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  1. AU=Tosoni Daniela
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  15. AU="van der Horst, A."
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  38. AU="Chiba, Kentaro"
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  1. Artikel ; Online: Correction to: Correlation between IPSET‑t risk at diagnosis and subsequent hemorrhage in patients with essential thrombocythemia; a single institution experience.

    Tosoni, Luca / Liberi, Matteo / Morelli, Gianluca / Zannier, Maria Elena / Lazzarotto, Davide / Filì, Carla / Simeone, Erica / Battaglia, Giulia / Callegari, Chiara / Fanin, Matteo / Damiani, Daniela / Fanin, Renato / Tiribelli, Mario

    Annals of hematology

    2023  Band 103, Heft 2, Seite(n) 449

    Sprache Englisch
    Erscheinungsdatum 2023-12-29
    Erscheinungsland Germany
    Dokumenttyp Published Erratum
    ZDB-ID 1064950-5
    ISSN 1432-0584 ; 0939-5555 ; 0945-8077
    ISSN (online) 1432-0584
    ISSN 0939-5555 ; 0945-8077
    DOI 10.1007/s00277-023-05608-5
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  2. Artikel ; Online: JAK2 V617F-mutated polycythemia vera developing in a patient with a 20-year-long chronic myeloid leukemia at the time of first molecular response.

    Tosoni, Luca / Fabbro, Dora / Pizzano, Umberto / Mullai, Rikard / Morelli, Gianluca / Franzoni, Alessandra / Damante, Giuseppe / Toffoletti, Eleonora / Damiani, Daniela / Fanin, Renato / Tiribelli, Mario

    Annals of hematology

    2023  Band 102, Heft 5, Seite(n) 1279–1280

    Mesh-Begriff(e) Humans ; Chronic Disease ; Janus Kinase 2/genetics ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/diagnosis ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive/genetics ; Leukemia, Myeloid ; Mutation ; Polycythemia Vera/diagnosis ; Polycythemia Vera/genetics
    Chemische Substanzen JAK2 protein, human (EC 2.7.10.2) ; Janus Kinase 2 (EC 2.7.10.2)
    Sprache Englisch
    Erscheinungsdatum 2023-03-22
    Erscheinungsland Germany
    Dokumenttyp Case Reports ; Letter
    ZDB-ID 1064950-5
    ISSN 1432-0584 ; 0939-5555 ; 0945-8077
    ISSN (online) 1432-0584
    ISSN 0939-5555 ; 0945-8077
    DOI 10.1007/s00277-023-05187-5
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  3. Artikel ; Online: Correlation between IPSET-t risk at diagnosis and subsequent hemorrhage in patients with essential thrombocythemia; a single institution experience.

    Tosoni, Luca / Liberi, Matteo / Morelli, Gianluca / Zannier, Maria Elena / Lazzarotto, Davide / Filì, Carla / Simeone, Erica / Battaglia, Giulia / Callegari, Chiara / Fanin, Matteo / Damiani, Daniela / Fanin, Renato / Tiribelli, Mario

    Annals of hematology

    2023  Band 103, Heft 2, Seite(n) 443–448

    Abstract: Essential thrombocythemia (ET) is a myeloproliferative neoplasm characterized by an increased risk of thrombotic and hemorrhagic events, that represent the leading causes of mortality and morbidity. Currently, while thrombotic risk is assessed through ... ...

    Abstract Essential thrombocythemia (ET) is a myeloproliferative neoplasm characterized by an increased risk of thrombotic and hemorrhagic events, that represent the leading causes of mortality and morbidity. Currently, while thrombotic risk is assessed through the IPSET-t and r-IPSET scores, there is no specific prognostic tool used to predict hemorrhagic risk in ET. The aim of the study was to define incidence and risk factors connected to hemorrhagic events by retrospectively analyzing 308 ET patients diagnosed between 1996 and 2022 at the Division of Hematology of Udine and treated according to the current international guidelines. According to molecular status, 193 patients (62.7%) were JAK2 mutated, 66 (21.4%) had a CALR mutation, 14 (4.5%) had a MPL mutation, 21 patients (6.8%) were "triple negative," and 14 patients (4.5%) were not evaluable. According to IPSET-t score, 49.7% patients were at high, 24.3% at intermediate, and 26.0% at low-risk, respectively. Twelve (3.9%) patients experienced bleeding at ET diagnosis, while 24 (7.8%) had at least one hemorrhagic event during follow-up at a median time of 103 months (range: 1-309). Forty hemorrhagic events were totally recorded and defined as minor in 22 cases, moderate in 11 cases, and severe in 7 cases. Cumulative incidence (CI) of hemorrhage at 10 and 20 years was 6.0% and 12.0%, respectively. A statistically significant correlation between hemorrhagic risk and IPSET-t score emerged: 10 years hemorrhage CI was 3.2% for low-risk, 2.9% for intermediate-risk, and 9.8% for high-risk patients, respectively (p=0.002). We found no correlation between hemorrhagic risk and gender or mutational status. Results of our study highlight the validity of IPSET-t score in predicting individual hemorrhagic risk among ET patients, suggesting a possible role of IPSET-t scoring system as a global evaluator for vascular events in ET patients.
    Mesh-Begriff(e) Humans ; Thrombocythemia, Essential/complications ; Thrombocythemia, Essential/diagnosis ; Thrombocythemia, Essential/genetics ; Retrospective Studies ; Thrombosis/epidemiology ; Risk Factors ; Prognosis ; Hemorrhage/etiology ; Hemorrhage/complications ; Mutation ; Janus Kinase 2/genetics ; Calreticulin/genetics
    Chemische Substanzen Janus Kinase 2 (EC 2.7.10.2) ; Calreticulin
    Sprache Englisch
    Erscheinungsdatum 2023-12-11
    Erscheinungsland Germany
    Dokumenttyp Journal Article
    ZDB-ID 1064950-5
    ISSN 1432-0584 ; 0939-5555 ; 0945-8077
    ISSN (online) 1432-0584
    ISSN 0939-5555 ; 0945-8077
    DOI 10.1007/s00277-023-05578-8
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  4. Artikel ; Online: miR-146 connects stem cell identity with metabolism and pharmacological resistance in breast cancer.

    Tordonato, Chiara / Marzi, Matteo Jacopo / Giangreco, Giovanni / Freddi, Stefano / Bonetti, Paola / Tosoni, Daniela / Di Fiore, Pier Paolo / Nicassio, Francesco

    The Journal of cell biology

    2021  Band 220, Heft 5

    Abstract: Although ectopic overexpression of miRNAs can influence mammary normal and cancer stem cells (SCs/CSCs), their physiological relevance remains uncertain. Here, we show that miR-146 is relevant for SC/CSC activity. MiR-146a/b expression is high in SCs/ ... ...

    Abstract Although ectopic overexpression of miRNAs can influence mammary normal and cancer stem cells (SCs/CSCs), their physiological relevance remains uncertain. Here, we show that miR-146 is relevant for SC/CSC activity. MiR-146a/b expression is high in SCs/CSCs from human/mouse primary mammary tissues, correlates with the basal-like breast cancer subtype, which typically has a high CSC content, and specifically distinguishes cells with SC/CSC identity. Loss of miR-146 reduces SC/CSC self-renewal in vitro and compromises patient-derived xenograft tumor growth in vivo, decreasing the number of tumor-initiating cells, thus supporting its pro-oncogenic function. Transcriptional analysis in mammary SC-like cells revealed that miR-146 has pleiotropic effects, reducing adaptive response mechanisms and activating the exit from quiescent state, through a complex network of finely regulated miRNA targets related to quiescence, transcription, and one-carbon pool metabolism. Consistent with these findings, SCs/CSCs display innate resistance to anti-folate chemotherapies either in vitro or in vivo that can be reversed by miR-146 depletion, unmasking a "hidden vulnerability" exploitable for the development of anti-CSC therapies.
    Mesh-Begriff(e) Animals ; Breast Neoplasms/genetics ; Carcinogenesis/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Drug Resistance, Neoplasm/genetics ; Female ; Gene Expression Regulation, Neoplastic/genetics ; Humans ; Mice ; MicroRNAs/genetics ; Neoplastic Stem Cells/metabolism
    Chemische Substanzen MicroRNAs ; Mirn146 microRNA, mouse
    Sprache Englisch
    Erscheinungsdatum 2021-05-02
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.202009053
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: The Ephrin tyrosine kinase a3 (EphA3) is a novel mediator of RAGE-prompted motility of breast cancer cells.

    Talia, Marianna / Cirillo, Francesca / Spinelli, Asia / Zicarelli, Azzurra / Scordamaglia, Domenica / Muglia, Lucia / De Rosis, Salvatore / Rigiracciolo, Damiano Cosimo / Filippelli, Gianfranco / Perrotta, Ida Daniela / Davoli, Mariano / De Rosa, Rosanna / Macirella, Rachele / Brunelli, Elvira / Miglietta, Anna Maria / Nardo, Bruno / Tosoni, Daniela / Pece, Salvatore / De Francesco, Ernestina Marianna /
    Belfiore, Antonino / Maggiolini, Marcello / Lappano, Rosamaria

    Journal of experimental & clinical cancer research : CR

    2023  Band 42, Heft 1, Seite(n) 164

    Abstract: Background: The receptor for advanced glycation-end products (RAGE) and its ligands have been implicated in obesity and associated inflammatory processes as well as in metabolic alterations like diabetes. In addition, RAGE-mediated signaling has been ... ...

    Abstract Background: The receptor for advanced glycation-end products (RAGE) and its ligands have been implicated in obesity and associated inflammatory processes as well as in metabolic alterations like diabetes. In addition, RAGE-mediated signaling has been reported to contribute to the metastatic progression of breast cancer (BC), although mechanistic insights are still required. Here, we provide novel findings regarding the transcriptomic landscape and the molecular events through which RAGE may prompt aggressive features in estrogen receptor (ER)-positive BC.
    Methods: MCF7 and T47D BC cells stably overexpressing human RAGE were used as a model system to evaluate important changes like cell protrusions, migration, invasion and colony formation both in vitro through scanning electron microscopy, clonogenic, migration and invasion assays and in vivo through zebrafish xenografts experiments. The whole transcriptome of RAGE-overexpressing BC cells was screened by high-throughput RNA sequencing. Thereafter, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses allowed the prediction of potential functions of differentially expressed genes (DEGs). Flow cytometry, real time-PCR, chromatin immunoprecipitation, immunofluorescence and western blot assays were performed to investigate the molecular network involved in the regulation of a novel RAGE target gene namely EphA3. The clinical significance of EphA3 was explored in the TCGA cohort of patients through the survivALL package, whereas the pro-migratory role of EphA3 signaling was ascertained in both BC cells and cancer-associated fibroblasts (CAFs). Statistical analysis was performed by t-tests.
    Results: RNA-seq findings and GSEA analysis revealed that RAGE overexpression leads to a motility-related gene signature in ER-positive BC cells. Accordingly, we found that RAGE-overexpressing BC cells exhibit long filopodia-like membrane protrusions as well as an enhanced dissemination potential, as determined by the diverse experimental assays. Mechanistically, we established for the first time that EphA3 signaling may act as a physical mediator of BC cells and CAFs motility through both homotypic and heterotypic interactions.
    Conclusions: Our data demonstrate that RAGE up-regulation leads to migratory ability in ER-positive BC cells. Noteworthy, our findings suggest that EphA3 may be considered as a novel RAGE target gene facilitating BC invasion and scattering from the primary tumor mass. Overall, the current results may provide useful insights for more comprehensive therapeutic approaches in BC, particularly in obese and diabetic patients that are characterized by high RAGE levels.
    Mesh-Begriff(e) Animals ; Female ; Humans ; Breast Neoplasms/genetics ; Receptor for Advanced Glycation End Products ; Receptor, EphA3/genetics ; Signal Transduction ; Zebrafish/genetics
    Chemische Substanzen EPHA3 protein, human (EC 2.7.10.1) ; Receptor for Advanced Glycation End Products ; Receptor, EphA3 (EC 2.7.10.1) ; AGER protein, human
    Sprache Englisch
    Erscheinungsdatum 2023-07-12
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 803138-1
    ISSN 1756-9966 ; 0392-9078
    ISSN (online) 1756-9966
    ISSN 0392-9078
    DOI 10.1186/s13046-023-02747-5
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  6. Artikel ; Online: Aberrant phosphorylation inactivates Numb in breast cancer causing expansion of the stem cell pool.

    Filippone, Maria Grazia / Freddi, Stefano / Zecchini, Silvia / Restelli, Silvia / Colaluca, Ivan Nicola / Bertalot, Giovanni / Pece, Salvatore / Tosoni, Daniela / Di Fiore, Pier Paolo

    The Journal of cell biology

    2022  Band 221, Heft 12

    Abstract: Asymmetric cell division is a key tumor suppressor mechanism that prevents the uncontrolled expansion of the stem cell (SC) compartment by generating daughter cells with alternative fates: one retains SC identity and enters quiescence and the other ... ...

    Abstract Asymmetric cell division is a key tumor suppressor mechanism that prevents the uncontrolled expansion of the stem cell (SC) compartment by generating daughter cells with alternative fates: one retains SC identity and enters quiescence and the other becomes a rapidly proliferating and differentiating progenitor. A critical player in this process is Numb, which partitions asymmetrically at SC mitosis and inflicts different proliferative and differentiative fates in the two daughters. Here, we show that asymmetric Numb partitioning per se is insufficient for the proper control of mammary SC dynamics, with differential phosphorylation and functional inactivation of Numb in the two progeny also required. The asymmetric phosphorylation/inactivation of Numb in the progenitor is mediated by the atypical PKCζ isoform. This mechanism is subverted in breast cancer via aberrant activation of PKCs that phosphorylate Numb in both progenies, leading to symmetric division and expansion of the cancer SC compartment, associated with aggressive disease. Thus, Numb phosphorylation represents a target for breast cancer therapy.
    Mesh-Begriff(e) Asymmetric Cell Division ; Breast Neoplasms/genetics ; Female ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mitosis ; Neoplastic Stem Cells/cytology ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Phosphorylation
    Chemische Substanzen Membrane Proteins ; Nerve Tissue Proteins ; NUMB protein, human
    Sprache Englisch
    Erscheinungsdatum 2022-10-06
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 218154-x
    ISSN 1540-8140 ; 0021-9525
    ISSN (online) 1540-8140
    ISSN 0021-9525
    DOI 10.1083/jcb.202112001
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  7. Artikel ; Online: p140Cap inhibits β-Catenin in the breast cancer stem cell compartment instructing a protective anti-tumor immune response.

    Salemme, Vincenzo / Vedelago, Mauro / Sarcinella, Alessandro / Moietta, Federico / Piccolantonio, Alessio / Moiso, Enrico / Centonze, Giorgia / Manco, Marta / Guala, Andrea / Lamolinara, Alessia / Angelini, Costanza / Morellato, Alessandro / Natalini, Dora / Calogero, Raffaele / Incarnato, Danny / Oliviero, Salvatore / Conti, Laura / Iezzi, Manuela / Tosoni, Daniela /
    Bertalot, Giovanni / Freddi, Stefano / Tucci, Francesco A / De Sanctis, Francesco / Frusteri, Cristina / Ugel, Stefano / Bronte, Vincenzo / Cavallo, Federica / Provero, Paolo / Gai, Marta / Taverna, Daniela / Turco, Emilia / Pece, Salvatore / Defilippi, Paola

    Nature communications

    2023  Band 14, Heft 1, Seite(n) 2350

    Abstract: The p140Cap adaptor protein is a tumor suppressor in breast cancer associated with a favorable prognosis. Here we highlight a function of p140Cap in orchestrating local and systemic tumor-extrinsic events that eventually result in inhibition of the ... ...

    Abstract The p140Cap adaptor protein is a tumor suppressor in breast cancer associated with a favorable prognosis. Here we highlight a function of p140Cap in orchestrating local and systemic tumor-extrinsic events that eventually result in inhibition of the polymorphonuclear myeloid-derived suppressor cell function in creating an immunosuppressive tumor-promoting environment in the primary tumor, and premetastatic niches at distant sites. Integrative transcriptomic and preclinical studies unravel that p140Cap controls an epistatic axis where, through the upstream inhibition of β-Catenin, it restricts tumorigenicity and self-renewal of tumor-initiating cells limiting the release of the inflammatory cytokine G-CSF, required for polymorphonuclear myeloid-derived suppressor cells to exert their local and systemic tumor conducive function. Mechanistically, p140Cap inhibition of β-Catenin depends on its ability to localize in and stabilize the β-Catenin destruction complex, promoting enhanced β-Catenin inactivation. Clinical studies in women show that low p140Cap expression correlates with reduced presence of tumor-infiltrating lymphocytes and more aggressive tumor types in a large cohort of real-life female breast cancer patients, highlighting the potential of p140Cap as a biomarker for therapeutic intervention targeting the β-Catenin/ Tumor-initiating cells /G-CSF/ polymorphonuclear myeloid-derived suppressor cell axis to restore an efficient anti-tumor immune response.
    Mesh-Begriff(e) Female ; Humans ; beta Catenin/metabolism ; Breast/pathology ; Breast Neoplasms/genetics ; Breast Neoplasms/immunology ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Immunity ; Neoplastic Stem Cells/immunology ; Neoplastic Stem Cells/metabolism
    Chemische Substanzen beta Catenin
    Sprache Englisch
    Erscheinungsdatum 2023-05-11
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-37824-y
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  8. Artikel ; Online: TFEB and TFE3 drive kidney cystogenesis and tumorigenesis.

    Di Malta, Chiara / Zampelli, Angela / Granieri, Letizia / Vilardo, Claudia / De Cegli, Rossella / Cinque, Laura / Nusco, Edoardo / Pece, Salvatore / Tosoni, Daniela / Sanguedolce, Francesca / Sorrentino, Nicolina Cristina / Merino, Maria J / Nielsen, Deborah / Srinivasan, Ramaprasad / Ball, Mark W / Ricketts, Christopher J / Vocke, Cathy D / Lang, Martin / Karim, Baktiar /
    Lanfrancone, Luisa / Schmidt, Laura S / Linehan, W Marston / Ballabio, Andrea

    EMBO molecular medicine

    2023  Band 15, Heft 5, Seite(n) e16877

    Abstract: Birt-Hogg-Dubé (BHD) syndrome is an inherited familial cancer syndrome characterized by the development of cutaneous lesions, pulmonary cysts, renal tumors and cysts and caused by loss-of-function pathogenic variants in the gene encoding the tumor- ... ...

    Abstract Birt-Hogg-Dubé (BHD) syndrome is an inherited familial cancer syndrome characterized by the development of cutaneous lesions, pulmonary cysts, renal tumors and cysts and caused by loss-of-function pathogenic variants in the gene encoding the tumor-suppressor protein folliculin (FLCN). FLCN acts as a negative regulator of TFEB and TFE3 transcription factors, master controllers of lysosomal biogenesis and autophagy, by enabling their phosphorylation by the mechanistic Target Of Rapamycin Complex 1 (mTORC1). We have previously shown that deletion of Tfeb rescued the renal cystic phenotype of kidney-specific Flcn KO mice. Using Flcn/Tfeb/Tfe3 double and triple KO mice, we now show that both Tfeb and Tfe3 contribute, in a differential and cooperative manner, to kidney cystogenesis. Remarkably, the analysis of BHD patient-derived tumor samples revealed increased activation of TFEB/TFE3-mediated transcriptional program and silencing either of the two genes rescued tumorigenesis in human BHD renal tumor cell line-derived xenografts (CDXs). Our findings demonstrate in disease-relevant models that both TFEB and TFE3 are key drivers of renal tumorigenesis and suggest novel therapeutic strategies based on the inhibition of these transcription factors.
    Mesh-Begriff(e) Humans ; Mice ; Animals ; Kidney/pathology ; Kidney Neoplasms/genetics ; Kidney Neoplasms/pathology ; Birt-Hogg-Dube Syndrome/genetics ; Birt-Hogg-Dube Syndrome/pathology ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics ; Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/metabolism ; Transcription Factors ; Carcinogenesis/genetics ; Cysts
    Chemische Substanzen Basic Helix-Loop-Helix Leucine Zipper Transcription Factors ; Transcription Factors ; TFE3 protein, human ; TFEB protein, human
    Sprache Englisch
    Erscheinungsdatum 2023-03-29
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2467145-9
    ISSN 1757-4684 ; 1757-4676
    ISSN (online) 1757-4684
    ISSN 1757-4676
    DOI 10.15252/emmm.202216877
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  9. Artikel ; Online: Author Correction: Direct stimulation of ERBB2 highlights a novel cytostatic signaling pathway driven by the receptor Thr

    Gaviraghi, Marco / Rabellino, Andrea / Andolfo, Annapaola / Brand, Matthias / Brombin, Chiara / Bagnato, Paola / De Feudis, Giuseppina / Raimondi, Andrea / Locatelli, Alberta / Tosoni, Daniela / Mazza, Davide / Gianni, Luca / Tonon, Giovanni / Yarden, Yosef / Tacchetti, Carlo / Daniele, Tiziana

    Scientific reports

    2021  Band 11, Heft 1, Seite(n) 18202

    Sprache Englisch
    Erscheinungsdatum 2021-09-08
    Erscheinungsland England
    Dokumenttyp Published Erratum
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-021-97699-1
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel ; Online: CAP (Cbl associated protein) regulates receptor-mediated endocytosis.

    Tosoni, Daniela / Cestra, Gianluca

    FEBS letters

    2009  Band 583, Heft 2, Seite(n) 293–300

    Abstract: CAP (c-Cbl associated protein)/ponsin belongs to a family of adaptor proteins implicated in cell adhesion and signaling. Here we show that CAP binds to and co-localizes with the essential endocytic factor dynamin. We demonstrate that CAP promotes the ... ...

    Abstract CAP (c-Cbl associated protein)/ponsin belongs to a family of adaptor proteins implicated in cell adhesion and signaling. Here we show that CAP binds to and co-localizes with the essential endocytic factor dynamin. We demonstrate that CAP promotes the formation of dynamin-decorated tubule like structures, which are also coated with actin filaments. Accordingly, we found that the expression of CAP leads to the inhibition of dynamin-mediated endocytosis and increases EGFR stability. Thus, we suggest that CAP may coordinate the function of dynamin with the regulation of the actin cytoskeleton during endocytosis.
    Mesh-Begriff(e) Actins/metabolism ; Animals ; COS Cells ; Cercopithecus aethiops ; Cytoskeleton/metabolism ; Cytoskeleton/ultrastructure ; Dynamin II/metabolism ; Endocytosis ; HeLa Cells ; Humans ; Immunoprecipitation ; Microfilament Proteins/metabolism ; Rats
    Chemische Substanzen Actins ; Microfilament Proteins ; ponsin ; Dynamin II (EC 3.6.5.5)
    Sprache Englisch
    Erscheinungsdatum 2009-01-22
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 212746-5
    ISSN 1873-3468 ; 0014-5793
    ISSN (online) 1873-3468
    ISSN 0014-5793
    DOI 10.1016/j.febslet.2008.12.047
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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