Zinc-finger proteins in health and disease

Cassandri, Matteo; Smirnov, Artem; Novelli, Flavia; Pitolli, Consuelo; Agostini, Massimiliano; Malewicz, Michal; Melino, Gerry; Raschellà, Giuseppe

doi:10.1038/cddiscovery.2017.71

Cited by 611 publications

(525 citation statements)

References 149 publications

(140 reference statements)

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“…We aligned LINC00115 sequence with other human RNAs and found that LINC00115 sequence from nucleotides 21-318 is almost identical to the 5 0 -UTR of zinc finger protein 596 (ZNF596) mRNA (99% identity) using BLAST (http:// blast.ncbi.nlm.nih.gov; Fig 5A and B). ZNF596 is a member of zinc finger protein family, which are functional diversity including transcriptional activation [33,34]. Moreover, LINC00115 knockdown inhibited ZNF596 mRNA ( Fig 5C) and protein ( Fig 5D) expression in 1123 and 528 GSCs.…”

Section: Znf596 Is Important For Linc00115-driven Gsc Tumorigenicitymentioning

confidence: 92%

TGF‐β‐activated lncRNA LINC00115 is a critical regulator of glioma stem‐like cell tumorigenicity

Tang

et al. 2019

EMBO Reports

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Long non‐coding RNAs (lncRNAs) are critical regulators in cancer. However, the involvement of lncRNAs in TGF‐β‐regulated tumorigenicity is still unclear. Here, we identify TGF‐β‐activated lncRNA LINC00115 as a critical regulator of glioma stem‐like cell (GSC) self‐renewal and tumorigenicity. LINC00115 is upregulated by TGF‐β, acts as a miRNA sponge, and upregulates ZEB1 by competitively binding of miR‐200s, thereby enhancing ZEB1 signaling and GSC self‐renewal. LINC00115 also promotes ZNF596 transcription by preventing binding of miR‐200s to the 5′‐UTR of ZNF596, resulting in augmented ZNF596/EZH2/STAT3 signaling and GBM tumor growth. Inhibition of EZH2 by genetic approaches or a small molecular inhibitor markedly suppresses LINC00115‐driven GSC self‐renewal and tumorigenicity. Moreover, LINC00115 is highly expressed in GBM, and LINC00115 expression or correlated co‐expression with ZEB1 or ZNF596 is prognostic for clinical GBM survival. Our work defines a critical role of LINC00115 in GSC self‐renewal and tumorigenicity, and suggests LINC00115 as a potential target for GBM treatment.

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Section: Znf596 Is Important For Linc00115-driven Gsc Tumorigenicitymentioning

confidence: 92%

TGF‐β‐activated lncRNA LINC00115 is a critical regulator of glioma stem‐like cell tumorigenicity

Tang

et al. 2019

EMBO Reports

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“…Biological software has predicted that TGEV Nsp2, an 85-kDa protein encoded by the replicase gene, is composed of several functional domains, including a ZnF structure. ZnFs are independently folded domains containing approximately 30 amino acids, which are maintained by a zinc ion, and coordinated through cysteine and histidine residues in different combinations [38]. They are implicated in the regulation of several cellular processes, including replication, signal transduction, cell proliferation, and apoptosis [38,39].…”

Section: Pk-15 Cells [29] Andmentioning

confidence: 99%

“…ZnFs are independently folded domains containing approximately 30 amino acids, which are maintained by a zinc ion, and coordinated through cysteine and histidine residues in different combinations [38]. They are implicated in the regulation of several cellular processes, including replication, signal transduction, cell proliferation, and apoptosis [38,39]. Interestingly, the ZnF of TGEV Nsp14 is reported to potentially play a role in modulating the expression of IFN-β, TNF-α, and interferon-stimulated genes in ST cells [37].…”

Section: Pk-15 Cells [29] Andmentioning

confidence: 99%

Porcine transmissible gastroenteritis virus nonstructural protein 2 contributes to inflammation via NF-κB activation

et al. 2018

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2018) Porcine transmissible gastroenteritis virus nonstructural protein 2 contributes to inflammation via NF-κB activation, ABSTRACT Transmissible gastroenteritis virus (TGEV) infection causes acute enteritis in swine of all ages, and especially in suckling piglets. Small intestinal inflammation is considered a central event in the pathogenesis of TGEV infections, and nuclear factor-kappa B (NF-κB) is a key transcription factor in the inflammatory response. However, it is unclear whether NF-κB is crucial for inducing inflammation during a TGEV infection. Our results show that NF-κB was activated in swine testicular (ST) cells and intestinal epithelial cell lines J2 (IPEC-J2) cells infected with TGEV, which is consistent with the up-regulation of pro-inflammatory cytokines. Treatment of TGEV-infected ST cells and IPEC-J2 cells with the NF-κB-specific inhibitor caused the down-regulation of pro-inflammatory cytokine expression, but did not significantly affect TGEV replication. Individual TGEV protein screening results demonstrated that Nsp2 exhibited a high potential for activating NF-κB and enhancing the expression of pro-inflammatory cytokines. Functional domain analyzes indicated that the first 120 amino acid residues of Nsp2 were essential for NF-κB activation. Taken together, these data suggested that NF-κB activation was a major contributor to TGEV infection-induced inflammation, and that Nsp2 was the key viral protein involved in the regulation of inflammation, with amino acids 1-120 playing a critical role in activating NF-κB. Abbreviations: TCID50: 50% tissue culture infectious dose; DMEM: Dulbecco's Modified Eagle Medium; eNOS: Endothelial nitric oxide synthase; FBS: fetal bovine serum; IFA: Indirect immunofluorescence; IκB: inhibitor of nuclear factor kappa-B; IL: interleukin; IPEC-J2: intestinal epithelial cell

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“…Zinc can either participate, directly, in chemical catalysis or, indirectly, by maintaining protein structure or stability. For this reason, it has an important regulatory role in a wide variety of biological processes, acting as a catalyst for more than 300 enzymes and is contained within thousands of proteins, as a zinc finger domain . Zinc plays a key role in fundamental cellular processes such as DNA synthesis, RNA transcription, cell division, and activation, as well as in prevention of cell apoptosis .…”

Section: Introductionmentioning

confidence: 99%

Zinc Nutrition and Inflammation in the Aging Retina

Gilbert

Pető²,

Lengyel³

et al. 2019

Molecular Nutrition Food Res

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Zinc is an essential nutrient for human health. It plays key roles in maintaining protein structure and stability, serves as catalytic factor for many enzymes, and regulates diverse fundamental cellular processes. Zinc is important in affecting signal transduction and, in particular, in the development and integrity of the immune system, where it affects both innate and adaptive immune responses. The eye, especially the retina‐choroid complex, has an unusually high concentration of zinc compared to other tissues. The highest amount of zinc is concentrated in the retinal pigment epithelium (RPE) (RPE‐choroid, 292 ± 98.5 µg g−1 dry tissue), followed by the retina (123±62.2 µg g−1 dry tissue). The interplay between zinc and inflammation has been explored in other parts of the body but, so far, has not been extensively researched in the eye. Several lines of evidence suggest that ocular zinc concentration decreases with age, especially in the context of age‐related disease. Thus, a hypothesis that retinal function could be modulated by zinc nutrition is proposed, and subsequently trialled clinically. In this review, the distribution and the potential role of zinc in the retina‐choroid complex is outlined, especially in relation to inflammation and immunity, and the clinical studies to date are summarized.

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Zinc-finger proteins in health and disease

Cited by 611 publications

References 149 publications

TGF‐β‐activated lncRNA LINC00115 is a critical regulator of glioma stem‐like cell tumorigenicity

TGF‐β‐activated lncRNA LINC00115 is a critical regulator of glioma stem‐like cell tumorigenicity

Porcine transmissible gastroenteritis virus nonstructural protein 2 contributes to inflammation via NF-κB activation

Zinc Nutrition and Inflammation in the Aging Retina

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