The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP)

Autores: Gil Rosas, Mauco Lucas; Centola, Cielo; Torres, Mercedes; Mouguelar, Valeria Soraya; David, Aldana Paula; Piga Marra, Ernesto José; Gomez, Dennis; Calcaterra, Nora Beatriz; Armas, Pablo; Coux, Gabriela
Año de publicación: 2024
Idioma: inglés
Tipo de recurso: artículo
Estado: versión publicada
Descripción: Treacle ribosome biogenesis factor 1 (TCOF1) is responsible for about 80% of mandibular dysostosis(MD) cases. We have formerly identifed a correlation between TCOF1 and CNBP (CCHC-type zincfnger nucleic acid binding protein) expression in human mesenchymal cells. Given the establishedrole of CNBP in gene regulation during rostral development, we explored the potential for CNBP tomodulate TCOF1 transcription. Computational analysis for CNBP binding sites (CNBP-BSs) in theTCOF1 promoter revealed several putative binding sites, two of which (Hs791 and Hs2160) overlapwith putative G-quadruplex (G4) sequences (PQSs). We validated the folding of these PQSs measuringcircular dichroism and fuorescence of appropriate synthetic oligonucleotides. In vitro studiesconfrmed binding of purifed CNBP to the target PQSs (both folded as G4 and unfolded) with Kdvalues in the nM range. ChIP assays conducted in HeLa cells chromatin detected the CNBP binding toTCOF1 promoter. Transient transfections of HEK293 cells revealed that Hs2160 cloned upstream SV40promoter increased transcription of downstream frefy luciferase reporter gene. We also detected aCNBP-BS and PQS (Dr2393) in the zebrafsh TCOF1 orthologue promoter (nolc1). Disrupting this G4in zebrafsh embryos by microinjecting DNA antisense oligonucleotides complementary to Dr2393reduced the transcription of nolc1 and recapitulated the craniofacial anomalies characteristic ofTreacher Collins Syndrome. Both cnbp overexpression and Morpholino-mediated knockdown inzebrafsh induced nolc1 transcription. These results suggest that CNBP modulates the transcriptionalexpression of TCOF1 through a mechanism involving G-quadruplex folding/unfolding, and that thisregulation is active in vertebrates as distantly related as bony fsh and humans. These fndings mayhave implications for understanding and treating MD.
Fil: Gil Rosas, Mauco Lucas. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina
Fil: Centola, Cielo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina
Fil: Torres, Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina
Fil: Mouguelar, Valeria Soraya. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina
Fil: David, Aldana Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina
Fil: Piga Marra, Ernesto José. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina
Fil: Gomez, Dennis. Universite de Toulose - Le Mirail; Francia
Fil: Calcaterra, Nora Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina
Fil: Armas, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina
Fil: Coux, Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina
Materia: TRANSCRIPTIONAL CONTROL
NON-CANONICAL DNA STRUCTURE
ZEBRAFISH
ZINC FINGER PROTEIN 9
Nivel de accesibilidad: acceso abierto
Condiciones de uso: https://creativecommons.org/licenses/by/2.5/ar/
Repositorio
Institución: Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador: oai:ri.conicet.gov.ar:11336/265405

Acceder

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network_acronym_str	CONICETDig
repository_id_str	3498
network_name_str	CONICET Digital (CONICET)
spelling	The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP)Gil Rosas, Mauco LucasCentola, CieloTorres, MercedesMouguelar, Valeria SorayaDavid, Aldana PaulaPiga Marra, Ernesto JoséGomez, DennisCalcaterra, Nora BeatrizArmas, PabloCoux, GabrielaTRANSCRIPTIONAL CONTROLNON-CANONICAL DNA STRUCTUREZEBRAFISHZINC FINGER PROTEIN 9https://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Treacle ribosome biogenesis factor 1 (TCOF1) is responsible for about 80% of mandibular dysostosis(MD) cases. We have formerly identifed a correlation between TCOF1 and CNBP (CCHC-type zincfnger nucleic acid binding protein) expression in human mesenchymal cells. Given the establishedrole of CNBP in gene regulation during rostral development, we explored the potential for CNBP tomodulate TCOF1 transcription. Computational analysis for CNBP binding sites (CNBP-BSs) in theTCOF1 promoter revealed several putative binding sites, two of which (Hs791 and Hs2160) overlapwith putative G-quadruplex (G4) sequences (PQSs). We validated the folding of these PQSs measuringcircular dichroism and fuorescence of appropriate synthetic oligonucleotides. In vitro studiesconfrmed binding of purifed CNBP to the target PQSs (both folded as G4 and unfolded) with Kdvalues in the nM range. ChIP assays conducted in HeLa cells chromatin detected the CNBP binding toTCOF1 promoter. Transient transfections of HEK293 cells revealed that Hs2160 cloned upstream SV40promoter increased transcription of downstream frefy luciferase reporter gene. We also detected aCNBP-BS and PQS (Dr2393) in the zebrafsh TCOF1 orthologue promoter (nolc1). Disrupting this G4in zebrafsh embryos by microinjecting DNA antisense oligonucleotides complementary to Dr2393reduced the transcription of nolc1 and recapitulated the craniofacial anomalies characteristic ofTreacher Collins Syndrome. Both cnbp overexpression and Morpholino-mediated knockdown inzebrafsh induced nolc1 transcription. These results suggest that CNBP modulates the transcriptionalexpression of TCOF1 through a mechanism involving G-quadruplex folding/unfolding, and that thisregulation is active in vertebrates as distantly related as bony fsh and humans. These fndings mayhave implications for understanding and treating MD.Fil: Gil Rosas, Mauco Lucas. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; ArgentinaFil: Centola, Cielo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; ArgentinaFil: Torres, Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; ArgentinaFil: Mouguelar, Valeria Soraya. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; ArgentinaFil: David, Aldana Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; ArgentinaFil: Piga Marra, Ernesto José. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; ArgentinaFil: Gomez, Dennis. Universite de Toulose - Le Mirail; FranciaFil: Calcaterra, Nora Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; ArgentinaFil: Armas, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; ArgentinaFil: Coux, Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; ArgentinaSpringer2024-03info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/265405Gil Rosas, Mauco Lucas; Centola, Cielo; Torres, Mercedes; Mouguelar, Valeria Soraya; David, Aldana Paula; et al.; The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP); Springer; Scientific Reports; 14; 1; 3-2024; 1-172045-2322CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/s41598-024-58255-9info:eu-repo/semantics/altIdentifier/doi/10.1038/s41598-024-58255-9info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-10-22T12:01:41Zoai:ri.conicet.gov.ar:11336/265405instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-10-22 12:01:41.715CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv	The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP)
title	The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP)
spellingShingle	The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP) Gil Rosas, Mauco Lucas TRANSCRIPTIONAL CONTROL NON-CANONICAL DNA STRUCTURE ZEBRAFISH ZINC FINGER PROTEIN 9
title_short	The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP)
title_full	The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP)
title_fullStr	The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP)
title_full_unstemmed	The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP)
title_sort	The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP)
dc.creator.none.fl_str_mv	Gil Rosas, Mauco Lucas Centola, Cielo Torres, Mercedes Mouguelar, Valeria Soraya David, Aldana Paula Piga Marra, Ernesto José Gomez, Dennis Calcaterra, Nora Beatriz Armas, Pablo Coux, Gabriela
author	Gil Rosas, Mauco Lucas
author_facet	Gil Rosas, Mauco Lucas Centola, Cielo Torres, Mercedes Mouguelar, Valeria Soraya David, Aldana Paula Piga Marra, Ernesto José Gomez, Dennis Calcaterra, Nora Beatriz Armas, Pablo Coux, Gabriela
author_role	author
author2	Centola, Cielo Torres, Mercedes Mouguelar, Valeria Soraya David, Aldana Paula Piga Marra, Ernesto José Gomez, Dennis Calcaterra, Nora Beatriz Armas, Pablo Coux, Gabriela
author2_role	author author author author author author author author author
dc.subject.none.fl_str_mv	TRANSCRIPTIONAL CONTROL NON-CANONICAL DNA STRUCTURE ZEBRAFISH ZINC FINGER PROTEIN 9
topic	TRANSCRIPTIONAL CONTROL NON-CANONICAL DNA STRUCTURE ZEBRAFISH ZINC FINGER PROTEIN 9
purl_subject.fl_str_mv	https://purl.org/becyt/ford/1.6 https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv	Treacle ribosome biogenesis factor 1 (TCOF1) is responsible for about 80% of mandibular dysostosis(MD) cases. We have formerly identifed a correlation between TCOF1 and CNBP (CCHC-type zincfnger nucleic acid binding protein) expression in human mesenchymal cells. Given the establishedrole of CNBP in gene regulation during rostral development, we explored the potential for CNBP tomodulate TCOF1 transcription. Computational analysis for CNBP binding sites (CNBP-BSs) in theTCOF1 promoter revealed several putative binding sites, two of which (Hs791 and Hs2160) overlapwith putative G-quadruplex (G4) sequences (PQSs). We validated the folding of these PQSs measuringcircular dichroism and fuorescence of appropriate synthetic oligonucleotides. In vitro studiesconfrmed binding of purifed CNBP to the target PQSs (both folded as G4 and unfolded) with Kdvalues in the nM range. ChIP assays conducted in HeLa cells chromatin detected the CNBP binding toTCOF1 promoter. Transient transfections of HEK293 cells revealed that Hs2160 cloned upstream SV40promoter increased transcription of downstream frefy luciferase reporter gene. We also detected aCNBP-BS and PQS (Dr2393) in the zebrafsh TCOF1 orthologue promoter (nolc1). Disrupting this G4in zebrafsh embryos by microinjecting DNA antisense oligonucleotides complementary to Dr2393reduced the transcription of nolc1 and recapitulated the craniofacial anomalies characteristic ofTreacher Collins Syndrome. Both cnbp overexpression and Morpholino-mediated knockdown inzebrafsh induced nolc1 transcription. These results suggest that CNBP modulates the transcriptionalexpression of TCOF1 through a mechanism involving G-quadruplex folding/unfolding, and that thisregulation is active in vertebrates as distantly related as bony fsh and humans. These fndings mayhave implications for understanding and treating MD. Fil: Gil Rosas, Mauco Lucas. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina Fil: Centola, Cielo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina Fil: Torres, Mercedes. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina Fil: Mouguelar, Valeria Soraya. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina Fil: David, Aldana Paula. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina Fil: Piga Marra, Ernesto José. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina Fil: Gomez, Dennis. Universite de Toulose - Le Mirail; Francia Fil: Calcaterra, Nora Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina Fil: Armas, Pablo. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina Fil: Coux, Gabriela. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - Rosario. Instituto de Biología Molecular y Celular de Rosario. Universidad Nacional de Rosario. Facultad de Ciencias Bioquímicas y Farmacéuticas. Instituto de Biología Molecular y Celular de Rosario; Argentina
description	Treacle ribosome biogenesis factor 1 (TCOF1) is responsible for about 80% of mandibular dysostosis(MD) cases. We have formerly identifed a correlation between TCOF1 and CNBP (CCHC-type zincfnger nucleic acid binding protein) expression in human mesenchymal cells. Given the establishedrole of CNBP in gene regulation during rostral development, we explored the potential for CNBP tomodulate TCOF1 transcription. Computational analysis for CNBP binding sites (CNBP-BSs) in theTCOF1 promoter revealed several putative binding sites, two of which (Hs791 and Hs2160) overlapwith putative G-quadruplex (G4) sequences (PQSs). We validated the folding of these PQSs measuringcircular dichroism and fuorescence of appropriate synthetic oligonucleotides. In vitro studiesconfrmed binding of purifed CNBP to the target PQSs (both folded as G4 and unfolded) with Kdvalues in the nM range. ChIP assays conducted in HeLa cells chromatin detected the CNBP binding toTCOF1 promoter. Transient transfections of HEK293 cells revealed that Hs2160 cloned upstream SV40promoter increased transcription of downstream frefy luciferase reporter gene. We also detected aCNBP-BS and PQS (Dr2393) in the zebrafsh TCOF1 orthologue promoter (nolc1). Disrupting this G4in zebrafsh embryos by microinjecting DNA antisense oligonucleotides complementary to Dr2393reduced the transcription of nolc1 and recapitulated the craniofacial anomalies characteristic ofTreacher Collins Syndrome. Both cnbp overexpression and Morpholino-mediated knockdown inzebrafsh induced nolc1 transcription. These results suggest that CNBP modulates the transcriptionalexpression of TCOF1 through a mechanism involving G-quadruplex folding/unfolding, and that thisregulation is active in vertebrates as distantly related as bony fsh and humans. These fndings mayhave implications for understanding and treating MD.
publishDate	2024
dc.date.none.fl_str_mv	2024-03
dc.type.none.fl_str_mv	info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion http://purl.org/coar/resource_type/c_6501 info:ar-repo/semantics/articulo
format	article
status_str	publishedVersion
dc.identifier.none.fl_str_mv	http://hdl.handle.net/11336/265405 Gil Rosas, Mauco Lucas; Centola, Cielo; Torres, Mercedes; Mouguelar, Valeria Soraya; David, Aldana Paula; et al.; The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP); Springer; Scientific Reports; 14; 1; 3-2024; 1-17 2045-2322 CONICET Digital CONICET
url	http://hdl.handle.net/11336/265405
identifier_str_mv	Gil Rosas, Mauco Lucas; Centola, Cielo; Torres, Mercedes; Mouguelar, Valeria Soraya; David, Aldana Paula; et al.; The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP); Springer; Scientific Reports; 14; 1; 3-2024; 1-17 2045-2322 CONICET Digital CONICET
dc.language.none.fl_str_mv	eng
language	eng
dc.relation.none.fl_str_mv	info:eu-repo/semantics/altIdentifier/url/https://www.nature.com/articles/s41598-024-58255-9 info:eu-repo/semantics/altIdentifier/doi/10.1038/s41598-024-58255-9
dc.rights.none.fl_str_mv	info:eu-repo/semantics/openAccess https://creativecommons.org/licenses/by/2.5/ar/
eu_rights_str_mv	openAccess
rights_invalid_str_mv	https://creativecommons.org/licenses/by/2.5/ar/
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dc.publisher.none.fl_str_mv	Springer
publisher.none.fl_str_mv	Springer
dc.source.none.fl_str_mv	reponame:CONICET Digital (CONICET) instname:Consejo Nacional de Investigaciones Científicas y Técnicas
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repository.mail.fl_str_mv	dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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The transcription of the main gene associated with Treacher–Collins syndrome (TCOF1) is regulated by G-quadruplexes and cellular nucleic acid binding protein (CNBP)

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