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MOLECULAR ONCOLOGY [10.1002/1878-0261.13056].";s:4:"data";s:4:"2021";s:2:"id";s:20:"PUBBLICAZIONE_425865";s:6:"handle";s:11:"2108/279782";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore BIO/10";s:9:"metadata4";N;s:9:"metadata5";s:61:"Global mapping of cancers: The Cancer Genome Atlas and beyond";s:9:"metadata6";s:327:"Ganini, C; Amelio, I; Bertolo, R; Bove, P; Buonomo, OC; Candi, E; Cipriani, C; Di Daniele, N; Juhl, H; Mauriello, A; Marani, C; Marshall, J; Melino, S; Marchetti, P; Montanaro, M; Natale, ME; Novelli, F; Palmieri, G; Piacentini, M; Rendina, EA; Roselli, M; Sica, G; Tesauro, M; Rovella, V; Tisone, G; Shi, Y; Wang, Y; Melino, G";s:9:"metadata7";s:23:"10.1002/1878-0261.13056";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:1;a:14:{s:9:"citazione";s:156:"Amelio, I., Bertolo, R., Bove, P., Buonomo, O.C., Candi, E., Chiocchi, M., et al. (2020). Liquid biopsies and cancer omics. CELL DEATH DISCOVERY, 6(1), 131.";s:4:"data";s:10:"2020-11-26";s:2:"id";s:20:"PUBBLICAZIONE_405225";s:6:"handle";s:11:"2108/261193";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore MED/18";s:9:"metadata4";s:1086:"The development of the sequencing technologies allowed the generation of huge amounts of molecular data from a single cancer specimen, allowing the clinical oncology to enter the era of the precision medicine. This massive amount of data is highlighting new details on cancer pathogenesis but still relies on tissue biopsies, which are unable to capture the dynamic nature of cancer through its evolution. This assumption led to the exploration of non-tissue sources of tumoral material opening the field of liquid biopsies. Blood, together with body fluids such as urines, or stool, from cancer patients, are analyzed applying the techniques used for the generation of omics data. With blood, this approach would allow to take into account tumor heterogeneity (since the circulating components such as CTCs, ctDNA, or ECVs derive from each cancer clone) in a time dependent manner, resulting in a somehow "real-time" understanding of cancer evolution. Liquid biopsies are beginning nowdays to be applied in many cancer contexts and are at the basis of many clinical trials in oncology.";s:9:"metadata5";s:32:"Liquid biopsies and cancer omics";s:9:"metadata6";s:266:"Amelio, I; Bertolo, R; Bove, P; Buonomo, OC; Candi, E; Chiocchi, M; Cipriani, C; Di Daniele, N; Ganini, C; Juhl, H; Mauriello, A; Marani, C; Marshall, J; Montanaro, M; Palmieri, G; Piacentini, M; Sica, G; Tesauro, M; Rovella, V; Tisone, G; Shi, Y; Wang, Y; Melino, G";s:9:"metadata7";s:26:"10.1038/s41420-020-00373-0";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:2;a:14:{s:9:"citazione";s:142:"Amelio, I., Bertolo, R., Bove, P., Candi, E., Chiocchi, M., Cipriani, C., et al. (2020). Cancer predictive studies. BIOLOGY DIRECT, 15(1), 18.";s:4:"data";s:10:"2020-10-14";s:2:"id";s:20:"PUBBLICAZIONE_404855";s:6:"handle";s:11:"2108/260853";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore MED/18";s:9:"metadata4";N;s:9:"metadata5";s:25:"Cancer predictive studies";s:9:"metadata6";s:253:"Amelio, I; Bertolo, R; Bove, P; Candi, E; Chiocchi, M; Cipriani, C; Di Daniele, N; Ganini, C; Juhl, H; Mauriello, A; Marani, C; Marshall, J; Montanaro, M; Palmieri, G; Piacentini, M; Sica, G; Tesauro, M; Rovella, V; Tisone, G; Shi, Y; Wang, Y; Melino, G";s:9:"metadata7";s:26:"10.1186/s13062-020-00274-3";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:3;a:14:{s:9:"citazione";s:204:"Niklison-Chirou, M.V., Agostini, M., Amelio, I., & Melino, G. (2020). Regulation of Adult Neurogenesis in Mammalian Brain. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 21(14), 1-21 [10.3390/ijms21144869].";s:4:"data";s:10:"2020-07-09";s:2:"id";s:20:"PUBBLICAZIONE_426781";s:6:"handle";s:11:"2108/280607";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore BIO/11";s:9:"metadata4";N;s:9:"metadata5";s:51:"Regulation of Adult Neurogenesis in Mammalian Brain";s:9:"metadata6";s:54:"Niklison-Chirou, MV; Agostini, M; Amelio, I; Melino, G";s:9:"metadata7";s:20:"10.3390/ijms21144869";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:4;a:14:{s:9:"citazione";s:263:"Di Giovanni, E., Buonvino, S., Amelio, I., & Melino, S. (2020). Glutathione-allylsulfur conjugates as mesenchymal stem cells stimulating agents for potential applications in tissue repair. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 21(5) [10.3390/ijms21051638].";s:4:"data";s:7:"2020-03";s:2:"id";s:20:"PUBBLICAZIONE_377839";s:6:"handle";s:11:"2108/237024";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore BIO/10";s:9:"metadata4";N;s:9:"metadata5";s:123:"Glutathione-allylsulfur conjugates as mesenchymal stem cells stimulating agents for potential applications in tissue repair";s:9:"metadata6";s:49:"Di Giovanni, E; Buonvino, S; Amelio, I; Melino, S";s:9:"metadata7";s:20:"10.3390/ijms21051638";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:5;a:14:{s:9:"citazione";s:297:"Amelio, I., Panatta, E., Niklison-Chirou, M.V., Steinert, J.R., Agostini, M., Morone, N., et al. (2020). The C terminus of p73 is essential for hippocampal development. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 117(27), 15694-15701 [10.1073/pnas.2000917117].";s:4:"data";s:4:"2020";s:2:"id";s:20:"PUBBLICAZIONE_426789";s:6:"handle";s:11:"2108/280615";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore BIO/11";s:9:"metadata4";N;s:9:"metadata5";s:62:"The C terminus of p73 is essential for hippocampal development";s:9:"metadata6";s:103:"Amelio, I; Panatta, E; Niklison-Chirou, MV; Steinert, JR; Agostini, M; Morone, N; Knight, RA; Melino, G";s:9:"metadata7";s:23:"10.1073/pnas.2000917117";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:6;a:14:{s:9:"citazione";s:239:"Cassandri, M., Butera, A., Amelio, I., Lena, A.M., Montanaro, M., Mauriello, A., et al. (2020). ZNF750 represses breast cancer invasion via epigenetic control of prometastatic genes. ONCOGENE, 39(22), 4331-4343 [10.1038/s41388-020-1277-5].";s:4:"data";s:4:"2020";s:2:"id";s:20:"PUBBLICAZIONE_426785";s:6:"handle";s:11:"2108/280611";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore BIO/11";s:9:"metadata4";N;s:9:"metadata5";s:85:"ZNF750 represses breast cancer invasion via epigenetic control of prometastatic genes";s:9:"metadata6";s:130:"Cassandri, M; Butera, A; Amelio, I; Lena, AM; Montanaro, M; Mauriello, A; Anemona, L; Candi, E; Knight, RA; Agostini, M; Melino, G";s:9:"metadata7";s:25:"10.1038/s41388-020-1277-5";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:7;a:14:{s:9:"citazione";s:159:"Noce, A., Santoro, M.L., Marrone, G., D'Agostini, C., Amelio, I., Duggento, A., et al. (2020). Serological determinants of COVID-19. BIOLOGY DIRECT, 15(1), 21.";s:4:"data";s:4:"2020";s:2:"id";s:20:"PUBBLICAZIONE_408379";s:6:"handle";s:11:"2108/263925";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore MED/09";s:9:"metadata4";N;s:9:"metadata5";s:36:"Serological determinants of COVID-19";s:9:"metadata6";s:98:"Noce, A; Santoro, ML; Marrone, G; D'Agostini, C; Amelio, I; Duggento, A; Tesauro, M; Di Daniele, N";s:9:"metadata7";s:26:"10.1186/s13062-020-00276-1";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:8;a:14:{s:9:"citazione";s:222:"Pentimalli, F., Grelli, S., Di Daniele, N., Melino, G., & Amelio, I. (2019). Cell death pathologies: targeting death pathways and the immune system for cancer therapy. GENES AND IMMUNITY, 20(7) [10.1038/s41435-018-0052-x].";s:4:"data";s:4:"2019";s:2:"id";s:20:"PUBBLICAZIONE_346839";s:6:"handle";s:11:"2108/211483";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:54:"Settore MED/07 - Microbiologia e Microbiologia Clinica";s:9:"metadata4";N;s:9:"metadata5";s:89:"Cell death pathologies: targeting death pathways and the immune system for cancer therapy";s:9:"metadata6";s:61:"Pentimalli, F; Grelli, S; Di Daniele, N; Melino, G; Amelio, I";s:9:"metadata7";s:25:"10.1038/s41435-018-0052-x";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:9;a:14:{s:9:"citazione";s:198:"Pitolli, C., Wang, Y., Candi, E., Shi, Y., Melino, G., & Amelio, I. (2019). p53-Mediated Tumor Suppression: DNA-Damage Response and Alternative Mechanisms. CANCERS, 11(12) [10.3390/cancers11121983].";s:4:"data";s:4:"2019";s:2:"id";s:20:"PUBBLICAZIONE_379038";s:6:"handle";s:11:"2108/238201";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore BIO/11";s:9:"metadata4";N;s:9:"metadata5";s:78:"p53-Mediated Tumor Suppression: DNA-Damage Response and Alternative Mechanisms";s:9:"metadata6";s:59:"Pitolli, C; Wang, Y; Candi, E; Shi, Y; Melino, G; Amelio, I";s:9:"metadata7";s:23:"10.3390/cancers11121983";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:10;a:14:{s:9:"citazione";s:194:"Pitolli, C., Wang, Y., Mancini, M., Shi, Y., Melino, G., & Amelio, I. (2019). Do Mutations Turn p53 into an Oncogene?. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 20(24) [10.3390/ijms20246241].";s:4:"data";s:4:"2019";s:2:"id";s:20:"PUBBLICAZIONE_379037";s:6:"handle";s:11:"2108/238209";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore BIO/11";s:9:"metadata4";N;s:9:"metadata5";s:39:"Do Mutations Turn p53 into an Oncogene?";s:9:"metadata6";s:61:"Pitolli, C; Wang, Y; Mancini, M; Shi, Y; Melino, G; Amelio, I";s:9:"metadata7";s:20:"10.3390/ijms20246241";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:11;a:14:{s:9:"citazione";s:224:"Lopriore, P., Capitanio, N., Panatta, E., Di Daniele, N., Gambacurta, A., Melino, G., et al. (2018). TAp73 regulates ATP7A: possible implications for ageing-related diseases. AGING, 10(12), 3745-3760 [10.18632/aging.101669].";s:4:"data";s:10:"2018-12-08";s:2:"id";s:20:"PUBBLICAZIONE_342364";s:6:"handle";s:11:"2108/207630";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";s:53:"ageing; cancer; copper; neurodegeneration; p53 family";s:9:"metadata3";s:14:"Settore BIO/11";s:9:"metadata4";s:1090:"The p53 family member p73 controls a wide range of cellular function. Deletion of p73 in mice results in increased tumorigenesis, infertility, neurological defects and altered immune system. Despite the extensive effort directed to define the molecular underlying mechanism of p73 function a clear definition of its transcriptional signature and the extent of overlap with the other p53 family members is still missing. Here we describe a novel TAp73 target, ATP7A a member of a large family of P-type ATPases implicated in human neurogenerative conditions and cancer chemoresistance. Modulation of TAp73 expression influences basal expression level of ATP7A in different cellular models and chromatin immunoprecipitation confirmed a physical direct binding of TAp73 on ATP7A genomic regions. Bioinformatic analysis of expression profile datasets of human lung cancer patients suggests a possible implication of TAp73/ATP7A axis in human cancer. These data provide a novel TAp73-dependent target which might have implications in ageing-related diseases such as cancer and neurodegeneration.";s:9:"metadata5";s:72:"TAp73 regulates ATP7A: possible implications for ageing-related diseases";s:9:"metadata6";s:89:"Lopriore, P; Capitanio, N; Panatta, E; Di Daniele, N; Gambacurta, A; Melino, G; Amelio, I";s:9:"metadata7";s:21:"10.18632/aging.101669";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:12;a:14:{s:9:"citazione";s:146:"Amelio, I., & Melino, G. (2018). Similar Domains for Different Regulations of p53 Family. STRUCTURE, 26(8), 1047-1049 [10.1016/j.str.2018.07.003].";s:4:"data";s:4:"2018";s:2:"id";s:20:"PUBBLICAZIONE_379056";s:6:"handle";s:11:"2108/238076";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore BIO/10";s:9:"metadata4";N;s:9:"metadata5";s:55:"Similar Domains for Different Regulations of p53 Family";s:9:"metadata6";s:20:"Amelio, I; Melino, G";s:9:"metadata7";s:25:"10.1016/j.str.2018.07.003";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:13;a:14:{s:9:"citazione";s:326:"Amelio, I., Mancini, M., Petrova, V., Cairns, R.A., Vikhreva, P., Nicolai, S., et al. (2018). p53 mutants cooperate with HIF-1 in transcriptional regulation of extracellular matrix components to promote tumor progression. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 115(46), E10869-E10878.";s:4:"data";s:4:"2018";s:2:"id";s:20:"PUBBLICAZIONE_379054";s:6:"handle";s:11:"2108/238080";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore BIO/11";s:9:"metadata4";N;s:9:"metadata5";s:126:"p53 mutants cooperate with HIF-1 in transcriptional regulation of extracellular matrix components to promote tumor progression";s:9:"metadata6";s:188:"Amelio, I; Mancini, M; Petrova, V; Cairns, RA; Vikhreva, P; Nicolai, S; Marini, A; Antonov, AA; Le Quesne, J; Acevedo, JDB; Dudek, K; Sozzi, G; Pastorino, U; Knight, RA; Mak, TW; Melino, G";s:9:"metadata7";s:23:"10.1073/pnas.1808314115";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:14;a:14:{s:9:"citazione";s:333:"Carbone, M., Amelio, I., Affar, E.B., Brugarolas, J., Cannon-Albright, L.A., Cantley, L.C., et al. (2018). Consensus report of the 8 and 9th Weinman Symposia on Gene x Environment Interaction in carcinogenesis: novel opportunities for precision medicine. CELL DEATH AND DIFFERENTIATION, 25(11), 1885-1904 [10.1038/s41418-018-0213-5].";s:4:"data";s:4:"2018";s:2:"id";s:20:"PUBBLICAZIONE_379058";s:6:"handle";s:11:"2108/238070";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore BIO/10";s:9:"metadata4";N;s:9:"metadata5";s:146:"Consensus report of the 8 and 9th Weinman Symposia on Gene x Environment Interaction in carcinogenesis: novel opportunities for precision medicine";s:9:"metadata6";s:315:"Carbone, M; Amelio, I; Affar, EB; Brugarolas, J; Cannon-Albright, LA; Cantley, LC; Cavenee, WK; Chen, Z; Croce, CM; D'Andrea, A; Gandara, D; Giorgi, C; Jia, W; Lan, Q; Mak, TW; Manley, JL; Mikoshiba, K; Onuchic, JN; Pass, HI; Pinton, P; Prives, C; Rothman, N; Sebti, SM; Turkson, J; Wu, X; Yang, H; Yu, H; Melino, G";s:9:"metadata7";s:25:"10.1038/s41418-018-0213-5";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:15;a:14:{s:9:"citazione";s:273:"Galluzzi, L., Vitale, I., Aaronson, S.a., Abrams, J.m., Adam, D., Agostinis, P., et al. (2018). Molecular mechanisms of cell death: Recommendations of the Nomenclature Committee on Cell Death 2018. CELL DEATH AND DIFFERENTIATION, 25(3), 486-541 [10.1038/s41418-017-0012-4].";s:4:"data";s:4:"2018";s:2:"id";s:20:"PUBBLICAZIONE_334306";s:6:"handle";s:11:"2108/201030";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore BIO/10";s:9:"metadata4";s:1125:"Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. 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CELL DEATH & DISEASE, 5(5), e1203 [10.1038/cddis.2014.113].";s:4:"data";s:4:"2014";s:2:"id";s:20:"PUBBLICAZIONE_231854";s:6:"handle";s:11:"2108/113677";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";s:270:"Antidepressive Agents; Autophagy; Binding Sites; Cell Line, Tumor; Clomipramine; Drug Synergism; Enzyme Inhibitors; High-Throughput Screening Assays; Humans; Models, Molecular; Protein Structure, Tertiary; Reproducibility of Results; Ubiquitin; Ubiquitin-Protein Ligases";s:9:"metadata3";s:14:"Settore BIO/10";s:9:"metadata4";s:1709:"Inhibition of distinct ubiquitin E3 ligases might represent a powerful therapeutic tool. ITCH is a HECT domain-containing E3 ligase that promotes the ubiquitylation and degradation of several proteins, including p73, p63, c-Jun, JunB, Notch and c-FLIP, thus affecting cell fate. Accordingly, ITCH depletion potentiates the effect of chemotherapeutic drugs, revealing ITCH as a potential pharmacological target in cancer therapy. Using high throughput screening of ITCH auto-ubiquitylation, we identified several putative ITCH inhibitors, one of which is clomipramine--a clinically useful antidepressant drug. Previously, we have shown that clomipramine inhibits autophagy by blocking autophagolysosomal fluxes and thus could potentiate chemotherapy in vitro. Here, we found that clomipramine specifically blocks ITCH auto-ubiquitylation, as well as p73 ubiquitylation. By screening structural homologs of clomipramine, we identified several ITCH inhibitors and putative molecular moieties that are essential for ITCH inhibition. Treating a panel of breast, prostate and bladder cancer cell lines with clomipramine, or its homologs, we found that they reduce cancer cell growth, and synergize with gemcitabine or mitomycin in killing cancer cells by blocking autophagy. We also discuss a potential mechanism of inhibition. 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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 414(2), 277-281 [10.1016/j.bbrc.2011.09.080].";s:4:"data";s:4:"2011";s:2:"id";s:20:"PUBBLICAZIONE_252166";s:6:"handle";s:11:"2108/131850";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";s:83:"Autophagy; Cell Death; Cell Survival; Humans; Neoplasms; Neurodegenerative Diseases";s:9:"metadata3";s:14:"Settore BIO/10";s:9:"metadata4";s:627:"Autophagy is a self-digesting mechanism that cells adopt to respond to stressful stimuli. Morphologically, cells dying by autophagy show multiple cytoplasmic double-membraned vacuoles, and, if prolonged, autophagy can lead to cell death, "autophagic cell death". Thus, autophagy can act both as a temporary protective mechanism during a brief stressful episode and be a mode of cell death in its own right. In this mini-review we focus on recent knowledge concerning the connection between autophagy and programmed cell death, evaluating their possible implications for therapy in pathologies like cancer and neurodegeneration.";s:9:"metadata5";s:77:"Cell death pathology: Cross-talk with autophagy and its clinical implications";s:9:"metadata6";s:42:"Melino, G; Amelio, I; Melino, G; Knight, R";s:9:"metadata7";s:26:"10.1016/j.bbrc.2011.09.080";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}i:56;a:14:{s:9:"citazione";s:245:"Lena, A.M., Cipollone, R., Amelio, I., Catani, M.V., Ramadan, S., Browne, G., et al. (2010). Skn-1a/Oct-11 and ΔNp63α exert antagonizing effects on human keratin expression. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 401(4), 568-573.";s:4:"data";s:10:"2010-10-29";s:2:"id";s:19:"PUBBLICAZIONE_33418";s:6:"handle";s:9:"2108/9234";s:9:"metadata1";s:19:"Articolo su rivista";s:9:"metadata2";N;s:9:"metadata3";s:14:"Settore BIO/10";s:9:"metadata4";N;s:9:"metadata5";s:81:"Skn-1a/Oct-11 and ΔNp63α exert antagonizing effects on human keratin expression";s:9:"metadata6";s:89:"Lena, AM; Cipollone, R; Amelio, I; Catani, MV; Ramadan, S; Browne, G; Melino, G; Candi, E";s:9:"metadata7";s:26:"10.1016/j.bbrc.2010.09.102";s:9:"metadata8";N;s:9:"metadata9";N;s:10:"metadata10";N;}}" } ["meta_keywords"]=> array(1) { [0]=> string(1) "," } ["reserved"]=> array(1) { [0]=> string(1) "0" } ["auth_ip"]=> array(1) { [0]=> string(1) "0" } } ["_fieldBoosts":protected]=> array(6) { ["content_id"]=> bool(false) ["content_title"]=> bool(false) ["description"]=> bool(false) ["meta_keywords"]=> bool(false) ["reserved"]=> bool(false) ["auth_ip"]=> bool(false) } } }