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Article ; Online: A genetic model of CEDNIK syndrome in zebrafish highlights the role of the SNARE protein Snap29 in neuromotor and epidermal development.

Mastrodonato, Valeria / Beznoussenko, Galina / Mironov, Alexandre / Ferrari, Laura / Deflorian, Gianluca / Vaccari, Thomas

Scientific reports

2019 Volume 9, Issue 1, Page(s) 1211

Abstract: Homozygous mutations in SNAP29, encoding a SNARE protein mainly involved in membrane fusion, cause CEDNIK (Cerebral Dysgenesis, Neuropathy, Ichthyosis and Keratoderma), a rare congenital neurocutaneous syndrome associated with short life expectancy, ... ...

Abstract	Homozygous mutations in SNAP29, encoding a SNARE protein mainly involved in membrane fusion, cause CEDNIK (Cerebral Dysgenesis, Neuropathy, Ichthyosis and Keratoderma), a rare congenital neurocutaneous syndrome associated with short life expectancy, whose pathogenesis is unclear. Here, we report the analysis of the first genetic model of CEDNIK in zebrafish. Strikingly, homozygous snap29 mutant larvae display CEDNIK-like features, such as microcephaly and skin defects. Consistent with Snap29 role in membrane fusion during autophagy, we observe accumulation of the autophagy markers p62 and LC3, and formation of aberrant multilamellar organelles and mitochondria. Importantly, we find high levels of apoptotic cell death during early development that might play a yet uncharacterized role in CEDNIK pathogenesis. Mutant larvae also display mouth opening problems, feeding impairment and swimming difficulties. These alterations correlate with defective trigeminal nerve formation and excess axonal branching. Since the paralog Snap25 is known to promote axonal branching, Snap29 might act in opposition with, or modulate Snap25 activity during neurodevelopment. Our vertebrate genetic model of CEDNIK extends the description in vivo of the multisystem defects due to loss of Snap29 and could provide the base to test compounds that might ameliorate traits of the disease.
MeSH term(s)	Animals ; Autophagy ; Humans ; Keratoderma, Palmoplantar/genetics ; Keratoderma, Palmoplantar/metabolism ; Keratoderma, Palmoplantar/physiopathology ; Membrane Fusion ; Models, Genetic ; Mutation ; Nervous System Malformations/metabolism ; Neurocutaneous Syndromes/genetics ; Neurocutaneous Syndromes/metabolism ; Neurocutaneous Syndromes/physiopathology ; Phenotype ; Protein Binding ; Qb-SNARE Proteins/metabolism ; Qc-SNARE Proteins/metabolism ; SNARE Proteins/metabolism ; SNARE Proteins/physiology ; Synaptosomal-Associated Protein 25/metabolism ; Synaptosomal-Associated Protein 25/physiology ; Zebrafish/metabolism ; Zebrafish Proteins/metabolism ; Zebrafish Proteins/physiology
Chemical Substances	Qb-SNARE Proteins ; Qc-SNARE Proteins ; SNAP29 protein, human ; SNARE Proteins ; Snap29 protein, zebrafish ; Synaptosomal-Associated Protein 25 ; Zebrafish Proteins
Language	English
Publishing date	2019-02-04
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-37780-4
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Article ; Online: MITO-Luc/GFP zebrafish model to assess spatial and temporal evolution of cell proliferation in vivo.

de Latouliere, Luisa / Manni, Isabella / Ferrari, Laura / Pisati, Federica / Totaro, Maria Grazia / Gurtner, Aymone / Marra, Emanuele / Pacello, Lucrezia / Pozzoli, Ombretta / Aurisicchio, Luigi / Capogrossi, Maurizio C / Deflorian, Gianluca / Piaggio, Giulia

Scientific reports

2021 Volume 11, Issue 1, Page(s) 671

Abstract: We developed a novel reporter transgenic zebrafish model called MITO-Luc/GFP zebrafish in which GFP and luciferase expression are under the control of the master regulator of proliferation NF-Y. In MITO-Luc/GFP zebrafish it is possible to visualize cell ... ...

Abstract	We developed a novel reporter transgenic zebrafish model called MITO-Luc/GFP zebrafish in which GFP and luciferase expression are under the control of the master regulator of proliferation NF-Y. In MITO-Luc/GFP zebrafish it is possible to visualize cell proliferation in vivo by fluorescence and bioluminescence. In this animal model, GFP and luciferase expression occur in early living embryos, becoming tissue specific in juvenile and adult zebrafish. By in vitro and ex vivo experiments we demonstrate that luciferase activity in adult animals occurs in intestine, kidney and gonads, where detectable proliferating cells are located. Further, by time lapse experiments in live embryos, we observed a wave of GFP positive cells following fin clip. In adult zebrafish, in addition to a bright bioluminescence signal on the regenerating tail, an early unexpected signal coming from the kidney occurs indicating not only a fin cell proliferation, but also a systemic response to tissue damage. Finally, we observed that luciferase activity was inhibited by anti-proliferative interventions, i.e. 5FU, cell cycle inhibitors and X-Rays. In conclusion, MITO-Luc/GFP zebrafish is a novel animal model that may be crucial to assess the spatial and temporal evolution of cell proliferation in vivo.
MeSH term(s)	Animals ; Animals, Genetically Modified/genetics ; Animals, Genetically Modified/growth & development ; Animals, Genetically Modified/metabolism ; Cell Proliferation ; Evolution, Molecular ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Luciferases/genetics ; Luciferases/metabolism ; Regeneration ; Spatio-Temporal Analysis ; Zebrafish/genetics ; Zebrafish/growth & development ; Zebrafish/metabolism
Chemical Substances	Green Fluorescent Proteins (147336-22-9) ; Luciferases (EC 1.13.12.-)
Language	English
Publishing date	2021-01-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-020-79530-5
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Article ; Online: Phage therapy against Pseudomonas aeruginosa infections in a cystic fibrosis zebrafish model.

Cafora, Marco / Deflorian, Gianluca / Forti, Francesca / Ferrari, Laura / Binelli, Giorgio / Briani, Federica / Ghisotti, Daniela / Pistocchi, Anna

Scientific reports

2019 Volume 9, Issue 1, Page(s) 1527

Abstract: Cystic fibrosis (CF) is a hereditary disease due to mutations in the CFTR gene and causes mortality in humans mainly due to respiratory infections caused by Pseudomonas aeruginosa. In a previous work we used phage therapy, which is a treatment with a mix ...

Abstract	Cystic fibrosis (CF) is a hereditary disease due to mutations in the CFTR gene and causes mortality in humans mainly due to respiratory infections caused by Pseudomonas aeruginosa. In a previous work we used phage therapy, which is a treatment with a mix of phages, to actively counteract acute P. aeruginosa infections in mice and Galleria mellonella larvae. In this work we apply phage therapy to the treatment of P. aeruginosa PAO1 infections in a CF zebrafish model. The structure of the CFTR channel is evolutionary conserved between fish and mammals and cftr-loss-of-function zebrafish embryos show a phenotype that recapitulates the human disease, in particular with destruction of the pancreas. We show that phage therapy is able to decrease lethality, bacterial burden, and the pro-inflammatory response caused by PAO1 infection. In addition, phage administration relieves the constitutive inflammatory state of CF embryos. To our knowledge, this is the first time that phage therapy is used to cure P. aeruginosa infections in a CF animal model. We also find that the curative effect against PAO1 infections is improved by combining phages and antibiotic treatments, opening a useful therapeutic approach that could reduce antibiotic doses and time of administration.
MeSH term(s)	Animals ; Anti-Bacterial Agents/therapeutic use ; Cystic Fibrosis/complications ; Disease Models, Animal ; Embryo, Nonmammalian/immunology ; Embryo, Nonmammalian/microbiology ; Embryo, Nonmammalian/virology ; Mice ; Pseudomonas Infections/immunology ; Pseudomonas Infections/microbiology ; Pseudomonas Infections/therapy ; Pseudomonas Infections/virology ; Pseudomonas Phages/growth & development ; Pseudomonas Phages/isolation & purification ; Pseudomonas aeruginosa/isolation & purification ; Pseudomonas aeruginosa/physiology ; Pseudomonas aeruginosa/virology ; Respiratory Tract Infections/microbiology ; Respiratory Tract Infections/therapy ; Zebrafish
Chemical Substances	Anti-Bacterial Agents
Language	English
Publishing date	2019-02-06
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-37636-x
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Article ; Online: Pharmacologic inhibition of vacuolar H+ ATPase reduces physiologic and oncogenic Notch signaling.

Kobia, Francis / Duchi, Serena / Deflorian, Gianluca / Vaccari, Thomas

Molecular oncology

2013 Volume 8, Issue 2, Page(s) 207–220

Abstract: Notch signaling in prominently involved in growth regulation in metazoan tissues. Because of this, Notch is often upregulated in cancer and current efforts point to developing drugs that block its activation. Notch receptor endocytosis towards acidic ... ...

Abstract	Notch signaling in prominently involved in growth regulation in metazoan tissues. Because of this, Notch is often upregulated in cancer and current efforts point to developing drugs that block its activation. Notch receptor endocytosis towards acidic compartments is a recently appreciated determinant of signaling activation. Vacuolar H(+) ATPase (V-ATPase) is responsible for acidification of endocytic organelles and mutants in V-ATPase subunit encoding genes in model organisms have been recently shown to display loss of Notch signaling. Here, we show that administration of BafilomycinA1 (BafA1), a highly specific V-ATPase inhibitor decreases Notch signaling during Drosophila and Zebrafish development, and in human cells in culture. In normal breast cells, we find that BafA1 treatment leads to accumulation of Notch in the endo-lysosomal system, and reduces its processing and signaling activity. In Notch-addicted breast cancer cells, BafA1 treatment reduces growth in cells expressing membrane tethered forms of Notch, while sparing cells expressing cytoplasmic forms. In contrast, we find that V-ATPase inhibition reduces growth of leukemia cells, without affecting Notch activatory cleavage. However, consistent with the emerging roles of V-ATPase in controlling multiple signaling pathways, in these cells Akt activation is reduced, as it is also the case in BafA1-treated breast cancer cells. Our data support V-ATPase inhibition as a novel therapeutic approach to counteract tumor growth via signaling pathways regulated at the endo-lysosomal level.
MeSH term(s)	Animals ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Cell Line, Tumor ; Drosophila Proteins/antagonists & inhibitors ; Drosophila Proteins/genetics ; Drosophila Proteins/metabolism ; Drosophila melanogaster ; Enzyme Inhibitors/pharmacology ; Female ; Humans ; Macrolides/pharmacology ; Neoplasm Proteins/antagonists & inhibitors ; Neoplasm Proteins/genetics ; Neoplasm Proteins/metabolism ; Receptors, Notch/antagonists & inhibitors ; Receptors, Notch/genetics ; Receptors, Notch/metabolism ; Signal Transduction ; Vacuolar Proton-Translocating ATPases/genetics ; Vacuolar Proton-Translocating ATPases/metabolism ; Zebrafish/genetics ; Zebrafish/metabolism ; Zebrafish Proteins/genetics ; Zebrafish Proteins/metabolism
Chemical Substances	Drosophila Proteins ; Enzyme Inhibitors ; Macrolides ; N protein, Drosophila ; Neoplasm Proteins ; Receptors, Notch ; Zebrafish Proteins ; bafilomycin A1 (88899-55-2) ; Vacuolar Proton-Translocating ATPases (EC 3.6.1.-)
Language	English
Publishing date	2013-11-18
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2415106-3
ISSN	1878-0261 ; 1574-7891
ISSN (online)	1878-0261
ISSN	1574-7891
DOI	10.1016/j.molonc.2013.11.002
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Article: HDAC8: A Promising Therapeutic Target for Acute Myeloid Leukemia.

Spreafico, Marco / Gruszka, Alicja M / Valli, Debora / Mazzola, Mara / Deflorian, Gianluca / Quintè, Arianna / Totaro, Maria Grazia / Battaglia, Cristina / Alcalay, Myriam / Marozzi, Anna / Pistocchi, Anna

Frontiers in cell and developmental biology

2020 Volume 8, Page(s) 844

Abstract: Histone deacetylase 8 (HDAC8), a class I HDAC that modifies non-histone proteins such as p53, is highly expressed in different hematological neoplasms including a subtype of acute myeloid leukemia (AML) bearing inversion of chromosome 16 [inv(16)]. To ... ...

Abstract	Histone deacetylase 8 (HDAC8), a class I HDAC that modifies non-histone proteins such as p53, is highly expressed in different hematological neoplasms including a subtype of acute myeloid leukemia (AML) bearing inversion of chromosome 16 [inv(16)]. To investigate HDAC8 contribution to hematopoietic stem cell maintenance and myeloid leukemic transformation, we generated a zebrafish model with Hdac8 overexpression and observed an increase in hematopoietic stem/progenitor cells, a phenotype that could be reverted using a specific HDAC8 inhibitor, PCI-34051 (PCI). In addition, we demonstrated that AML cell lines respond differently to PCI treatment: HDAC8 inhibition elicits cytotoxic effect with cell cycle arrest followed by apoptosis in THP-1 cells, and cytostatic effect in HL60 cells that lack p53. A combination of cytarabine, a standard anti-AML chemotherapeutic, with PCI resulted in a synergistic effect in all the cell lines tested. We, then, searched for a mechanism behind cell cycle arrest caused by HDAC8 inhibition in the absence of functional p53 and demonstrated an involvement of the canonical WNT signaling in zebrafish and in cell lines. Together, we provide the evidence for the role of HDAC8 in hematopoietic stem cell differentiation in zebrafish and AML cell lines, suggesting HDAC8 inhibition as a therapeutic target in hematological malignancies. Accordingly, we demonstrated the utility of a highly specific HDAC8 inhibition as a therapeutic strategy in combination with standard chemotherapy.
Language	English
Publishing date	2020-09-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2737824-X
ISSN	2296-634X
ISSN	2296-634X
DOI	10.3389/fcell.2020.00844
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Article ; Online: IRSp53 controls plasma membrane shape and polarized transport at the nascent lumen in epithelial tubules.

Bisi, Sara / Marchesi, Stefano / Rizvi, Abrar / Carra, Davide / Beznoussenko, Galina V / Ferrara, Ines / Deflorian, Gianluca / Mironov, Alexander / Bertalot, Giovanni / Pisati, Federica / Oldani, Amanda / Cattaneo, Angela / Saberamoli, Ghazaleh / Pece, Salvatore / Viale, Giuseppe / Bachi, Angela / Tripodo, Claudio / Scita, Giorgio / Disanza, Andrea

Nature communications

2020 Volume 11, Issue 1, Page(s) 3516

Abstract: It is unclear whether the establishment of apical-basal cell polarity during the generation of epithelial lumens requires molecules acting at the plasma membrane/actin interface. Here, we show that the I-BAR-containing IRSp53 protein controls lumen ... ...

Abstract	It is unclear whether the establishment of apical-basal cell polarity during the generation of epithelial lumens requires molecules acting at the plasma membrane/actin interface. Here, we show that the I-BAR-containing IRSp53 protein controls lumen formation and the positioning of the polarity determinants aPKC and podocalyxin. Molecularly, IRSp53 acts by regulating the localization and activity of the small GTPase RAB35, and by interacting with the actin capping protein EPS8. Using correlative light and electron microscopy, we further show that IRSp53 ensures the shape and continuity of the opposing plasma membrane of two daughter cells, leading to the formation of a single apical lumen. Genetic removal of IRSp53 results in abnormal renal tubulogenesis, with altered tubular polarity and architectural organization. Thus, IRSp53 acts as a membrane curvature-sensing platform for the assembly of multi-protein complexes that control the trafficking of apical determinants and the integrity of the luminal plasma membrane.
MeSH term(s)	Actins/metabolism ; Cell Membrane/metabolism ; Cell Polarity/genetics ; Cell Polarity/physiology ; Epithelial Cells/metabolism ; Female ; Humans ; Morphogenesis/genetics ; Morphogenesis/physiology ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Protein Transport/genetics ; Protein Transport/physiology ; Sialoglycoproteins/genetics ; Sialoglycoproteins/metabolism ; rab GTP-Binding Proteins/genetics ; rab GTP-Binding Proteins/metabolism
Chemical Substances	Actins ; BAIAP2 protein, human ; Nerve Tissue Proteins ; Sialoglycoproteins ; podocalyxin ; RAB35 protein, human (EC 3.6.1.-) ; rab GTP-Binding Proteins (EC 3.6.5.2)
Language	English
Publishing date	2020-07-14
Publishing country	England
Document type	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/s41467-020-17091-x
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Article ; Online: Nucleophosmin leukemogenic mutant activates Wnt signaling during zebrafish development.

Barbieri, Elisa / Deflorian, Gianluca / Pezzimenti, Federica / Valli, Debora / Saia, Marco / Meani, Natalia / Gruszka, Alicja M / Alcalay, Myriam

Oncotarget

2016 Volume 7, Issue 34, Page(s) 55302–55312

Abstract: Nucleophosmin (NPM1) is a ubiquitous multifunctional phosphoprotein with both oncogenic and tumor suppressor functions. Mutations of the NPM1 gene are the most frequent genetic alterations in acute myeloid leukemia (AML) and result in the expression of a ...

Abstract	Nucleophosmin (NPM1) is a ubiquitous multifunctional phosphoprotein with both oncogenic and tumor suppressor functions. Mutations of the NPM1 gene are the most frequent genetic alterations in acute myeloid leukemia (AML) and result in the expression of a mutant protein with aberrant cytoplasmic localization, NPMc+. Although NPMc+ causes myeloproliferation and AML in animal models, its mechanism of action remains largely unknown. Here we report that NPMc+ activates canonical Wnt signaling during the early phases of zebrafish development and determines a Wnt-dependent increase in the number of progenitor cells during primitive hematopoiesis. Coherently, the canonical Wnt pathway is active in AML blasts bearing NPMc+ and depletion of the mutant protein in the patient derived OCI-AML3 cell line leads to a decrease in the levels of active β-catenin and of Wnt target genes. Our results reveal a novel function of NPMc+ and provide insight into the molecular pathogenesis of AML bearing NPM1 mutations.
Language	English
Publishing date	2016-08-23
Publishing country	United States
Document type	Journal Article
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.10878
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Article ; Online: A ligand-insensitive UNC5B splicing isoform regulates angiogenesis by promoting apoptosis.

Nature communications

2021 Volume 12, Issue 1, Page(s) 4872

Abstract: The Netrin-1 receptor UNC5B is an axon guidance regulator that is also expressed in endothelial cells (ECs), where it finely controls developmental and tumor angiogenesis. In the absence of Netrin-1, UNC5B induces apoptosis that is blocked upon Netrin-1 ... ...

Abstract	The Netrin-1 receptor UNC5B is an axon guidance regulator that is also expressed in endothelial cells (ECs), where it finely controls developmental and tumor angiogenesis. In the absence of Netrin-1, UNC5B induces apoptosis that is blocked upon Netrin-1 binding. Here, we identify an UNC5B splicing isoform (called UNC5B-Δ8) expressed exclusively by ECs and generated through exon skipping by NOVA2, an alternative splicing factor regulating vascular development. We show that UNC5B-Δ8 is a constitutively pro-apoptotic splicing isoform insensitive to Netrin-1 and required for specific blood vessel development in an apoptosis-dependent manner. Like NOVA2, UNC5B-Δ8 is aberrantly expressed in colon cancer vasculature where its expression correlates with tumor angiogenesis and poor patient outcome. Collectively, our data identify a mechanism controlling UNC5B's necessary apoptotic function in ECs and suggest that the NOVA2/UNC5B circuit represents a post-transcriptional pathway regulating angiogenesis.
MeSH term(s)	Alternative Splicing ; Animals ; Apoptosis ; Blood Vessels/growth & development ; Colonic Neoplasms/blood supply ; Colonic Neoplasms/metabolism ; Endothelial Cells ; Humans ; Morphogenesis ; Neovascularization, Pathologic/metabolism ; Nerve Tissue Proteins/genetics ; Nerve Tissue Proteins/metabolism ; Netrin Receptors/genetics ; Netrin Receptors/metabolism ; Netrin-1/metabolism ; RNA Isoforms/genetics ; RNA Isoforms/metabolism ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Survival Analysis ; Zebrafish
Chemical Substances	NOVA2 protein, human ; Nerve Tissue Proteins ; Netrin Receptors ; RNA Isoforms ; RNA-Binding Proteins ; Netrin-1 (158651-98-0)
Language	English
Publishing date	2021-08-11
Publishing country	England
Document type	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/s41467-021-24998-6
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Article ; Online: The tumor suppressor PRDM5 regulates Wnt signaling at early stages of zebrafish development.

Meani, Natalia / Pezzimenti, Federica / Deflorian, Gianluca / Mione, Marina / Alcalay, Myriam

PloS one

2009 Volume 4, Issue 1, Page(s) e4273

Abstract: PRDM genes are a family of transcriptional regulators that modulate cellular processes such as differentiation, cell growth and apoptosis. Some family members are involved in tissue or organ maturation, and are differentially expressed in specific phases ...

Abstract	PRDM genes are a family of transcriptional regulators that modulate cellular processes such as differentiation, cell growth and apoptosis. Some family members are involved in tissue or organ maturation, and are differentially expressed in specific phases of embryonic development. PRDM5 is a recently identified family member that functions as a transcriptional repressor and behaves as a putative tumor suppressor in different types of cancer. Using gene expression profiling, we found that transcriptional targets of PRDM5 in human U2OS cells include critical genes involved in developmental processes, and specifically in regulating wnt signaling. We therefore assessed PRDM5 function in vivo by performing loss-of-function and gain-of-function experiments in zebrafish embryos. Depletion of prdm5 resulted in impairment of morphogenetic movements during gastrulation and increased the occurrence of the masterblind phenotype in axin+/- embryos, characterized by the loss of eyes and telencephalon. Overexpression of PRDM5 mRNA had opposite effects on the development of anterior neural structures, and resulted in embryos with a shorter body axis due to posterior truncation, a bigger head and abnormal somites. In situ hybridization experiments aimed at analyzing the integrity of wnt pathways during gastrulation at the level of the prechordal plate revealed inhibition of non canonical PCP wnt signaling in embryos overexpressing PRDM5, and over-activation of wnt/beta-catenin signaling in embryos lacking Prdm5. Our data demonstrate that PRDM5 regulates the expression of components of both canonical and non canonical wnt pathways and negatively modulates wnt signaling in vivo.
MeSH term(s)	Animals ; Cell Line, Tumor ; DNA-Binding Proteins/metabolism ; Gene Expression Profiling ; Gene Expression Regulation ; Genes, Tumor Suppressor ; Humans ; In Situ Hybridization ; Neurons/metabolism ; Oligonucleotide Array Sequence Analysis ; Phenotype ; RNA, Messenger/metabolism ; Signal Transduction ; Transcription Factors/metabolism ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/physiology ; Wnt Proteins/metabolism ; Zebrafish ; Zebrafish Proteins/genetics ; Zebrafish Proteins/physiology
Chemical Substances	DNA-Binding Proteins ; PRDM5 protein, human ; PRDM5 protein, zebrafish ; RNA, Messenger ; Transcription Factors ; Tumor Suppressor Proteins ; Wnt Proteins ; Zebrafish Proteins
Language	English
Publishing date	2009-01-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0004273
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Article ; Online: NIPBL

Mazzola, Mara / Deflorian, Gianluca / Pezzotta, Alex / Ferrari, Laura / Fazio, Grazia / Bresciani, Erica / Saitta, Claudia / Ferrari, Luca / Fumagalli, Monica / Parma, Matteo / Marasca, Federica / Bodega, Beatrice / Riva, Paola / Cotelli, Franco / Biondi, Andrea / Marozzi, Anna / Cazzaniga, Gianni / Pistocchi, Anna

Haematologica

2019 Volume 104, Issue 7, Page(s) 1332–1341

Abstract: The nucleophosmin 1 gene ( ...

Abstract	The nucleophosmin 1 gene (
MeSH term(s)	Adult ; Animals ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; Cell Differentiation ; Chromosomal Proteins, Non-Histone/genetics ; Chromosomal Proteins, Non-Histone/metabolism ; Embryo, Nonmammalian/metabolism ; Embryo, Nonmammalian/pathology ; Gene Expression Regulation, Neoplastic ; Hematopoiesis ; Humans ; Leukemia, Myeloid, Acute/genetics ; Leukemia, Myeloid, Acute/metabolism ; Leukemia, Myeloid, Acute/pathology ; Mutation ; Nuclear Proteins/genetics ; Nucleophosmin ; Phenotype ; Wnt Signaling Pathway ; Zebrafish ; Cohesins
Chemical Substances	Cell Cycle Proteins ; Chromosomal Proteins, Non-Histone ; NIPBL protein, human ; NPM1 protein, human ; Nuclear Proteins ; Nucleophosmin (117896-08-9)
Language	English
Publishing date	2019-01-10
Publishing country	Italy
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2333-4
ISSN	1592-8721 ; 0017-6567 ; 0390-6078
ISSN (online)	1592-8721
ISSN	0017-6567 ; 0390-6078
DOI	10.3324/haematol.2018.200899
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