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Embryonic lethal abnormal vision-like HuR-dependent mRNA stability regulates post-transcriptional expression of cyclin-dependent kinase inhibitor p27Kip1

Standard

Embryonic lethal abnormal vision-like HuR-dependent mRNA stability regulates post-transcriptional expression of cyclin-dependent kinase inhibitor p27Kip1. / Ziegeler, Gudrun; Ming, Jie; Koseki, Jana C; Sevinc, Sema; Chen, Ting; Ergun, Suleyman; Qin, Xuebin; Aktas, Bertal H.

In: J BIOL CHEM, Vol. 285, No. 20, 14.05.2010, p. 15408-19.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Ziegeler, G, Ming, J, Koseki, JC, Sevinc, S, Chen, T, Ergun, S, Qin, X & Aktas, BH 2010, 'Embryonic lethal abnormal vision-like HuR-dependent mRNA stability regulates post-transcriptional expression of cyclin-dependent kinase inhibitor p27Kip1', J BIOL CHEM, vol. 285, no. 20, pp. 15408-19. https://doi.org/10.1074/jbc.M110.113365

APA

Ziegeler, G., Ming, J., Koseki, J. C., Sevinc, S., Chen, T., Ergun, S., Qin, X., & Aktas, B. H. (2010). Embryonic lethal abnormal vision-like HuR-dependent mRNA stability regulates post-transcriptional expression of cyclin-dependent kinase inhibitor p27Kip1. J BIOL CHEM, 285(20), 15408-19. https://doi.org/10.1074/jbc.M110.113365

Vancouver

Ziegeler G, Ming J, Koseki JC, Sevinc S, Chen T, Ergun S et al. Embryonic lethal abnormal vision-like HuR-dependent mRNA stability regulates post-transcriptional expression of cyclin-dependent kinase inhibitor p27Kip1. J BIOL CHEM. 2010 May 14;285(20):15408-19. https://doi.org/10.1074/jbc.M110.113365

Bibtex

@article{0cc67a1b973a4967806233c61a2b5afc,
title = "Embryonic lethal abnormal vision-like HuR-dependent mRNA stability regulates post-transcriptional expression of cyclin-dependent kinase inhibitor p27Kip1",
abstract = "The cyclin-dependent kinase inhibitor p27(Kip1) plays a critical role in regulating entry into and exit from the cell cycle. Post-transcriptional regulation of p27(Kip1) expression is of significant interest. The embryonic lethal abnormal vision (ELAV)-like RNA-binding protein HuR is thought be important for the translation of p27(Kip1), however, different reports attributed diametrically opposite roles to HuR. We report here an alternative mechanism wherein HuR regulates stability of the p27(Kip1) mRNA. Specifically, human and mouse p27(Kip1) mRNAs interact with HuR protein through multiple U-rich elements in both 5' and 3' untranslated regions (UTR). These interactions, which occur in vitro and in vivo, stabilize p27(Kip1) mRNA and play a critical role in its accumulation. Deleting HuR binding sites or knocking down HuR expression destabilizes p27(Kip1) mRNA and reduces its accumulation. We also identified a CT repeat in the 5' UTR of full-length p27(Kip1) mRNA isoforms that interact with a approximately 41-kDa protein and represses p27(Kip1) expression. This CT-rich element and diffuse elements in the 3' UTR regulate post-transcriptional expression of p27(Kip1) at the level of translation. This is the first demonstration that HuR-dependent mRNA stability and HuR-independent mRNA translation plays a critical role in the regulation of post-transcriptional p27(Kip1) expression.",
keywords = "3' Untranslated Regions, Animals, Antigens, Surface, Cell Cycle, Cyclin-Dependent Kinase Inhibitor p27, ELAV Proteins, ELAV-Like Protein 1, Gene Expression Regulation, Humans, Mice, NIH 3T3 Cells, RNA Processing, Post-Transcriptional, RNA, Messenger, RNA-Binding Proteins, Journal Article",
author = "Gudrun Ziegeler and Jie Ming and Koseki, {Jana C} and Sema Sevinc and Ting Chen and Suleyman Ergun and Xuebin Qin and Aktas, {Bertal H}",
year = "2010",
month = may,
day = "14",
doi = "10.1074/jbc.M110.113365",
language = "English",
volume = "285",
pages = "15408--19",
journal = "J BIOL CHEM",
issn = "0021-9258",
publisher = "American Society for Biochemistry and Molecular Biology Inc.",
number = "20",

}

RIS

TY - JOUR

T1 - Embryonic lethal abnormal vision-like HuR-dependent mRNA stability regulates post-transcriptional expression of cyclin-dependent kinase inhibitor p27Kip1

AU - Ziegeler, Gudrun

AU - Ming, Jie

AU - Koseki, Jana C

AU - Sevinc, Sema

AU - Chen, Ting

AU - Ergun, Suleyman

AU - Qin, Xuebin

AU - Aktas, Bertal H

PY - 2010/5/14

Y1 - 2010/5/14

N2 - The cyclin-dependent kinase inhibitor p27(Kip1) plays a critical role in regulating entry into and exit from the cell cycle. Post-transcriptional regulation of p27(Kip1) expression is of significant interest. The embryonic lethal abnormal vision (ELAV)-like RNA-binding protein HuR is thought be important for the translation of p27(Kip1), however, different reports attributed diametrically opposite roles to HuR. We report here an alternative mechanism wherein HuR regulates stability of the p27(Kip1) mRNA. Specifically, human and mouse p27(Kip1) mRNAs interact with HuR protein through multiple U-rich elements in both 5' and 3' untranslated regions (UTR). These interactions, which occur in vitro and in vivo, stabilize p27(Kip1) mRNA and play a critical role in its accumulation. Deleting HuR binding sites or knocking down HuR expression destabilizes p27(Kip1) mRNA and reduces its accumulation. We also identified a CT repeat in the 5' UTR of full-length p27(Kip1) mRNA isoforms that interact with a approximately 41-kDa protein and represses p27(Kip1) expression. This CT-rich element and diffuse elements in the 3' UTR regulate post-transcriptional expression of p27(Kip1) at the level of translation. This is the first demonstration that HuR-dependent mRNA stability and HuR-independent mRNA translation plays a critical role in the regulation of post-transcriptional p27(Kip1) expression.

AB - The cyclin-dependent kinase inhibitor p27(Kip1) plays a critical role in regulating entry into and exit from the cell cycle. Post-transcriptional regulation of p27(Kip1) expression is of significant interest. The embryonic lethal abnormal vision (ELAV)-like RNA-binding protein HuR is thought be important for the translation of p27(Kip1), however, different reports attributed diametrically opposite roles to HuR. We report here an alternative mechanism wherein HuR regulates stability of the p27(Kip1) mRNA. Specifically, human and mouse p27(Kip1) mRNAs interact with HuR protein through multiple U-rich elements in both 5' and 3' untranslated regions (UTR). These interactions, which occur in vitro and in vivo, stabilize p27(Kip1) mRNA and play a critical role in its accumulation. Deleting HuR binding sites or knocking down HuR expression destabilizes p27(Kip1) mRNA and reduces its accumulation. We also identified a CT repeat in the 5' UTR of full-length p27(Kip1) mRNA isoforms that interact with a approximately 41-kDa protein and represses p27(Kip1) expression. This CT-rich element and diffuse elements in the 3' UTR regulate post-transcriptional expression of p27(Kip1) at the level of translation. This is the first demonstration that HuR-dependent mRNA stability and HuR-independent mRNA translation plays a critical role in the regulation of post-transcriptional p27(Kip1) expression.

KW - 3' Untranslated Regions

KW - Animals

KW - Antigens, Surface

KW - Cell Cycle

KW - Cyclin-Dependent Kinase Inhibitor p27

KW - ELAV Proteins

KW - ELAV-Like Protein 1

KW - Gene Expression Regulation

KW - Humans

KW - Mice

KW - NIH 3T3 Cells

KW - RNA Processing, Post-Transcriptional

KW - RNA, Messenger

KW - RNA-Binding Proteins

KW - Journal Article

U2 - 10.1074/jbc.M110.113365

DO - 10.1074/jbc.M110.113365

M3 - SCORING: Journal article

C2 - 20332085

VL - 285

SP - 15408

EP - 15419

JO - J BIOL CHEM

JF - J BIOL CHEM

SN - 0021-9258

IS - 20

ER -