What's new about CNBP? Divergent functions and activities for a conserved nucleic acid binding protein

Armas, Pablo; Coux, Gabriela; Weiner, Andrea M. J.; Calcaterra, Nora B.

doi:10.1016/j.bbagen.2021.129996

Cited by 18 publications

(16 citation statements)

References 111 publications

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“…If AONs target CNBP pre-mRNA, this would also reduce CNBP mRNA levels, leading to a reduction in CNBP protein. Since CNBP has essential functions in normal cells (reviewed in [ 88 ]), the reduction in CNBP should be avoided. The mutant CCUG RNA could be also degraded by the normalization of the Dead-box 5 (DDX5) RNA-helicase p68 [ 89 ] ( Figure 4 ).…”

Section: Therapeutic Studies In Dm2mentioning

confidence: 99%

“…There is also a possibility to correct DM2 by improving some potential modifying factors, associated with DM2, such as CNBP. CNBP is a DNA- and RNA-binding protein that regulates gene expression at the levels of transcription and translation [ 88 ]. It plays a significant role in development, immune system and tumorigenesis.…”

Section: Therapeutic Studies In Dm2mentioning

confidence: 99%

“…Therefore, a reduction in CNBP might be associated with at least some symptoms in DM2. It has been shown that CNBP stability could be regulated by phosphorylation by AMPK kinase (reviewed in [ 88 ]). Small molecules increasing CNBP stability might normalize CNBP levels, contributing to the correction of DM2 pathogenesis.…”

Section: Therapeutic Studies In Dm2mentioning

confidence: 99%

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Development of Therapeutic Approaches for Myotonic Dystrophies Type 1 and Type 2

Timchenko

2022

IJMS

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Myotonic Dystrophies type 1 (DM1) and type 2 (DM2) are complex multisystem diseases without disease-based therapies. These disorders are caused by the expansions of unstable CTG (DM1) and CCTG (DM2) repeats outside of the coding regions of the disease genes: DMPK in DM1 and CNBP in DM2. Multiple clinical and molecular studies provided a consensus for DM1 pathogenesis, showing that the molecular pathophysiology of DM1 is associated with the toxicity of RNA CUG repeats, which cause multiple disturbances in RNA metabolism in patients’ cells. As a result, splicing, translation, RNA stability and transcription of multiple genes are misregulated in DM1 cells. While mutant CCUG repeats are the main cause of DM2, additional factors might play a role in DM2 pathogenesis. This review describes current progress in the translation of mechanistic knowledge in DM1 and DM2 to clinical trials, with a focus on the development of disease-specific therapies for patients with adult forms of DM1 and congenital DM1 (CDM1).

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Section: Therapeutic Studies In Dm2mentioning

confidence: 99%

Section: Therapeutic Studies In Dm2mentioning

confidence: 99%

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Development of Therapeutic Approaches for Myotonic Dystrophies Type 1 and Type 2

Timchenko

2022

IJMS

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“…CNBP is a conserved small single-stranded nucleic acid-binding protein present in most eukaryotes as both a transcriptional and translational regulator that controls cell death and proliferation . All CNBP orthologs contain six or seven CCHC-type (Cys–Cys–His–Cys) zinc knuckles (tiny zinc fingers) . CNBP also contains an RG-rich motif that is considered a novel G4 interaction motif .…”

Section: Cellular G4-binding Proteinsmentioning

confidence: 99%

Targeting the RNA G-Quadruplex and Protein Interactome for Antiviral Therapy

et al. 2022

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In recent years, G-quadruplexes (G4s), types of noncanonical four-stranded nucleic acid structures, have been identified in many viruses that threaten human health, such as HIV and Epstein–Barr virus. In this context, G4 ligands were designed to target the G4 structures, among which some have shown promising antiviral effects. In this Perspective, we first summarize the diversified roles of RNA G4s in different viruses. Next, we introduce small-molecule ligands developed as G4 modulators and highlight their applications in antiviral studies. In addition to G4s, we comprehensively review the medical intervention of G4-interacting proteins from both the virus (N protein, viral-encoded helicases, severe acute respiratory syndrome-unique domain, and Epstein–Barr nuclear antigen 1) and the host (heterogeneous nuclear ribonucleoproteins, RNA helicases, zinc-finger cellular nucelic acid-binding protein, and nucleolin) by inhibitors as an alternative way to disturb the normal functions of G4s. Finally, we discuss the challenges and opportunities in G4-based antiviral therapy.

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“…Cellular nucleic acid binding protein (CNBP) is a small human single-stranded nucleic acid-binding protein and is involved in transcription regulation by binding to both single-stranded DNA and RNA molecules and by activating or repressing the expression of many genes [ 85 ]. A heterozygous CNBP knock-out ( Cnbp −/+) mouse model showed some of the multi-organ phenotypic features of myotonic dystrophy, including muscle histopathology, myotonic discharges and heart conduction abnormalities.…”

Section: Postulated Pathomechanismsmentioning

confidence: 99%

Myotonic Dystrophies: A Genetic Overview

Soltanzadeh

2022

Genes

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Myotonic dystrophies (DM) are the most common muscular dystrophies in adults, which can affect other non-skeletal muscle organs such as the heart, brain and gastrointestinal system. There are two genetically distinct types of myotonic dystrophy: myotonic dystrophy type 1 (DM1) and myotonic dystrophy type 2 (DM2), both dominantly inherited with significant overlap in clinical manifestations. DM1 results from CTG repeat expansions in the 3′-untranslated region (3′UTR) of the DMPK (dystrophia myotonica protein kinase) gene on chromosome 19, while DM2 is caused by CCTG repeat expansions in intron 1 of the CNBP (cellular nucleic acid-binding protein) gene on chromosome 3. Recent advances in genetics and molecular biology, especially in the field of RNA biology, have allowed better understanding of the potential pathomechanisms involved in DM. In this review article, core clinical features and genetics of DM are presented followed by a discussion on the current postulated pathomechanisms and therapeutic approaches used in DM, including the ones currently in human clinical trial phase.

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What's new about CNBP? Divergent functions and activities for a conserved nucleic acid binding protein

Cited by 18 publications

References 111 publications

Development of Therapeutic Approaches for Myotonic Dystrophies Type 1 and Type 2

Development of Therapeutic Approaches for Myotonic Dystrophies Type 1 and Type 2

Targeting the RNA G-Quadruplex and Protein Interactome for Antiviral Therapy

Myotonic Dystrophies: A Genetic Overview

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