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Article ; Online: Silencing of Ago-2 Interacting Protein SERBP1 Relieves KCC2 Repression by miR-92 in Neurons.

Barbato, Christian / Frisone, Paola / Braccini, Laura / D'Aguanno, Simona / Pieroni, Luisa / Ciotti, Maria Teresa / Catalanotto, Caterina / Cogoni, Carlo / Ruberti, Francesca

Cells

2022 Volume 11, Issue 6

Abstract: RNA-binding proteins (RBPs) play important roles in modulating miRNA-mediated mRNA target repression. Argonaute2 (Ago2) is an essential component of the RNA-induced silencing complex (RISC) that plays a central role in silencing mechanisms via small non- ... ...

Abstract	RNA-binding proteins (RBPs) play important roles in modulating miRNA-mediated mRNA target repression. Argonaute2 (Ago2) is an essential component of the RNA-induced silencing complex (RISC) that plays a central role in silencing mechanisms via small non-coding RNA molecules known as siRNAs and miRNAs. Small RNAs loaded into Argonaute proteins catalyze endoribonucleolytic cleavage of target RNAs or recruit factors responsible for translational silencing and mRNA target destabilization. In previous studies we have shown that KCC2, a neuronal Cl (-) extruding K (+) Cl (-) co-transporter 2, is regulated by miR-92 in neuronal cells. Searching for Ago2 partners by immunoprecipitation and LC-MS/MS analysis, we isolated among other proteins the Serpine mRNA binding protein 1 (SERBP1) from SH-SY5Y neuroblastoma cells. Exploring the role of SERBP1 in miRNA-mediated gene silencing in SH-SY5Y cells and primary hippocampal neurons, we demonstrated that SERBP1 silencing regulates KCC2 expression through the 3' untranslated region (UTR). In addition, we found that SERBP1 as well as Ago2/miR-92 complex bind to KCC2 3'UTR. Finally, we demonstrated the attenuation of miR-92-mediated repression of KCC2 3'UTR by SERBP1 silencing. These findings advance our knowledge regarding the miR-92-mediated modulation of KCC2 translation in neuronal cells and highlight SERBP1 as a key component of this gene regulation.
MeSH term(s)	3' Untranslated Regions ; Chromatography, Liquid ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neurons/metabolism ; RNA, Messenger/genetics ; RNA-Induced Silencing Complex/genetics ; Symporters/genetics ; Tandem Mass Spectrometry
Chemical Substances	3' Untranslated Regions ; MicroRNAs ; RNA, Messenger ; RNA-Induced Silencing Complex ; Symporters
Language	English
Publishing date	2022-03-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11061052
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Article ; Online: PI3K signaling: a crossroads of metabolic regulation.

Braccini, Laura / Ciraolo, Elisa / Morello, Fulvio / Lu, Xiaoyun / Hirsch, Emilio

Expert review of endocrinology & metabolism

2019 Volume 4, Issue 4, Page(s) 349–357

Abstract: Insulin exerts a fundamental role in glucose metabolism. Several lines of evidence have established PI3Ks as crucial signaling crossroads of metabolic regulation. These kinases play a key role in glucose homeostasis through the generation of lipid ... ...

Abstract	Insulin exerts a fundamental role in glucose metabolism. Several lines of evidence have established PI3Ks as crucial signaling crossroads of metabolic regulation. These kinases play a key role in glucose homeostasis through the generation of lipid secondary messengers upon membrane receptor activation, thus regulating liver gluconeogenesis and glycogen synthesis. While class IA Pl3Kα historically appeared as the major PI3K isoform involved in insulin-mediated glucose metabolism, emerging evidence has demonstrated the contribution of other PI3K isoforms. In this review, we focus on the prototypical insulin receptor-PI3K pathway and on the effects of its impairment on metabolism, insulin sensitivity and the molecular pathophysiology of diabetes mellitus.
Language	English
Publishing date	2019-02-19
Publishing country	England
Document type	Journal Article
ISSN	1744-8417
ISSN (online)	1744-8417
DOI	10.1586/eem.09.19
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Article: PI3K inhibition in inflammation: Toward tailored therapies for specific diseases

Ghigo, Alessandra / Damilano, Federico / Braccini, Laura / Hirsch, Emilio

BioEssays. 2010 Mar., v. 32, no. 3

2010

Abstract: In the past decade, the availability of genetically modified animals has enabled the discovery of interesting roles for phosphatidylinositol 3-kinase-γ (PI3Kγ) and -δ (PI3Kδ) in different cell types orchestrating innate and adaptive immune responses. ... ...

Abstract	In the past decade, the availability of genetically modified animals has enabled the discovery of interesting roles for phosphatidylinositol 3-kinase-γ (PI3Kγ) and -δ (PI3Kδ) in different cell types orchestrating innate and adaptive immune responses. Therefore, these PI3K isoforms appear to be attractive drug targets for the treatment of diseases caused by unrestrained immune reactions. Currently, pharmacological targeting of PI3Kγ and/or PI3Kδ represents one of the most promising challenges for companies interested in the development of novel safe treatments for inflammatory diseases. In this review we provide a general outline of PI3Kγ- and PI3Kδ-specific functions in distinct subsets of inflammatory cells. We also discuss the therapeutic impact of novel compounds targeting PI3Kγ, PI3Kδ or both, in mouse models of autoimmune disorders (systemic lupus erythematosus (SLE) and rheumatoid arthritis), respiratory diseases (allergic asthma and chronic obstructive pulmonary disease) and cardiovascular dysfunctions (atherosclerosis and myocardial infarction).
Language	English
Dates of publication	2010-03
Size	p. 185-196.
Publishing place	Wiley-VCH Verlag
Document type	Article
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.200900150
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Article ; Online: PI3K/AKT signaling pathway and cancer: an updated review.

Martini, Miriam / De Santis, Maria Chiara / Braccini, Laura / Gulluni, Federico / Hirsch, Emilio

Annals of medicine

2014 Volume 46, Issue 6, Page(s) 372–383

Abstract: Despite development of novel agents targeting oncogenic pathways, matching targeted therapies to the genetic status of individual tumors is proving to be a daunting task for clinicians. To improve the clinical efficacy and to reduce the toxic side ... ...

Abstract	Despite development of novel agents targeting oncogenic pathways, matching targeted therapies to the genetic status of individual tumors is proving to be a daunting task for clinicians. To improve the clinical efficacy and to reduce the toxic side effects of treatments, a deep characterization of genetic alterations in different tumors is required. The mutational profile often evidences a gain of function or hyperactivity of phosphoinositide 3-kinases (PI3Ks) in tumors. These enzymes are activated downstream tyrosine kinase receptors (RTKs) and/or G proteins coupled receptors (GPCRs) and, via AKT, are able to induce mammalian target of rapamycin (mTOR) stimulation. Here, we elucidate the impact of class I (p110α, β, γ, and δ) catalytic subunit mutations on AKT-mediated cellular processes that control crucial mechanisms in tumor development. Moreover, the interrelation of PI3K signaling with mTOR, ERK, and RAS pathways will be discussed, exploiting the potential benefits of PI3K signaling inhibitors in clinical use.
MeSH term(s)	Animals ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/physiopathology ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphatidylinositol 3-Kinases/physiology ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; Proto-Oncogene Proteins c-akt/physiology ; Signal Transduction/physiology
Chemical Substances	Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
Language	English
Publishing date	2014-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1004226-x
ISSN	1365-2060 ; 1651-2219 ; 0785-3890 ; 1743-1387
ISSN (online)	1365-2060 ; 1651-2219
ISSN	0785-3890 ; 1743-1387
DOI	10.3109/07853890.2014.912836
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Article ; Online: PI3K inhibition in inflammation: Toward tailored therapies for specific diseases.

Ghigo, Alessandra / Damilano, Federico / Braccini, Laura / Hirsch, Emilio

BioEssays : news and reviews in molecular, cellular and developmental biology

2009 Volume 32, Issue 3, Page(s) 185–196

Abstract: In the past decade, the availability of genetically modified animals has enabled the discovery of interesting roles for phosphatidylinositol 3-kinase-gamma (PI3Kgamma) and -delta (PI3Kdelta) in different cell types orchestrating innate and adaptive ... ...

Abstract	In the past decade, the availability of genetically modified animals has enabled the discovery of interesting roles for phosphatidylinositol 3-kinase-gamma (PI3Kgamma) and -delta (PI3Kdelta) in different cell types orchestrating innate and adaptive immune responses. Therefore, these PI3K isoforms appear to be attractive drug targets for the treatment of diseases caused by unrestrained immune reactions. Currently, pharmacological targeting of PI3Kgamma and/or PI3Kdelta represents one of the most promising challenges for companies interested in the development of novel safe treatments for inflammatory diseases. In this review we provide a general outline of PI3Kgamma- and PI3Kdelta-specific functions in distinct subsets of inflammatory cells. We also discuss the therapeutic impact of novel compounds targeting PI3Kgamma, PI3Kdelta or both, in mouse models of autoimmune disorders (systemic lupus erythematosus (SLE) and rheumatoid arthritis), respiratory diseases (allergic asthma and chronic obstructive pulmonary disease) and cardiovascular dysfunctions (atherosclerosis and myocardial infarction).
MeSH term(s)	Animals ; Asthma/drug therapy ; Autoimmune Diseases/drug therapy ; B-Lymphocytes/immunology ; Cardiovascular Diseases/drug therapy ; Chemotaxis, Leukocyte/physiology ; Eosinophils/immunology ; Humans ; Immune System/enzymology ; Inflammation/drug therapy ; Inflammation/enzymology ; Leukocytes/immunology ; Mast Cells/immunology ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoinositide-3 Kinase Inhibitors ; Protein Subunits/antagonists & inhibitors ; Protein Subunits/metabolism ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Signal Transduction/immunology ; T-Lymphocytes/immunology
Chemical Substances	Phosphoinositide-3 Kinase Inhibitors ; Protein Subunits
Language	English
Publishing date	2009-10-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	50140-2
ISSN	1521-1878 ; 0265-9247
ISSN (online)	1521-1878
ISSN	0265-9247
DOI	10.1002/bies.200900150
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Article: Twice upon a time: PI3K's secret double life exposed.

Hirsch, Emilio / Braccini, Laura / Ciraolo, Elisa / Morello, Fulvio / Perino, Alessia

Trends in biochemical sciences

2009 Volume 34, Issue 5, Page(s) 244–248

Abstract: Class I phosphoinositide 3-kinases (PI3Ks) are heterodimeric enzymes involved in signal transduction triggered by growth factors and G-protein-coupled receptors. The catalytic function of PI3Ks is well known to promote a wide variety of biological ... ...

Abstract	Class I phosphoinositide 3-kinases (PI3Ks) are heterodimeric enzymes involved in signal transduction triggered by growth factors and G-protein-coupled receptors. The catalytic function of PI3Ks is well known to promote a wide variety of biological processes, including proliferation, survival and migration, but a new layer of complexity in the function of PI3Ks has recently emerged, indicating that these proteins function not only as kinases but also as scaffold proteins. Knockout mice that lack PI3K protein expression show a different phenotype from knock-in mice expressing PI3K mutants that have lost their kinase activity, providing evidence for this novel role of PI3Ks. We will discuss such findings, highlighting the crucial scaffold function of PI3Kgamma in cAMP homeostasis and PI3Kbeta in receptor recycling.
MeSH term(s)	Animals ; Class Ib Phosphatidylinositol 3-Kinase ; Cyclic AMP/metabolism ; Humans ; Isoenzymes/classification ; Isoenzymes/genetics ; Isoenzymes/physiology ; Models, Biological ; Phosphatidylinositol 3-Kinases/classification ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/physiology ; Phylogeny ; Signal Transduction/genetics ; Signal Transduction/physiology
Chemical Substances	Isoenzymes ; Cyclic AMP (E0399OZS9N) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Class Ib Phosphatidylinositol 3-Kinase (EC 2.7.1.137) ; PIK3CG protein, human (EC 2.7.1.137) ; Pik3cg protein, mouse (EC 2.7.1.153)
Language	English
Publishing date	2009-04-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	194216-5
ISSN	1362-4326 ; 0968-0004 ; 0376-5067
ISSN (online)	1362-4326
ISSN	0968-0004 ; 0376-5067
DOI	10.1016/j.tibs.2009.02.003
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Article: L'ADHD e l'intervento multimodale.

Rea, Monica / Braccini, Laura / Laviola, Giovanni / Ferri, Rosa

Annali dell'Istituto superiore di sanita

2006 Volume 42, Issue 2, Page(s) 231–245

Abstract: During the year 2003, the National Register of the Attention deficit hyperactivity disorder (ADHD) has been implemented in Italy. It was commissioned by the Ministry of Health to the Istituto Superiore di Sanità, which is its leading technical and ... ...

Title translation	ADHD and multimodal intervention.
Abstract	During the year 2003, the National Register of the Attention deficit hyperactivity disorder (ADHD) has been implemented in Italy. It was commissioned by the Ministry of Health to the Istituto Superiore di Sanità, which is its leading technical and scientific body, with the aim to set up a sound database gathering detailed information on the prescription of Ritalin at the national level. The latter represents the most diffused elective drug treatment for such an early-onset neuropsychiatric syndrome. To this aim, the more prevalent theories on the pathogenesis of ADHD and the debate on therapy are reviewed and discussed. This paper is aimed at emphasizing that this kind of systematic data gathering of such a Register has not to be meant an unconditional approval of a therapeutical approach based on drug therapy only. Pharmacological therapies may or may not be included within the frame of a multimodal complex treatment plan which should also rely on psychological intervention.
MeSH term(s)	Attention Deficit Disorder with Hyperactivity/diagnosis ; Attention Deficit Disorder with Hyperactivity/drug therapy ; Attention Deficit Disorder with Hyperactivity/etiology ; Attention Deficit Disorder with Hyperactivity/therapy ; Combined Modality Therapy ; Humans ; Psychotherapy
Language	Italian
Publishing date	2006
Publishing country	Italy
Document type	English Abstract ; Journal Article
ZDB-ID	950344-4
ISSN	0021-2571
ISSN	0021-2571
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Article: Ago1 and Ago2 differentially affect cell proliferation, motility and apoptosis when overexpressed in SH-SY5Y neuroblastoma cells

Parisi, Chiara / Giorgi, Corinna / Batassa, Enrico Maria / Braccini, Laura / Maresca, Giovanna / D’agnano, Igea / Caputo, Viviana / Salvatore, Annamaria / Pietrolati, Flavia / Cogoni, Carlo / Catalanotto, Caterina

FEBS letters. 2011 Oct. 3, v. 585, no. 19

2011

Abstract: Argonaute are a conserved class of proteins central to the microRNA pathway. We have highlighted a novel and non-redundant function of Ago1 versus Ago2; the two core factors of the miRNA-associated RISC complex. Stable overexpression of Ago1 in ... ...

Abstract	Argonaute are a conserved class of proteins central to the microRNA pathway. We have highlighted a novel and non-redundant function of Ago1 versus Ago2; the two core factors of the miRNA-associated RISC complex. Stable overexpression of Ago1 in neuroblastoma cells causes the cell cycle to slow down, a decrease in cellular motility and a stronger apoptotic response upon UV irradiation. These effects, together with a significant increase in p53 levels, suggest that Ago1 may act as a tumor-suppressor factor, a function also supported by GEO Profiles microarrays that inversely correlate Ago1 expression levels with cell proliferation rates.
Keywords	apoptosis ; cell cycle ; cell movement ; cell proliferation ; microRNA ; microarray technology ; proteins ; ultraviolet radiation
Language	English
Dates of publication	2011-1003
Size	p. 2965-2971.
Publishing place	Elsevier B.V.
Document type	Article
ZDB-ID	212746-5
ISSN	1873-3468 ; 0014-5793
ISSN (online)	1873-3468
ISSN	0014-5793
DOI	10.1016/j.febslet.2011.08.003
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Article ; Online: PI3K-C2γ is a Rab5 effector selectively controlling endosomal Akt2 activation downstream of insulin signalling.

Braccini, Laura / Ciraolo, Elisa / Campa, Carlo C / Perino, Alessia / Longo, Dario L / Tibolla, Gianpaolo / Pregnolato, Marco / Cao, Yanyan / Tassone, Beatrice / Damilano, Federico / Laffargue, Muriel / Calautti, Enzo / Falasca, Marco / Norata, Giuseppe D / Backer, Jonathan M / Hirsch, Emilio

Nature communications

2015 Volume 6, Page(s) 7400

Abstract: In the liver, insulin-mediated activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway is at the core of metabolic control. Multiple PI3K and Akt isoenzymes are found in hepatocytes and whether isoform-selective interplays exist is currently ... ...

Abstract	In the liver, insulin-mediated activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway is at the core of metabolic control. Multiple PI3K and Akt isoenzymes are found in hepatocytes and whether isoform-selective interplays exist is currently unclear. Here we report that insulin signalling triggers the association of the liver-specific class II PI3K isoform γ (PI3K-C2γ) with Rab5-GTP, and its recruitment to Rab5-positive early endosomes. In these vesicles, PI3K-C2γ produces a phosphatidylinositol-3,4-bisphosphate pool specifically required for delayed and sustained endosomal Akt2 stimulation. Accordingly, loss of PI3K-C2γ does not affect insulin-dependent Akt1 activation as well as S6K and FoxO1-3 phosphorylation, but selectively reduces Akt2 activation, which specifically inhibits glycogen synthase activity. As a consequence, PI3K-C2γ-deficient mice display severely reduced liver accumulation of glycogen and develop hyperlipidemia, adiposity as well as insulin resistance with age or after consumption of a high-fat diet. Our data indicate PI3K-C2γ supports an isoenzyme-specific forking of insulin-mediated signal transduction to an endosomal pool of Akt2, required for glucose homeostasis.
MeSH term(s)	Adiposity/genetics ; Aging/genetics ; Animals ; Diet, High-Fat ; Endosomes/metabolism ; Forkhead Transcription Factors/metabolism ; Glucose/metabolism ; Glycogen/metabolism ; Glycogen Synthase/metabolism ; Hepatocytes/metabolism ; Homeostasis ; Hyperlipidemias/genetics ; Insulin/metabolism ; Insulin Resistance/genetics ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Phosphatidylinositol 3-Kinases/genetics ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphatidylinositol Phosphates/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Ribosomal Protein S6 Kinases/metabolism ; Signal Transduction ; rab5 GTP-Binding Proteins/metabolism
Chemical Substances	Forkhead Transcription Factors ; Insulin ; Phosphatidylinositol Phosphates ; phosphatidylinositol 3,4-diphosphate ; Glycogen (9005-79-2) ; Glycogen Synthase (EC 2.4.1.11) ; Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Pik3c2g protein, mouse (EC 2.7.1.137) ; Akt1 protein, mouse (EC 2.7.11.1) ; Akt2 protein, mouse (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Ribosomal Protein S6 Kinases (EC 2.7.11.1) ; rab5 GTP-Binding Proteins (EC 3.6.5.2) ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2015-06-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; 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/ncomms8400
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Article ; Online: The post-transcriptional gene silencing machinery functions independently of DNA methylation to repress a LINE1-like retrotransposon in Neurospora crassa.

Nolan, Tony / Braccini, Laura / Azzalin, Gianluca / De Toni, Arianna / Macino, Giuseppe / Cogoni, Carlo

Nucleic acids research

2005 Volume 33, Issue 5, Page(s) 1564–1573

Abstract: Post-transcriptional gene silencing (PTGS) involving small interfering RNA (siRNA)-directed degradation of RNA transcripts and transcriptional silencing via DNA methylation have each been proposed as mechanisms of genome defence against invading nucleic ... ...

Abstract	Post-transcriptional gene silencing (PTGS) involving small interfering RNA (siRNA)-directed degradation of RNA transcripts and transcriptional silencing via DNA methylation have each been proposed as mechanisms of genome defence against invading nucleic acids, such as transposons and viruses. Furthermore, recent data from plants indicates that many transposons are silenced via a combination of the two mechanisms, and siRNAs can direct methylation of transposon sequences. We investigated the contribution of DNA methylation and the PTGS pathway to transposon control in the filamentous fungus Neurospora crassa. We found that repression of the LINE1-like transposon, Tad, requires the Argonaute protein QDE2 and Dicer, each of which are required for transgene-induced PTGS (quelling) in N.crassa. Interestingly, unlike quelling, the RNA-dependent RNA polymerase QDE1 and the RecQ DNA helicase QDE3 were not required for Tad control, suggesting the existence of specialized silencing pathways for diverse kinds of repetitive elements. In contrast, Tad elements were not significantly methylated and the DIM2 DNA methyltransferase, responsible for all known DNA methylation in Neurospora, had no effect on Tad control. Thus, an RNAi-related transposon silencing mechanism operates during the vegetative phase of N.crassa that is independent of DNA methylation, highlighting a major difference between this organism and other methylation-proficient species.
MeSH term(s)	DNA Methylation ; Gene Expression Regulation, Fungal ; Long Interspersed Nucleotide Elements ; Mutation ; Neurospora crassa/genetics ; Neurospora crassa/metabolism ; RNA Interference ; RNA, Small Interfering/biosynthesis ; Ribonuclease III/genetics
Chemical Substances	RNA, Small Interfering ; Ribonuclease III (EC 3.1.26.3)
Language	English
Publishing date	2005
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2205588-5
ISSN	1362-4962 ; 1746-8272 ; 0305-1048 ; 0261-3166
ISSN (online)	1362-4962 ; 1746-8272
ISSN	0305-1048 ; 0261-3166
DOI	10.1093/nar/gki300
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