Erythroid Kruppel-like factor regulates the G1 Cdk inhibitor p18

Tallacka, Michael R., Keysa, Janelle R. and Perkins, Andrew C. (2007). Erythroid Kruppel-like factor regulates the G1 Cdk inhibitor p18. In: Blood cells, molecules and diseases. Abstracts of the 15th Conference on Hemoglobin Switching. 15th Conference on Hemoglobin Switching 2006, Oxford, United Kingdom, (168-168). 14-18 September 2006. doi:10.1016/j.bcmd.2006.10.111

Author Tallacka, Michael R.
Keysa, Janelle R.
Perkins, Andrew C.
Title of paper Erythroid Kruppel-like factor regulates the G1 Cdk inhibitor p18
Conference name 15th Conference on Hemoglobin Switching 2006
Conference location Oxford, United Kingdom
Conference dates 14-18 September 2006
Proceedings title Blood cells, molecules and diseases. Abstracts of the 15th Conference on Hemoglobin Switching   Check publisher's open access policy
Journal name Blood Cells Molecules and Diseases   Check publisher's open access policy
Place of Publication London, UK
Publisher Elsevier
Publication Year 2007
Sub-type Published abstract
DOI 10.1016/j.bcmd.2006.10.111
Open Access Status Not Open Access
ISSN 1079-9796
Volume 38
Issue 2
Start page 168
End page 168
Total pages 1
Language eng
Abstract/Summary Erythroid Kruppel-like Factornext term (EKLF) is a zinc finger transcription previous termfactornext term that is expressed specifically in erythrocytes throughout development. Its major function is the activation of β-globin gene expression, by binding to CACCC box motifs, however further roles in erythrocyte development appear likely. A transcriptional profiling experiment comparing the global gene expression in EKLF-null and wild-type erythrocytes has identified many differentially expressed genes. The Cyclin-dependent kinase (previous termCdk) inhibitor p18next term was identified as a potential EKLF target gene, and found to be down-regulated in EKLF-null mice as confirmed by real-time PCR. The previous termp18next term protein functions as an previous terminhibitornext term of Cdk4 and Cdk6 activity during early previous termG1next term phase of the cell cycle to control its progression. The search throughout the previous termp18next term gene locus for phylogenetically conserved extended CACC box elements (CCNCNCCC) found two closely associated CACC sites not, vert, similar 1 kb upstream of the transcriptional start site. We show EKLF binding to these sites by gel shift assay and have demonstrated that these sites are capable of driving EKLF-dependent transcription in luciferase reporter assays. We also show by chromatin immunoprecipitation (ChIP) assay that this region of the previous termp18next term promoter is specifically occupied by EKLF in vivo. These results suggest that EKLF acts to control the switch from proliferation to differentiation in erythrocytes by regulating previous termp18next term gene expression and thereby controlling passage through the previous termG1next term–S transition.
Subjects 1103 Clinical Sciences
1102 Cardiovascular Medicine and Haematology
Q-Index Code EX
Q-Index Status Provisional Code
Institutional Status Unknown

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Created: Fri, 05 Mar 2010, 21:14:21 EST by Laura McTaggart on behalf of Institute for Molecular Bioscience