Abstract：
:The present study was attempted to identify transcriptionally regulated genes of the normal neurocytes responsive to iron availability. Postnatal rat hippocampus cells were primarily cultured either under the iron-loaded or depleted conditions. These cultured cells were applied for the generation of subtracted complementary DNA libraries by the suppression subtraction hybridization (SSH) and for the subsequent identification of differentially expressed transcripts by reverse Northern blot. The differentially expressed genes were chosen to perform sequencing, and then some of them were performed by Northern blot analysis for observation of their expression in the hippocampus of rats with the different iron status. The results indicated that five unique transcripts were strong candidates for differential expression in cellular iron repletion, one of them is a novel sequence (GenBank No. AF 433878), while 26 unique transcripts were strong candidates for differential expression in cellular iron deprivation, one of them is a novel sequence (GenBank No. AY 912101). The revealed known genes responsive to iron availability were previously unknown to respond to iron availability, or have not been determined in the brain, have not even been currently determined in their physiological and biological functions. Interestingly, the proteins encoded by most of the known genes are either directly pointed to or indirectly associated with the molecules that play important, even key roles in cellular signal transduction and the cell cycle. These findings lead to the important suggestion that the cellular responses to iron availability involve extensive transcriptional regulation and cellular signal transduction. Therefore, iron may serve as a signal, which directly and/or indirectly regulates or modulates cell functions.
journal_name
Mol Cell Biochemjournal_title
Molecular and cellular biochemistryauthors
Liu M,Xiao DS,Qian ZMdoi
10.1007/s11010-006-9377-2subject
Has Abstractpub_date
2007-06-01 00:00:00pages
139-47issue
1-2eissn
0300-8177issn
1573-4919journal_volume
300pub_type
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