Affinage

NOP56

Nucleolar protein 56 · UniProt O00567

Length
594 aa
Mass
66.0 kDa
Annotated
2026-06-10
38 papers in source corpus 18 papers cited in narrative 19 extracted findings
Cross-family judge vs UniProt: Affinage preferred faithfulness: 7/7 claims corpus-supported (100%)

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

NOP56 is a core scaffolding subunit of box C/D small nucleolar ribonucleoprotein (snoRNP) complexes that guide 2'-O-methylation of rRNA (PMID:12020815, PMID:16601205). It bridges the methyltransferase fibrillarin to the snoRNP through its N-terminal domain, which mediates an exceptionally stable, RNA-independent interaction with fibrillarin's alpha-helix domain (PMID:19331828, PMID:22496443); crystallographic work on archaeal and eukaryotic complexes shows that this NTD interface recruits and positions fibrillarin, and that eukaryotic NOP56 engages fibrillarin through a protein-protein interface distinct from the archaeal arrangement (PMID:33483369, PMID:17617422). Beyond scaffolding, NOP56 contributes directly to catalysis: its coiled-coil domain is dispensable for assembly but required for sRNP-guided methylation, NOP56/fibrillarin and NOP56 self-dimerization are mutually exclusive, and the protein contacts the target RNA substrate (PMID:16601205, PMID:22496443). NOP56 production is autoregulated by a feedback loop in which excess snoRNP core proteins drive the intron-hosted snoRNA SNORD86 to redirect NOP56 pre-mRNA splicing toward a nonsense-mediated decay fate, coupling core protein availability to NOP56 levels (PMID:30220559). The gene is essential for vertebrate CNS development, as nop56 loss in zebrafish causes cerebellar agenesis and neurodegeneration (PMID:36009362). In cancer, NOP56 acts downstream of Myc as a rate-limiting effector of ribosome biogenesis and transformation (PMID:24013231), and NOP56 depletion in KRAS-mutant cells raises ROS and confers synthetic lethality with mTOR inhibition (PMID:35039048). Pathogenic intronic GGCCTG hexanucleotide repeat expansions in NOP56 cause spinocerebellar ataxia type 36 (SCA36) via RNA gain-of-function, with RNA foci that sequester SRSF2 (PMID:21683323) and repeat-associated non-AUG (RAN) translation producing dipeptide repeat proteins (PMID:32375063, PMID:40015643).

Mechanistic history

Synthesis pass · year-by-year structured walk · 13 steps
  1. 2002 Medium

    Established that NOP56 is a constitutive component of box C/D snoRNPs, defining its baseline role in the 2'-O-methylation machinery rather than in snoRNA stabilization.

    Evidence cDNA cloning, co-immunoprecipitation with box C/D snoRNPs, 5' end mapping and polysome analysis in Xenopus laevis

    PMID:12020815

    Open questions at the time
    • Did not resolve which domains mediate snoRNP incorporation
    • No structural or catalytic role defined
  2. 2006 High

    Separated NOP56 assembly from catalysis by showing the coiled-coil domain is dispensable for binding but required for methylation, and that self- and fibrillarin-dimerization are mutually exclusive.

    Evidence Site-directed mutagenesis, pull-down, in vitro methylation assays and nuclease probing of archaeal box C/D sRNPs

    PMID:16601205

    Open questions at the time
    • Archaeal system; eukaryotic coiled-coil requirement not directly tested
    • Mechanism by which coiled-coil shapes RNP structure not resolved
  3. 2007 High

    Resolved the architecture and conformational flexibility of the Nop56/58-fibrillarin complex, explaining how hinge motion could position catalytic sites at bipartite guide RNA targets.

    Evidence X-ray crystallography of Pyrococcus furiosus complex bound to SAM with normal-mode analysis

    PMID:17617422

    Open questions at the time
    • Archaeal; eukaryotic dynamics not captured
    • Catalytic positioning inferred, not directly visualized in turnover
  4. 2009 Medium

    Demonstrated that NOP56 and fibrillarin interact directly in vivo before snoRNP assembly via fibrillarin's alpha-helix domain, independent of RNA, establishing the pre-assembly scaffolding step.

    Evidence Relocalization/affinity-tag delocalization with co-immunoprecipitation and localization analysis in mammalian cells

    PMID:19331828

    Open questions at the time
    • Single lab
    • NOP56 domain mediating the interaction not mapped here
  5. 2012 High

    Revealed that the NOP56 N-terminal domain not only binds fibrillarin extremely stably but contributes directly to methyltransferase activity and contacts the substrate RNA, extending its role beyond passive scaffolding.

    Evidence Mutagenesis, in vitro methylation, denaturation, RNA cross-linking and 1.7 Å crystallography of archaeal NTD

    PMID:22496443

    Open questions at the time
    • Archaeal NTD; eukaryotic NTD catalytic contribution inferred
    • Exact catalytic step NOP56 influences not defined
  6. 2011 Medium

    Identified the molecular basis of SCA36 as an intronic GGCCTG repeat expansion acting through RNA gain-of-function, with foci that sequester SRSF2.

    Evidence Genetic linkage, FISH for RNA foci and gel-shift assay in patient lymphoblastoid cells

    PMID:21683323

    Open questions at the time
    • Functional consequence of SRSF2 sequestration on splicing not established
    • Contribution of foci versus protein loss to disease unresolved
  7. 2013 Medium

    Placed NOP56 downstream of Myc as a necessary, rate-limiting effector of Myc-driven transformation, connecting ribosome biogenesis machinery to oncogenesis.

    Evidence Expression profiling, RNAi/overexpression with transformation and in vivo tumor growth assays

    PMID:24013231

    Open questions at the time
    • Whether transformation requires snoRNP/methylation activity not tested
    • Direct Myc regulation of NOP56 not dissected here
  8. 2018 High

    Defined the autoregulatory circuit controlling NOP56 abundance, showing the intronic snoRNA SNORD86 senses snoRNP core protein excess and redirects splicing toward NMD.

    Evidence Alternative splicing analysis, NMD reporter assays, RNA structure probing and snoRNP protein perturbation in human cells

    PMID:30220559

    Open questions at the time
    • Which core proteins trigger the conformational switch not fully enumerated
    • Physiological conditions activating the loop in vivo unclear
  9. 2020 Medium

    Showed SCA36 repeats undergo RAN translation producing soluble dipeptide repeat proteins, distinguishing its molecular pathology from aggregation-prone c9ALS/FTD.

    Evidence RAN translation detection and DPR immunoassays in patient tissue with solubility profiling

    PMID:32375063

    Open questions at the time
    • Pathogenic contribution of DPRs versus RNA foci not quantified
    • No model linking DPRs to neurodegeneration
  10. 2021 High

    Solved the eukaryotic Nop1/fibrillarin-Nop56 NTD structure, establishing that eukaryotic recruitment occurs through a protein interface distinct from archaea.

    Evidence X-ray crystallography of S. cerevisiae complex with comparison to archaeal structures

    PMID:33483369

    Open questions at the time
    • Full eukaryotic snoRNP not crystallized
    • Catalytic mechanism in eukaryotes not directly tested
  11. 2022 Medium

    Linked NOP56 to redox and growth-signaling control in cancer, revealing synthetic lethality between NOP56 depletion and mTOR inhibition in KRAS-mutant cells.

    Evidence RNAi/CRISPR knockdown/knockout, ROS flow cytometry, inhibitor screen and xenografts

    PMID:35039048

    Open questions at the time
    • Whether ROS effect depends on rRNA methylation not resolved
    • Direct molecular target connecting NOP56 to ROS unknown
  12. 2022 Medium

    Established NOP56 as essential for vertebrate CNS development, with loss causing cerebellar agenesis and neurodegeneration in zebrafish.

    Evidence Zebrafish loss-of-function mutant with microscopy, apoptosis assays and gene expression analysis

    PMID:36009362

    Open questions at the time
    • Cell-autonomous versus systemic basis of neurodegeneration not separated
    • Link to SCA36 disease mechanism not established
  13. 2025 Medium

    Detailed the cap-dependent, multi-frame initiation of SCA36 RAN translation, showing near-cognate start usage and repeat-length-dependent enhancement.

    Evidence Cell-free translation with reporter constructs and mutagenesis

    PMID:40015643

    Open questions at the time
    • In vivo relevance of frameshifting not confirmed
    • Cellular factors regulating initiation not identified

Open questions

Synthesis pass · forward-looking unresolved questions
  • How NOP56's core snoRNP/rRNA-methylation function mechanistically connects to its diverse cancer signaling roles (Myc, mTOR/ROS, SIRT1/p300-p53) and to SCA36 neuronal vulnerability remains unresolved.
  • Cancer signaling interactions (PI3K/AKT, SIRT1/p300) rest on single Co-IP studies without reciprocal/structural validation
  • Whether disease phenotypes arise from snoRNP loss-of-function versus repeat RNA/DPR gain-of-function not disentangled
  • No structure of the intact human box C/D snoRNP

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060090 molecular adaptor activity 3 GO:0003723 RNA binding 2 GO:0140098 catalytic activity, acting on RNA 2
Localization
GO:0005730 nucleolus 2
Pathway
R-HSA-8953854 Metabolism of RNA 3 R-HSA-1643685 Disease 2
Partners
FBLSNORD86SRSF2
Complex memberships
box C/D snoRNP

Evidence

Reading pass · 19 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
2018 The intron-hosted box C/D snoRNA snoRD86 acts in cis as a sensor controlling NOP56 levels: excess snoRNP core proteins cause snoRD86 to adopt alternative RNP conformations that dictate usage of nearby alternative splice donors in the NOP56 pre-mRNA, triggering generation of a cytoplasmic snoRD86-containing NOP56-derived lncRNA via the nonsense-mediated decay pathway — a feedback mechanism that couples snoRNP core protein availability to NOP56 production. Alternative splicing analysis, NMD reporter assays, RNA structure probing, overexpression/depletion of snoRNP core proteins with functional readouts in human cells Molecular Cell High 30220559
2009 Fibrillarin and NOP56 directly interact in vivo prior to assembly into box C/D snoRNPs; this interaction requires the alpha-helix domain of fibrillarin (not the GAR or RNA-binding domain) and does not require RNA. Disrupting either protein's localization impairs their association with box C/D snoRNPs. Relocalization/affinity-tag delocalization of core box C/D proteins followed by co-immunoprecipitation and localization analysis in mammalian cells Experimental Cell Research Medium 19331828
2021 High-resolution crystal structure of eukaryotic Nop1 (fibrillarin) from S. cerevisiae bound to the amino-terminal domain of Nop56 was solved; the interaction interface differs substantially from the archaeal orthologs, demonstrating that eukaryotic Nop56 recruits the methyltransferase to the box C/D RNP through a protein-protein interface distinct from that in archaea. X-ray crystallography with functional comparison to archaeal structures RNA High 33483369
2007 Crystal structure of archaeal Nop56/58-fibrillarin complex from Pyrococcus furiosus (at 2.7 Å) bound to S-adenosyl-L-methionine confirmed the generality of the bipartite/symmetric dimer arrangement; the distinct conformation of Nop56/58 compared to the Archaeoglobus fulgidus structure revealed flexibility via hinge motion, repositioning fibrillarin catalytic sites, suggesting simultaneous positioning of two catalytic sites at two target sites of a bipartite guide RNA. X-ray crystallography and computational normal mode analysis Journal of Molecular Biology High 17617422
2006 In archaeal box C/D sRNPs, the coiled-coil domain of Nop56/58 is dispensable for core protein binding and sRNP assembly but is required for sRNP-guided nucleotide 2'-O-methylation; Nop56/58 self-dimerization and Nop56/58-fibrillarin dimerization are mutually exclusive interactions; deletion of the coiled-coil domain disrupts RNP structure essential for methylation without preventing assembly. Site-directed mutagenesis, protein pull-down assays, in vitro methylation assays, nuclease probing of sRNP structure RNA High 16601205
2012 The N-terminal domain (NTD) of archaeal Nop56/58 mediates an exceptionally stable interaction with fibrillarin; mutations that did not affect fibrillarin binding or sRNP assembly still disrupted sRNP-guided nucleotide modification, revealing a direct role for Nop56/58 in methyltransferase activity beyond scaffolding. Cross-linking confirmed Nop56/58 contacts the target RNA substrate. The NTD crystal structure (1.7 Å) showed conservation despite low sequence identity among archaeal homologs. Site-directed mutagenesis, in vitro methylation assay, chemical and thermal denaturation, RNA cross-linking, X-ray crystallography Journal of Biological Chemistry High 22496443
2002 Xenopus laevis NOP56 (XNop56p) was identified as a common component of X. laevis box C/D snoRNPs; it is not essential for snoRNA stability; its transcript initiates with a pyrimidine tract and contains an intronic snoRNA, but it is not translationally regulated in a growth-dependent manner (i.e., it is not a TOP gene). cDNA cloning, co-immunoprecipitation with box C/D snoRNPs, 5' end mapping, polysome analysis Biochimica et Biophysica Acta Medium 12020815
2013 NOP56 (Nol5a) was identified as a gene hyperactivated by Burkitt's lymphoma-associated Myc mutants and was shown to be necessary for Myc-induced cell transformation; Nol5a/NOP56 enhances wild-type Myc-induced cell transformation and increases the size of Myc-induced tumors, placing NOP56 downstream of Myc as a rate-limiting effector for transformation. Gene expression profiling, RNAi knockdown/overexpression with transformation assays and in vivo tumor growth assays Oncogene Medium 24013231
2022 NOP56 depletion in KRAS-mutant lung cancer cells increases ROS levels and creates synthetic lethality with mTOR inhibition; mechanistically, cells with reduced NOP56 rely on mTOR signaling to balance oxidative stress, and IRE1α-mediated unfolded protein response activates mTOR through p38 MAPK in this context. Co-targeting NOP56 and mTOR profoundly enhances tumor cell death in vitro and in vivo. RNAi/shRNA knockdown, CRISPR/Cas9 knockout, flow cytometry for ROS, Western blot, chemical inhibitor screen, xenograft models Journal of Experimental & Clinical Cancer Research Medium 35039048
2022 Loss-of-function of nop56 in zebrafish causes severe neurodegeneration characterized by absence of cerebellum, reduced spinal cord neurons, high CNS apoptosis, and impaired movement, with disrupted expression of genes related to the C/D box complex, balance, and CNS development, establishing NOP56 as essential for vertebrate CNS development and function. Zebrafish loss-of-function mutant, fluorescence microscopy, apoptosis assays, gene expression analysis Biomedicines Medium 36009362
2011 Expansion of an intronic GGCCTG hexanucleotide repeat in NOP56 causes SCA36; RNA foci form in lymphoblastoid cells from affected subjects, and the expanded (GGCCUG)n RNA binds the RNA-binding protein SRSF2 (but not CUG6), as shown by gel-shift assay, indicating RNA gain-of-function toxicity. Genetic linkage analysis, FISH for RNA foci, gel-shift assay, segregation analysis American Journal of Human Genetics Medium 21683323
2020 The intronic GGCCTG repeat expansion in NOP56 undergoes repeat-associated non-AUG (RAN) translation to produce dipeptide repeat proteins (DPRs) including poly(GP) and poly(PR); poly(GP) in SCA36 is produced via canonical AUG-mediated translation from intron-retained repeat RNAs and exists as a soluble species without TDP-43 pathology, in contrast to c9ALS/FTD where chimeric DPR species cause aggregation. RAN translation detection in patient tissue, immunoassays for DPR proteins, comparison of solubility profiles Neuron Medium 32375063
2025 NOP56 intron 1 GGCCTG repeat RAN translation occurs in all reading frames of the sense strand; translation initiates in a 5'-cap-dependent manner from near-cognate start codons upstream of the repeat in each frame; longer GGCCTG repeats enhance RAN translation; and a frameshift occurs within the GGCCUG repeat during translation. Cell-free translation systems with reporter constructs and mutagenesis Journal of Biological Chemistry Medium 40015643
2013 NOP56 protein levels progressively decrease selectively in large motor neurons of lumbar and cervical spinal cord in SOD1-G93A ALS model mice from the early symptomatic stage, preceding reductions in TDP-43 and FUS, implicating early NOP56 loss in motor neuron degeneration. Immunohistochemistry and protein expression analysis across disease stages in transgenic ALS mice Neurological Research Low 23582672
2026 NOP56 interacts with fibrillarin (FBL) and activates the PI3K/AKT/CREB signaling pathway in hepatocellular carcinoma; NOP56 knockdown lowers FBL levels and suppresses PI3K/AKT/CREB activity, while FBL overexpression partially rescues apoptotic effects of NOP56 silencing. Co-immunoprecipitation, Western blot, RNAi knockdown, overexpression rescue, xenograft models Frontiers in Oncology Low 41568368
2026 NOP56 promotes p53 degradation in colorectal cancer through suppression of SIRT1 and activation of p300; NOP56 depletion increases p53 stability and acetylation via the SIRT1/p300 axis, as supported by evidence of direct interaction and colocalization of NOP56 with SIRT1 and p300. RNAi knockdown, co-immunoprecipitation, colocalization, Western blot, xenograft models International Journal of Biological Sciences Low 42157947
2026 NOP56 activates MYC signaling by regulating IRES-dependent translation, and MYC in turn transcriptionally upregulates NOP56 expression, creating a positive feedback loop that enhances ribosome biogenesis and drives NSCLC progression; promoter hypomethylation also contributes to NOP56 upregulation. Luciferase reporter assay for IRES translation, chromatin immunoprecipitation, bisulfite DNA sequencing, RNA sequencing, functional overexpression/knockdown assays Cancers Low 41827688
2021 In miiuy croaker, NOP56 negatively regulates MyD88-mediated NF-κB signaling; the NOSIC domain of NOP56 is responsible for suppressing MyD88 protein expression; NOP56 overexpression inhibits MyD88 protein levels while NOP56 siRNA knockdown increases them. Overexpression, siRNA knockdown, Western blot, domain deletion analysis in fish cells Fish & Shellfish Immunology Low 34774735
2025 In a preprint, NOP56 expression was downregulated by unfolded protein response (UPR) alongside FBL and NHP2L1; reduced C/D box snoRNP function during UPR alters rRNA 2'-O-methylation and translational fidelity including effects on nonsense suppression, frameshifts, ribosome pausing, and IRES-dependent translation initiation. qRT-PCR for expression, FBL knockdown with rRNA methylation assay and translational fidelity reporter assays bioRxivpreprint Low

Source papers

Stage 0 corpus · 38 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Expansion of intronic GGCCTG hexanucleotide repeat in NOP56 causes SCA36, a type of spinocerebellar ataxia accompanied by motor neuron involvement. American journal of human genetics 216 21683323
2012 Clinical features of SCA36: a novel spinocerebellar ataxia with motor neuron involvement (Asidan). Neurology 73 22744658
2018 Box C/D snoRNP Autoregulation by a cis-Acting snoRNA in the NOP56 Pre-mRNA. Molecular cell 67 30220559
2020 Chimeric Peptide Species Contribute to Divergent Dipeptide Repeat Pathology in c9ALS/FTD and SCA36. Neuron 60 32375063
2013 Burkitt's lymphoma-associated c-Myc mutations converge on a dramatically altered target gene response and implicate Nol5a/Nop56 in oncogenesis. Oncogene 44 24013231
2020 Hexanucleotide Repeat Expansions in c9FTD/ALS and SCA36 Confer Selective Patterns of Neurodegeneration In Vivo. Cell reports 38 32375043
2007 Alternative conformations of the archaeal Nop56/58-fibrillarin complex imply flexibility in box C/D RNPs. Journal of molecular biology 30 17617422
2006 The coiled-coil domain of the Nop56/58 core protein is dispensable for sRNP assembly but is critical for archaeal box C/D sRNP-guided nucleotide methylation. RNA (New York, N.Y.) 29 16601205
2022 Metabolic synthetic lethality by targeting NOP56 and mTOR in KRAS-mutant lung cancer. Journal of experimental & clinical cancer research : CR 25 35039048
2018 Structural and Dynamical Characterization of DNA and RNA Quadruplexes Obtained from the GGGGCC and GGGCCT Hexanucleotide Repeats Associated with C9FTD/ALS and SCA36 Diseases. ACS chemical neuroscience 24 29281254
2018 Frequency of SCA8, SCA10, SCA12, SCA36, FXTAS and C9orf72 repeat expansions in SCA patients negative for the most common SCA subtypes. BMC neurology 23 29316893
2009 Fibrillarin and Nop56 interact before being co-assembled in box C/D snoRNPs. Experimental cell research 23 19331828
2019 Suppression of the yeast elongation factor Spt4 ortholog reduces expanded SCA36 GGCCUG repeat aggregation and cytotoxicity. Brain research 17 30610877
2018 Nucleolar Division in the Promastigote Stage of Leishmania major Parasite: A Nop56 Point of View. BioMed research international 12 30406129
2015 Spinocerebellar ataxia 36 (SCA36): «Costa da Morte ataxia». Neurologia (Barcelona, Spain) 12 25593102
2020 Cerebellar Cognitive Affective Syndrome in Costa da Morte Ataxia (SCA36). Cerebellum (London, England) 11 32270466
2023 The roles of NOP56 in cancer and SCA36. Pathology oncology research : POR 10 36741964
2022 A nop56 Zebrafish Loss-of-Function Model Exhibits a Severe Neurodegenerative Phenotype. Biomedicines 10 36009362
2021 Repeats expansions in ATXN2, NOP56, NIPA1 and ATXN1 are not associated with ALS in Africans. IBRO neuroscience reports 10 34179866
2013 Early and selective reduction of NOP56 (Asidan) and RNA processing proteins in the motor neuron of ALS model mice. Neurological research 10 23582672
2012 Structurally conserved Nop56/58 N-terminal domain facilitates archaeal box C/D ribonucleoprotein-guided methyltransferase activity. The Journal of biological chemistry 10 22496443
2023 Repeat expansions in NOP56 are a cause of spinocerebellar ataxia Type 36 in the British population. Brain communications 9 37810464
2022 RNA G-quadruplex in live cells lighted-up by a thiazole orange analogue for SCA36 identification. International journal of biological macromolecules 8 36572080
2023 A Chinese SCA36 pedigree analysis of NOP56 expansion region based on long-read sequencing. Frontiers in genetics 6 37051597
2021 NOP56 negatively regulates MyD88-mediated NF-κB signaling in miiuy croaker, Miichthys miiuy. Fish & shellfish immunology 6 34774735
2022 Long-read sequencing identified intronic (GGCCTG)n expansion in NOP56 in one SCA36 family and literature review. Clinical neurology and neurosurgery 5 36368168
2021 High-resolution structure of eukaryotic Fibrillarin interacting with Nop56 amino-terminal domain. RNA (New York, N.Y.) 5 33483369
2025 Dissecting the mechanism of NOP56 GGCCUG repeat-associated non-AUG translation using cell-free translation systems. The Journal of biological chemistry 4 40015643
2025 Structural Insights into an Antiparallel Chair-Type G-Quadruplex From the Intron of NOP56 Oncogene. Advanced science (Weinheim, Baden-Wurttemberg, Germany) 4 40047221
2002 Characterization of the sequences encoding for Xenopus laevis box C/D snoRNP Nop56 protein. Biochimica et biophysica acta 4 12020815
2000 Dnop56, a Drosophila gene homologous to the yeast nucleolar NOP56 gene. Genetica 3 11430491
2024 Hexanucleotide repeat expansion in SCA36 reduces the expression of genes involved in ribosome biosynthesis and protein translation. Journal of human genetics 2 38811808
2022 Identification of Malignancy in PAP Smear Samples Using the CGB3 and NOP56 Genes as Methylation Markers. Asian Pacific journal of cancer prevention : APJCP 2 36308381
2026 NOP56 interacts with Fibrarin to regulate the PI3K/AKT signaling pathway and inhibit apoptosis of hepatocellular carcinoma. Frontiers in oncology 0 41568368
2026 A DNA Methylation-Dependent NOP56/MYC Positive Feedback Loop Promotes the Proliferation and Migration of Non-Small Cell Lung Cancer Through Regulating Ribosome Biogenesis. Cancers 0 41827688
2026 NOP56 Drives Colorectal Cancer Progression by Modulating p53 Acetylation through SIRT1/p300. International journal of biological sciences 0 42157947
2025 A fly model of SCA36 reveals combinatorial neurotoxicity of hexanucleotide and dipeptide repeats. PLoS genetics 0 41337098
2024 Investigating Repeat Expansions in NIPA1, NOP56, and NOTCH2NLC Genes: A Closer Look at Amyotrophic Lateral Sclerosis Patients from Southern Italy. Cells 0 38667292

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