Cross-talk between signaling pathways regulates alternative splicing: A novel role for JNK

The regulation of alternative splicing by extracellular signals represents a key event in the control of gene expression. There is increasing evidence showing that many extracellular cues regulate alternative splicing. Nevertheless, the broad picture regarding the role of different signaling pathway...

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Publicado:	2005
Materias:	Biological membranes Cells Computer simulation Enzyme inhibition Enzymes Genes Mathematical models Stresses Fibronectin genes Gene expression Laminin Splicing Biochemistry fibronectin laminin mitogen activated protein kinase phosphatidylinositol 3 kinase stress activated protein kinase alternative RNA splicing article basement membrane breast epithelium controlled study culture medium dephosphorylation epithelium cell gene expression human human cell mesenchyme cell model priority journal protein function signal transduction 1-Phosphatidylinositol 3-Kinase Alternative Splicing Basement Membrane Breast Neoplasms Carcinoma, Hepatocellular Cell Line, Tumor Epithelial Cells Extracellular Signal-Regulated MAP Kinases Humans JNK Mitogen-Activated Protein Kinases Mesoderm Protein-Serine-Threonine Kinases Proto-Oncogene Proteins Proto-Oncogene Proteins c-akt Signal Transduction Transfection
Acceso en línea:	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219258_v280_n27_p25461_Pelisch http://hdl.handle.net/20.500.12110/paper_00219258_v280_n27_p25461_Pelisch
Aporte de:	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires

id	paper:paper_00219258_v280_n27_p25461_Pelisch
record_format	dspace
spelling	paper:paper_00219258_v280_n27_p25461_Pelisch2023-06-08T14:43:26Z Cross-talk between signaling pathways regulates alternative splicing: A novel role for JNK Biological membranes Cells Computer simulation Enzyme inhibition Enzymes Genes Mathematical models Stresses Fibronectin genes Gene expression Laminin Splicing Biochemistry fibronectin laminin mitogen activated protein kinase phosphatidylinositol 3 kinase stress activated protein kinase alternative RNA splicing article basement membrane breast epithelium controlled study culture medium dephosphorylation epithelium cell gene expression human human cell mesenchyme cell model priority journal protein function signal transduction 1-Phosphatidylinositol 3-Kinase Alternative Splicing Basement Membrane Breast Neoplasms Carcinoma, Hepatocellular Cell Line, Tumor Epithelial Cells Extracellular Signal-Regulated MAP Kinases Humans JNK Mitogen-Activated Protein Kinases Laminin Mesoderm Protein-Serine-Threonine Kinases Proto-Oncogene Proteins Proto-Oncogene Proteins c-akt Signal Transduction Transfection The regulation of alternative splicing by extracellular signals represents a key event in the control of gene expression. There is increasing evidence showing that many extracellular cues regulate alternative splicing. Nevertheless, the broad picture regarding the role of different signaling pathways and their interaction remains incomplete. Using the fibronectin gene as a model, we show that a laminin-rich basement membrane regulates the alternative splicing of two out of three regions of the transcript (extra domain I and type III connecting segment) in mammary epithelial cells, through a non-stress c-Jun N-terminal kinase (JNK) signaling pathway. We propose that dephosphorylation of the extracellular signal-regulated kinase is involved in this regulatory process. Furthermore, the laminin-rich basement membrane blocks the effect of a mammary mesenchymal cell-conditioned medium, which stimulates the inclusion of extra domain I and type III connecting segment through a phosphatidylinositol 3-kinase-dependent cascade, indicating that JNK signaling can inhibit the phosphatidylinositol 3-kinase-mediated splicing regulation. These results implicate JNK in the regulation of alternative splicing and provide new evi-dence on how extracellular stimuli are converted into changes in splicing patterns, strengthening the view that the control of alternative splicing is as complex and relevant as transcriptional control, together accounting for the spatiotemporal requirements of gene expression. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc. 2005 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219258_v280_n27_p25461_Pelisch http://hdl.handle.net/20.500.12110/paper_00219258_v280_n27_p25461_Pelisch
institution	Universidad de Buenos Aires
institution_str	I-28
repository_str	R-134
collection	Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic	Biological membranes Cells Computer simulation Enzyme inhibition Enzymes Genes Mathematical models Stresses Fibronectin genes Gene expression Laminin Splicing Biochemistry fibronectin laminin mitogen activated protein kinase phosphatidylinositol 3 kinase stress activated protein kinase alternative RNA splicing article basement membrane breast epithelium controlled study culture medium dephosphorylation epithelium cell gene expression human human cell mesenchyme cell model priority journal protein function signal transduction 1-Phosphatidylinositol 3-Kinase Alternative Splicing Basement Membrane Breast Neoplasms Carcinoma, Hepatocellular Cell Line, Tumor Epithelial Cells Extracellular Signal-Regulated MAP Kinases Humans JNK Mitogen-Activated Protein Kinases Laminin Mesoderm Protein-Serine-Threonine Kinases Proto-Oncogene Proteins Proto-Oncogene Proteins c-akt Signal Transduction Transfection
spellingShingle	Biological membranes Cells Computer simulation Enzyme inhibition Enzymes Genes Mathematical models Stresses Fibronectin genes Gene expression Laminin Splicing Biochemistry fibronectin laminin mitogen activated protein kinase phosphatidylinositol 3 kinase stress activated protein kinase alternative RNA splicing article basement membrane breast epithelium controlled study culture medium dephosphorylation epithelium cell gene expression human human cell mesenchyme cell model priority journal protein function signal transduction 1-Phosphatidylinositol 3-Kinase Alternative Splicing Basement Membrane Breast Neoplasms Carcinoma, Hepatocellular Cell Line, Tumor Epithelial Cells Extracellular Signal-Regulated MAP Kinases Humans JNK Mitogen-Activated Protein Kinases Laminin Mesoderm Protein-Serine-Threonine Kinases Proto-Oncogene Proteins Proto-Oncogene Proteins c-akt Signal Transduction Transfection Cross-talk between signaling pathways regulates alternative splicing: A novel role for JNK
topic_facet	Biological membranes Cells Computer simulation Enzyme inhibition Enzymes Genes Mathematical models Stresses Fibronectin genes Gene expression Laminin Splicing Biochemistry fibronectin laminin mitogen activated protein kinase phosphatidylinositol 3 kinase stress activated protein kinase alternative RNA splicing article basement membrane breast epithelium controlled study culture medium dephosphorylation epithelium cell gene expression human human cell mesenchyme cell model priority journal protein function signal transduction 1-Phosphatidylinositol 3-Kinase Alternative Splicing Basement Membrane Breast Neoplasms Carcinoma, Hepatocellular Cell Line, Tumor Epithelial Cells Extracellular Signal-Regulated MAP Kinases Humans JNK Mitogen-Activated Protein Kinases Laminin Mesoderm Protein-Serine-Threonine Kinases Proto-Oncogene Proteins Proto-Oncogene Proteins c-akt Signal Transduction Transfection
description	The regulation of alternative splicing by extracellular signals represents a key event in the control of gene expression. There is increasing evidence showing that many extracellular cues regulate alternative splicing. Nevertheless, the broad picture regarding the role of different signaling pathways and their interaction remains incomplete. Using the fibronectin gene as a model, we show that a laminin-rich basement membrane regulates the alternative splicing of two out of three regions of the transcript (extra domain I and type III connecting segment) in mammary epithelial cells, through a non-stress c-Jun N-terminal kinase (JNK) signaling pathway. We propose that dephosphorylation of the extracellular signal-regulated kinase is involved in this regulatory process. Furthermore, the laminin-rich basement membrane blocks the effect of a mammary mesenchymal cell-conditioned medium, which stimulates the inclusion of extra domain I and type III connecting segment through a phosphatidylinositol 3-kinase-dependent cascade, indicating that JNK signaling can inhibit the phosphatidylinositol 3-kinase-mediated splicing regulation. These results implicate JNK in the regulation of alternative splicing and provide new evi-dence on how extracellular stimuli are converted into changes in splicing patterns, strengthening the view that the control of alternative splicing is as complex and relevant as transcriptional control, together accounting for the spatiotemporal requirements of gene expression. © 2005 by The American Society for Biochemistry and Molecular Biology, Inc.
title	Cross-talk between signaling pathways regulates alternative splicing: A novel role for JNK
title_short	Cross-talk between signaling pathways regulates alternative splicing: A novel role for JNK
title_full	Cross-talk between signaling pathways regulates alternative splicing: A novel role for JNK
title_fullStr	Cross-talk between signaling pathways regulates alternative splicing: A novel role for JNK
title_full_unstemmed	Cross-talk between signaling pathways regulates alternative splicing: A novel role for JNK
title_sort	cross-talk between signaling pathways regulates alternative splicing: a novel role for jnk
publishDate	2005
url	https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_00219258_v280_n27_p25461_Pelisch http://hdl.handle.net/20.500.12110/paper_00219258_v280_n27_p25461_Pelisch
_version_	1768545723841773568

Cross-talk between signaling pathways regulates alternative splicing: A novel role for JNK

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