| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on April 2, 2002
Accepted on August 27, 2002
1 Laboratory of Genetics and Physiology, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Bethesda, MD 20892, USA; Department of Biochemistry, School of Dentistry, The University of Tokushima, Tokushima, Japan; Department of Molecular Cell Biology, Max Planck Institute of Biophysical Chemistry, Goettingen, Germany; Institut National de la Recherche Agronomique, Jouy-en-Josas Cedex, France; Basic Research Laboratory, NCI, NIH, Bethesda, MD 20892, USA; Agricultural Research Organization, Volcani Center, Bet Dagan, Israel.
* To whom correspondence should be addressed. E-mail: traudl{at}nih.gov.
Mammary alveolar development during pregnancy is triggered by hormone signals. The PrlR/Jak2/Stat5 signal transduction pathway is the principal mediator of these cues and alveolar development is abrogated in its absence. The loss of the basic helix-loop-helix protein Id2 results in a similar defect. To investigate the role of Id2 in mammary epithelium we performed structural and molecular analyses. Id2-null mammary epithelial cells were unable to form alveoli, the epithelial architecture was disorganized and dissimilar from early stages of alveologenesis in wild type glands. The epithelial cells retained the ductal marker NKCC1. Nuclear localization of Stat5a and down-regulation of NKCC1 was observed in some areas indicating a limited response to pregnancy signals. The differentiation status of Id2-null tissue at term was further characterized with cDNA microarrays enriched in mammary specific sequences ("mammochip"). Some of the early differentiation markers for mammary epithelium were expressed in the Id2-null tissue, while genes that are expressed at later stages of pregnancy were not induced. From these results we conclude that in the absence of Id2 mammary epithelial development is arrested at an early stage of pregnancy.
This article has been cited by other articles:
 |
|
 |
|
  R. Fernandez-Valdivia, A. Mukherjee, C. J. Creighton, A. C. Buser, F. J. DeMayo, D. P. Edwards, and J. P. Lydon Transcriptional Response of the Murine Mammary Gland to Acute Progesterone Exposure Endocrinology, December 1, 2008; 149(12): 6236 - 6250. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. N. Johnstone, P. S. Mongroo, A. S. Rich, M. Schupp, M. J. Bowser, A. S. deLemos, J. W. Tobias, Y. Liu, G. E. Hannigan, and A. K. Rustgi Parvin- Inhibits Breast Cancer Tumorigenicity and Promotes CDK9-Mediated Peroxisome Proliferator-Activated Receptor Gamma 1 Phosphorylation Mol. Cell. Biol., January 15, 2008; 28(2): 687 - 704. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Zhao, C. Johansson, T. Tran, R. Bettencourt, Y. Itahana, P.-Y. Desprez, and S. F. Konieczny Identification of a Basic Helix-Loop-Helix Transcription Factor Expressed in Mammary Gland Alveolar Cells and Required for Maintenance of the Differentiated State Mol. Endocrinol., September 1, 2006; 20(9): 2187 - 2198. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N.-S. Kim, H.-J. Kim, B.-K. Koo, M.-C. Kwon, Y.-W. Kim, Y. Cho, Y. Yokota, J. M. Penninger, and Y.-Y. Kong Receptor Activator of NF-{kappa}B Ligand Regulates the Proliferation of Mammary Epithelial Cells via Id2 Mol. Cell. Biol., February 1, 2006; 26(3): 1002 - 1013. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. C. Mallory, G. Crudden, A. Oliva, C. Saunders, A. Stromberg, and R. J. Craven A Novel Group of Genes Regulates Susceptibility to Antineoplastic Drugs in Highly Tumorigenic Breast Cancer Cells Mol. Pharmacol., December 1, 2005; 68(6): 1747 - 1756. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. L. Grimm, A. Contreras, M.-H. Barcellos-Hoff, and J. M. Rosen Cell Cycle Defects Contribute to a Block in Hormone-induced Mammary Gland Proliferation in CCAAT/Enhancer-binding Protein (C/EBP{beta})-null Mice J. Biol. Chem., October 28, 2005; 280(43): 36301 - 36309. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Itahana, J. Singh, T. Sumida, J.-P. Coppe, S. Parrinello, J. L. Bennington, and P.-Y. Desprez Role of Id-2 in the Maintenance of a Differentiated and Noninvasive Phenotype in Breast Cancer Cells Cancer Res., November 1, 2003; 63(21): 7098 - 7105. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. M. Siegel, W. Shu, and J. Massague Mad Upregulation and Id2 Repression Accompany Transforming Growth Factor (TGF)-{beta}-mediated Epithelial Cell Growth Suppression J. Biol. Chem., September 12, 2003; 278(37): 35444 - 35450. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |
| Endocrinology | Endocrine Reviews | J. Clin. End. & Metab. |
| Molecular Endocrinology | Recent Prog. Horm. Res. | All Endocrine Journals |
