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MiR-21 is under control of STAT5 but is dispensable for mammary development and lactation
Year:
2014
Source of publication :
PLoS ONE
Authors :
Shamay, Avi
;
.
Volume :
9
Co-Authors:
Feuermann, Y., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States
Kang, K., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States
Shamay, A., Animal Science Departments, Volcani Center, Ministry of Agriculture, Bet Dagan, Israel
Robinson, G.W., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States
Hennighausen, L., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States
Facilitators :
From page:
To page:
(
Total pages:
1
)
Abstract:
Development of mammary alveolar epithelium during pregnancy is controlled by prolactin, through the transcription factors STAT5A/B that activate specific sets of target genes. Here we asked whether some of STAT5's functions are mediated by microRNAs. The miR-21 promoter sequence contains a bona-fide STAT5 binding site and miR-21 levels increased in HC11 mammary cells upon prolactin treatment. In vivo miR-21 was abundantly expressed in mammary epithelium at day 6 of pregnancy. Analysis of mice lacking miR-21 revealed that their mammary tissue developed normally during pregnancy and dams were able to nurse their pups. Our study demonstrated that although expression of miR-21 is under prolactin control through the transcription factors STAT5A/B its presence is dispensable for mammary development and lactation.
Note:
Related Files :
Animal
Animals
Cell Proliferation
Female
gene expression
Genetics
lactation
metabolism
pregnancy
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More details
DOI :
10.1371/journal.pone.0085123
Article number:
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
30725
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:56
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Scientific Publication
MiR-21 is under control of STAT5 but is dispensable for mammary development and lactation
9
Feuermann, Y., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States
Kang, K., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States
Shamay, A., Animal Science Departments, Volcani Center, Ministry of Agriculture, Bet Dagan, Israel
Robinson, G.W., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States
Hennighausen, L., Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, United States
MiR-21 is under control of STAT5 but is dispensable for mammary development and lactation
Development of mammary alveolar epithelium during pregnancy is controlled by prolactin, through the transcription factors STAT5A/B that activate specific sets of target genes. Here we asked whether some of STAT5's functions are mediated by microRNAs. The miR-21 promoter sequence contains a bona-fide STAT5 binding site and miR-21 levels increased in HC11 mammary cells upon prolactin treatment. In vivo miR-21 was abundantly expressed in mammary epithelium at day 6 of pregnancy. Analysis of mice lacking miR-21 revealed that their mammary tissue developed normally during pregnancy and dams were able to nurse their pups. Our study demonstrated that although expression of miR-21 is under prolactin control through the transcription factors STAT5A/B its presence is dispensable for mammary development and lactation.
Scientific Publication
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