Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow Print PDF (652K) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (13)
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Kim, Y.-S.
Right arrow Articles by Jetten, A. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kim, Y.-S.
Right arrow Articles by Jetten, A. M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 2003, Vol. 31, No. 19 5513-5525
© 2003 Oxford University Press

GLIS3, a novel member of the GLIS subfamily of Krüppel-like zinc finger proteins with repressor and activation functions

Yong-Sik Kim, Gen Nakanishi, Mark Lewandoski1 and Anton M. Jetten*

Cell Biology Section, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Department of Health and Human Services, Research Triangle Park, NC 27709, USA and 1 Laboratory of Cancer and Developmental Biology, National Cancer Institute–Frederick, National Institutes of Health, Frederick, MD 21702, USA

*To whom correspondence should be addressed. Tel: +1 919 541 2768; Fax: +1 919 541 4133; Email: jetten{at}niehs.nih.gov

In this study, we describe the identification and characterization of a novel transcription factor GLI-similar 3 (GLIS3). GLIS3 is an 83.8 kDa nuclear protein containing five C2H2-type Krüppel-like zinc finger motifs that exhibit 93% identity with those of GLIS1, however, little homology exists outside their zinc finger domains. GLIS3 can function as a repressor and activator of transcription. Deletion mutant analysis determined that the N- and C-termini are required for optimal transcriptional activity. GLIS3 binds to the GLI-RE consensus sequence and is able to enhance GLI-RE-dependent transcription. GLIS3({Delta}C496), a dominant-negative mutant, inhibits transcriptional activation by GLIS3 and GLI1. Whole mount in situ hybridization on mouse embryos from stage E6.5 through E14.5 demonstrated that GLIS3 is expressed in specific regions in developing kidney and testis and in a highly dynamic pattern during neurulation. From E11.5 through E12.5 GLIS3 was strongly expressed in the interdigital regions, which are fated to undergo apoptosis. The temporal and spatial pattern of GLIS3 expression observed during embryonic development suggests that it may play a critical role in the regulation of a variety of cellular processes during development. Both the repressor and activation functions of GLIS3 may be involved in this control.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Mol. Cell. Biol.Home page
H. S. Kang, Y.-S. Kim, G. ZeRuth, J. Y. Beak, K. Gerrish, G. Kilic, B. Sosa-Pineda, J. Jensen, J. Foley, and A. M. Jetten
Transcription Factor Glis3, a Novel Critical Player in the Regulation of Pancreatic {beta}-Cell Development and Insulin Gene Expression
Mol. Cell. Biol., December 15, 2009; 29(24): 6366 - 6379.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
H. S. Kang, J. Y. Beak, Y.-S. Kim, R. Herbert, and A. M. Jetten
Glis3 Is Associated with Primary Cilia and Wwtr1/TAZ and Implicated in Polycystic Kidney Disease
Mol. Cell. Biol., May 15, 2009; 29(10): 2556 - 2569.
[Abstract] [Full Text] [PDF]

Home page
 Nucleic Acids ResHome page
Y. Yang, B. H.-J. Chang, S. L. Samson, M. V. Li, and L. Chan
The Kruppel-like zinc finger protein Glis3 directly and indirectly activates insulin gene transcription
Nucleic Acids Res., May 1, 2009; 37(8): 2529 - 2538.
[Abstract] [Full Text] [PDF]

Home page
 Endocr. Rev.Home page
L. Aguilar-Bryan and J. Bryan
Neonatal Diabetes Mellitus
Endocr. Rev., May 1, 2008; 29(3): 265 - 291.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
Y.-S. Kim, H. S. Kang, R. Herbert, J. Y. Beak, J. B. Collins, S. F. Grissom, and A. M. Jetten
Kruppel-Like Zinc Finger Protein Glis2 Is Essential for the Maintenance of Normal Renal Functions
Mol. Cell. Biol., April 1, 2008; 28(7): 2358 - 2367.
[Abstract] [Full Text] [PDF]

Home page
 Nucleic Acids ResHome page
J. Y. Beak, H. S. Kang, Y.-S. Kim, and A. M. Jetten
Functional analysis of the zinc finger and activation domains of Glis3 and mutant Glis3(NDH1)
Nucleic Acids Res., March 1, 2008; 36(5): 1690 - 1702.
[Abstract] [Full Text] [PDF]

Home page
 J Mol EndocrinolHome page
M. A Meester-Smoor, A. C Molijn, Y. Zhao, N. A Groen, C. A H Groffen, M. Boogaard, D. van Dalsum-Verbiest, G. C Grosveld, and E. C Zwarthoff
The MN1 oncoprotein activates transcription of the IGFBP5 promoter through a CACCC-rich consensus sequence
J. Mol. Endocrinol., January 1, 2007; 38(1): 113 - 125.
[Abstract] [Full Text] [PDF]

Home page
 Nucleic Acids ResHome page
S.-C. Kim, Y.-S. Kim, and A. M. Jetten
Kruppel-like zinc finger protein Gli-similar 2 (Glis2) represses transcription through interaction with C-terminal binding protein 1 (CtBP1)
Nucleic Acids Res., December 2, 2005; 33(21): 6805 - 6815.
[Abstract] [Full Text] [PDF]

Home page
 Nucleic Acids ResHome page
T. Nakajima, S. Fujino, G. Nakanishi, Y.-S. Kim, and A. M. Jetten
TIP27: a novel repressor of the nuclear orphan receptor TAK1/TR4
Nucleic Acids Res., August 9, 2004; 32(14): 4194 - 4204.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.