53 mutants
    Amir Zalcenstein
    Department of Molecular Cell Biology, Weizmann Institute of Science, PO Box 26, Rehovot, 76100, Israel
    Oncogene 22:5667-76. 2003
    ..Hence, the CD95 promoter is likely to be a direct target for downregulation by mutant p53. This activity of mutant p53 may contribute to its gain of function effects in oncogenesis...
  70. pmc New plays in the p53 theater
    Yael Aylon
    Department of Molecular Cell Biology, The Weizmann Institute of Science, PO Box 26, Rechovot 76100, Israel
    Curr Opin Genet Dev 21:86-92. 2011
    ..These include genes encoding for proteins that impinge on a broad spectrum of cellular functions, from cell metabolism to stem cell renewal. The p53 story is still far from being fully told...
  71. pmc Tyrosine phosphorylation of Mdm2 by c-Abl: implications for p53 regulation
    Zehavit Goldberg
    Lautenberg Center for General and Tumor Immunology, The Hebrew University Hadassah Medical School, Jerusalem 91120, Israel
    EMBO J 21:3715-27. 2002
    ..Our results suggest that phosphorylation of Mdm2 by c-Abl impairs the inhibition of p53 by Mdm2, hence defining a novel mechanism by which c-Abl activates p53...
  72. ncbi request reprint DeltaN-p53, a natural isoform of p53 lacking the first transactivation domain, counteracts growth suppression by wild-type p53
    Stéphanie Courtois
    Group of Molecular Carcinogenesis, International Agency for Research on Cancer, 150 cours Albert Thomas, 69372 Lyon Cedex 08, France
    Oncogene 21:6722-8. 2002
    ..These results suggest that DeltaN-p53 may play a role as a transient, negative regulator of p53 during cell cycle progression...
  73. pmc TAp63alpha induces apoptosis by activating signaling via death receptors and mitochondria
    Olav Gressner
    Department of Internal Medicine IV, Hepatology and Gastroenterology, University Hospital, Heidelberg, Germany
    EMBO J 24:2458-71. 2005
    ..Thus, beyond its importance in development and differentiation, we describe an important role for TAp63alpha in the induction of apoptosis and chemosensitivity...
  74. ncbi request reprint Regulation of the p73 protein stability and degradation
    Andrew Oberst
    IDI IRCCS Biochemistry Lab, c o Department of Experimental Medicine, University of Rome Tor Vergata, Rome 00133, Italy
    Biochem Biophys Res Commun 331:707-12. 2005
    ....
  75. ncbi request reprint Critical role of p63 in the development of a normal esophageal and tracheobronchial epithelium
    Yaron Daniely
    Cell Biology Section, Division of Intramural Research, National Institute of Environmental Health Sciences, Triangle Park, NC 27709, USA
    Am J Physiol Cell Physiol 287:C171-81. 2004
    ....
  76. pmc Siah-1b is a direct transcriptional target of p53: identification of the functional p53 responsive element in the siah-1b promoter
    Giusy Fiucci
    Molecular Engines Laboratories, 20 Rue Bouvier, 75011 Paris, France
    Proc Natl Acad Sci U S A 101:3510-5. 2004
    ..Thus, the siah-1b gene is a direct transcriptional target of p53...
  77. ncbi request reprint Cell cycle regulation and p53 activation by protein phosphatase 2C alpha
    Paula Ofek
    Department of Cell Research and Immunology, Tel Aviv University, Israel
    J Biol Chem 278:14299-305. 2003
    ..The role of PP2C alpha in p53 activation is discussed...
  78. ncbi request reprint Conditional RNA interference in vivo to study mutant p53 oncogenic gain of function on tumor malignancy
    Gianluca Bossi
    Department of Experimental Oncology, Regina Elena Cancer Institute, Rome, Italy
    Cell Cycle 7:1870-9. 2008
    ..Results are confirmatory that depletion of mutant p53 protein impacts on tumor malignancy and validated the inducible lentiviral-based system as an efficient tool to study the gain of function activity of human tumor derived p53 mutants...
  79. pmc The Nedd4-binding partner 1 (N4BP1) protein is an inhibitor of the E3 ligase Itch
    Andrew Oberst
    Biochemistry Laboratory, Istituto Dermopatico dell Immacolata Istituto di Ricovero e Cura a Carattere Scientifico, University of Rome Tor Vergata, 00133 Rome, Italy
    Proc Natl Acad Sci U S A 104:11280-5. 2007
    ....
  80. ncbi request reprint Physical interaction with human tumor-derived p53 mutants inhibits p63 activities
    Sabrina Strano
    Molecular Oncogenesis Laboratory, Regina Elena Cancer Institute, Rome 00158, Italy
    J Biol Chem 277:18817-26. 2002
    ..Thus, inactivation of p53 family members may contribute to the biological properties of specific p53 mutants in promoting tumorigenesis and in conferring selective survival advantage to cancer cells...
  81. ncbi request reprint The Wip1 Phosphatase acts as a gatekeeper in the p53-Mdm2 autoregulatory loop
    Xiongbin Lu
    Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, USA
    Cancer Cell 12:342-54. 2007
    ..Thus, Wip1 acts as a gatekeeper in the Mdm2-p53 regulatory loop by stabilizing Mdm2 and promoting Mdm2-mediated proteolysis of p53...
  82. ncbi request reprint BCL6 is regulated by p53 through a response element frequently disrupted in B-cell non-Hodgkin lymphoma
    Ofer Margalit
    Pediatric Hematology Oncology, Safra Children s Hospital, Chaim Sheba Medical Center, Tel Hashomer 52621, Israel
    Blood 107:1599-607. 2006
    ..The increase in BCL6 mRNA levels was attenuated by the p53 inhibitor PFT-alpha. Thus, we define the BCL6 gene as a new p53 target, regulated through a RE frequently disrupted in BNHL...

Research Grants1

  1. FUNCTIOINAL ANALYSIS OF THE P53 TUMOR SUPPRESSOR
    Moshe Oren; Fiscal Year: 2002
    ..Finally, p53 activity will be monitored in vivo in transgenic reporter mice subjected to ischemia. P53 may play a role as a mediator of tissue damage in this clinically important condition. ..