STAT5 transcriptional activity is impaired by LIF in a mammary epithelial cell line
Gene regulation mediated by STAT factors has been implicated in cellular functions with relevance to a variety of processes. Particularly, STAT5 and STAT3 play a crucial role in mammary epithelium displaying reciprocal activation kinetics during pregnancy, lactation and involution. Here, we show tha...
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todo:paper_0006291X_v356_n3_p727_RodriguezGranillo2023-10-03T14:03:53Z STAT5 transcriptional activity is impaired by LIF in a mammary epithelial cell line Rodriguez Granillo, A. Boffi, J.C. Barañao, L. Kordon, E. Pecci, A. Guberman, A. Gene expression HC11 Involution LIF Mammary epithelium Prolactin Signal transduction STAT3 STAT5 leukemia inhibitory factor prolactin STAT3 protein STAT5 protein article breast epithelium controlled study gene control gene expression regulation gene repression human human cell involution priority journal promoter region protein phosphorylation signal transduction transcription regulation Animals bcl-X Protein CCAAT-Enhancer-Binding Protein-delta Dexamethasone Epithelium Insulin Leukemia Inhibitory Factor Mammary Glands, Animal Mice Phosphorylation Prolactin Promoter Regions (Genetics) Proto-Oncogene Proteins c-fos STAT3 Transcription Factor STAT5 Transcription Factor Gene regulation mediated by STAT factors has been implicated in cellular functions with relevance to a variety of processes. Particularly, STAT5 and STAT3 play a crucial role in mammary epithelium displaying reciprocal activation kinetics during pregnancy, lactation and involution. Here, we show that LIF treatment of mammary epithelial HC11 cells reduces the phosphorylation levels and transcriptional activity of p-STAT5 in correlation with STAT3 phosphorylation. We have also found that STAT5 activity is negatively modulated by this cytokine, both on a gene whose expression is induced, as well as on a promoter repressed by STAT5. Besides, our results show that lactogenic hormones increase LIF effect on gene induction without modifying STAT3 phosphorylation state. Our findings strongly suggest that there is crosstalk between STAT5 and STAT3 pathways that could modulate their ability to regulate gene expression. © 2007 Elsevier Inc. All rights reserved. Fil:Rodriguez Granillo, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Boffi, J.C. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Barañao, L. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Kordon, E. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Pecci, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. Fil:Guberman, A. Universidad de Buenos Aires. Facultad de Ciencias Exactas y Naturales; Argentina. JOUR info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by/2.5/ar http://hdl.handle.net/20.500.12110/paper_0006291X_v356_n3_p727_RodriguezGranillo |
institution |
Universidad de Buenos Aires |
institution_str |
I-28 |
repository_str |
R-134 |
collection |
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) |
topic |
Gene expression HC11 Involution LIF Mammary epithelium Prolactin Signal transduction STAT3 STAT5 leukemia inhibitory factor prolactin STAT3 protein STAT5 protein article breast epithelium controlled study gene control gene expression regulation gene repression human human cell involution priority journal promoter region protein phosphorylation signal transduction transcription regulation Animals bcl-X Protein CCAAT-Enhancer-Binding Protein-delta Dexamethasone Epithelium Insulin Leukemia Inhibitory Factor Mammary Glands, Animal Mice Phosphorylation Prolactin Promoter Regions (Genetics) Proto-Oncogene Proteins c-fos STAT3 Transcription Factor STAT5 Transcription Factor |
spellingShingle |
Gene expression HC11 Involution LIF Mammary epithelium Prolactin Signal transduction STAT3 STAT5 leukemia inhibitory factor prolactin STAT3 protein STAT5 protein article breast epithelium controlled study gene control gene expression regulation gene repression human human cell involution priority journal promoter region protein phosphorylation signal transduction transcription regulation Animals bcl-X Protein CCAAT-Enhancer-Binding Protein-delta Dexamethasone Epithelium Insulin Leukemia Inhibitory Factor Mammary Glands, Animal Mice Phosphorylation Prolactin Promoter Regions (Genetics) Proto-Oncogene Proteins c-fos STAT3 Transcription Factor STAT5 Transcription Factor Rodriguez Granillo, A. Boffi, J.C. Barañao, L. Kordon, E. Pecci, A. Guberman, A. STAT5 transcriptional activity is impaired by LIF in a mammary epithelial cell line |
topic_facet |
Gene expression HC11 Involution LIF Mammary epithelium Prolactin Signal transduction STAT3 STAT5 leukemia inhibitory factor prolactin STAT3 protein STAT5 protein article breast epithelium controlled study gene control gene expression regulation gene repression human human cell involution priority journal promoter region protein phosphorylation signal transduction transcription regulation Animals bcl-X Protein CCAAT-Enhancer-Binding Protein-delta Dexamethasone Epithelium Insulin Leukemia Inhibitory Factor Mammary Glands, Animal Mice Phosphorylation Prolactin Promoter Regions (Genetics) Proto-Oncogene Proteins c-fos STAT3 Transcription Factor STAT5 Transcription Factor |
description |
Gene regulation mediated by STAT factors has been implicated in cellular functions with relevance to a variety of processes. Particularly, STAT5 and STAT3 play a crucial role in mammary epithelium displaying reciprocal activation kinetics during pregnancy, lactation and involution. Here, we show that LIF treatment of mammary epithelial HC11 cells reduces the phosphorylation levels and transcriptional activity of p-STAT5 in correlation with STAT3 phosphorylation. We have also found that STAT5 activity is negatively modulated by this cytokine, both on a gene whose expression is induced, as well as on a promoter repressed by STAT5. Besides, our results show that lactogenic hormones increase LIF effect on gene induction without modifying STAT3 phosphorylation state. Our findings strongly suggest that there is crosstalk between STAT5 and STAT3 pathways that could modulate their ability to regulate gene expression. © 2007 Elsevier Inc. All rights reserved. |
format |
JOUR |
author |
Rodriguez Granillo, A. Boffi, J.C. Barañao, L. Kordon, E. Pecci, A. Guberman, A. |
author_facet |
Rodriguez Granillo, A. Boffi, J.C. Barañao, L. Kordon, E. Pecci, A. Guberman, A. |
author_sort |
Rodriguez Granillo, A. |
title |
STAT5 transcriptional activity is impaired by LIF in a mammary epithelial cell line |
title_short |
STAT5 transcriptional activity is impaired by LIF in a mammary epithelial cell line |
title_full |
STAT5 transcriptional activity is impaired by LIF in a mammary epithelial cell line |
title_fullStr |
STAT5 transcriptional activity is impaired by LIF in a mammary epithelial cell line |
title_full_unstemmed |
STAT5 transcriptional activity is impaired by LIF in a mammary epithelial cell line |
title_sort |
stat5 transcriptional activity is impaired by lif in a mammary epithelial cell line |
url |
http://hdl.handle.net/20.500.12110/paper_0006291X_v356_n3_p727_RodriguezGranillo |
work_keys_str_mv |
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1782025722934591488 |