Advertisement
JBC

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Originally published In Press as doi:10.1074/jbc.M501481200 on June 6, 2005

J. Biol. Chem., Vol. 280, Issue 30, 28152-28161, July 29, 2005
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
280/30/28152    most recent
M501481200v1
Right arrow Submit a Letter to Editor
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowRequest Permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Torrano, V.
Right arrow Articles by Delgado, M. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Torrano, V.
Right arrow Articles by Delgado, M. D.
Social Bookmarking
 Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

CTCF Regulates Growth and Erythroid Differentiation of Human Myeloid Leukemia Cells*

Verónica Torrano{ddagger}§, Igor Chernukhin¶, France Docquier¶, Vivien D'Arcy¶, Javier León{ddagger}, Elena Klenova¶||**, and M. Dolores Delgado{ddagger}||{ddagger}{ddagger}

From the {ddagger}Grupo de Biología Molecular del Cáncer, Departamento de Biologia Molecular, Unidad de Biomedicina-CSIC, Universidad de Cantabria, 39011 Santander, Spain and the Department of Biological Sciences, Central Campus, University of Essex, Wivenhoe Park, Colchester, Essex CO4 3SQ, United Kingdom

CTCF is a transcription factor and a candidate tumor suppressor that contains a DNA-binding domain composed of 11 zinc fingers. We reported previously that CTCF is differentially regulated during differentiation of human myeloid leukemia cells. In this study we aimed to investigate the role of CTCF in myeloid cell differentiation. A human cell line, K562, that can be chemically induced to differentiate into various hematopoietic lineages was chosen as a model system for this study. Several K562 cell lines with constitutive and conditional expression of CTCF have been generated. By using these model systems we demonstrated that: (i) ectopic expression of CTCF in K562 cells led to growth retardation and promotion of differentiation into the erythroid lineage; (ii) CTCF knock-down significantly inhibited differentiation of K562 cells into erythroid lineage; (iii) differentiation of K562 into the megakaryocytic lineage was not significantly affected; and (iv) down-regulation of MYC has been identified as one of the mechanisms by which CTCF promotes erythroid differentiation. Taken together our results demonstrate that CTCF is involved in the control of myeloid cell growth and differentiation.


Received for publication, February 8, 2005 , and in revised form, May 31, 2005.

* This work was supported in part by Grants FIS01-1129 and FISPI041083 from the Spanish Ministerio de Sanidad y Consumo (to M. D. D.), Grant SAF02-4193 from Spanish Ministerio de Educación (to J. L.), a Biomedical Research Collaboration Grant from the Wellcome Trust (to E. K., M. D. D., and J. L.), the Breast Cancer Campaign (to F. D. and E. K.), and the Research Promotion Fund from the University of Essex (to I. C., F. D., and E. K.). The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

§ Supported by a predoctoral fellowship from the Fondo Investigacion Sanitaria (FIS) and the University of Cantabria.

|| Both authors contributed equally to this article.

** To whom correspondence may be addressed: Dept. Biological Sciences, University of Essex, Wivenhoe Park, Colchester, Essex CO4 3SQ, United Kingdom. Tel.: 44-1206-874868; Fax: 44-1206-872592; E-mail: klenovae{at}essex.ac.uk.

{ddagger}{ddagger} To whom correspondence may be addressed: Dept. Biología Molecular, Facultad de Medicina, 39011-Santander, Spain. Tel.: 34-942-201955; Fax: 34-942-201945; E-mail: delgadmd{at}unican.es.


Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
Mol. Cell. Biol.Home page
I. Chernukhin, S. Shamsuddin, S. Y. Kang, R. Bergstrom, Y.-W. Kwon, W. Yu, J. Whitehead, R. Mukhopadhyay, F. Docquier, D. Farrar, et al.
CTCF Interacts with and Recruits the Largest Subunit of RNA Polymerase II to CTCF Target Sites Genome-Wide
Mol. Cell. Biol., March 1, 2007; 27(5): 1631 - 1648.
[Abstract] [Full Text] [PDF]


Home page
J. Cell Sci.Home page
V. Torrano, J. Navascues, F. Docquier, R. Zhang, L. J. Burke, I. Chernukhin, D. Farrar, J. Leon, M. T. Berciano, R. Renkawitz, et al.
Targeting of CTCF to the nucleolus inhibits nucleolar transcription through a poly(ADP-ribosyl)ation-dependent mechanism
J. Cell Sci., May 1, 2006; 119(9): 1746 - 1759.
[Abstract] [Full Text] [PDF]




HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2005 by the American Society for Biochemistry and Molecular Biology.
Advertisement
spacer
Advertisement
Advertisement