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Publication : Loss of CCAAT/enhancer binding protein delta promotes chromosomal instability.

First Author  Huang AM Year  2004
Journal  Oncogene Volume  23
Issue  8 Pages  1549-57
PubMed ID  14716301 Mgi Jnum  J:121195
Mgi Id  MGI:3709512 Doi  10.1038/sj.onc.1207285
Citation  Huang AM, et al. (2004) Loss of CCAAT/enhancer binding protein delta promotes chromosomal instability. Oncogene 23(8):1549-57
abstractText  The transcription factor CCAAT/enhancer binding protein delta (Cebpd, also known as C/EBPdelta, CRP3, CELF, NF-IL6beta) is implicated in diverse cellular functions such as the acute phase response, adipocyte differentiation, learning and memory, and mammary epithelial cell growth control. Here, we report that lack of Cebpd causes genomic instability and centrosome amplifications in primary embryonic fibroblasts derived from 129S1 mice. Upon spontaneous immortalization, Cebpd-deficient fibroblasts acquire transformed features such as impaired contact inhibition and reduced serum dependence. These data identify a novel role for Cebpd in the maintenance of chromosomal stability and suggest a potential tumor suppressor function in vivo.
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