Biomedical subjects

Chun Ren Lim

Publications and source records attributed to Chun Ren Lim.

3 recordsLinked to original sources

PubMed2005

Psychophysiological stress-regulated gene expression in mice.

Eight genes showed significant changes in expression in mice under psychophysiological stress provided by cage-restraint and water-immersion. The transcription level of most of these genes was affected in all the tissues analyzed, and some of them were responsive genes in several different stress systems. Peculiarly, the expression level of one gene, cdc2-like kinase 1 (CLK1), was reduced only in the brain, while the balance of partially- and alternatively-spliced CLK1 mRNA species changed in all the tissues including the brain. These results suggest that some stress-response mechanisms, including transcriptional and post-transcriptional events, are coordinated in the whole body in mice under psychophysiological stress.

Animals↗

PubMed2004

Gene expression profiling of mouse postnatal cerebellar development using cDNA microarrays.

The cerebellum serves as a model system for developmental studies of the mammalian nervous system. Classical analysis of individual genes is insufficient to address the complex regulatory circuits underlying the developmental process. In this study, the postnatal cerebellar development of mice aged 2, 4, 8, 12, 16, 21 and 42 days old was studied using a microarray spotted with 5494 cDNA clones collected from the cerebellum and the cerebrum of C57BL/6J mice. We were able to cluster the expression patterns into four groups and each was highly correlated with gene function. Housekeeping genes are in a cluster in which the expression pattern peaks at the neonatal stage, while genes related to brain function peak at the adult stage. The other two clusters, characterized by transiently upregulated or downregulated expression during days 8-16, contain genes with different functions, most notably related to cell differentiation and cell cycle progression. Based on this categorization and on motif scanning, we were able to assign hypothetical functions to functionally undetermined genes. The result indicates that expression profiling is an efficient method for generation of new hypotheses for the developmental study of the cerebellum. When combined with other studies such as pharmacology etc., data generated in this study may have application in the elucidation of genetic networks underlying developmental disorder.

Amino Acid Motifs↗

PubMed2003

Impairment of the DNA binding activity of the TATA-binding protein renders the transcriptional function of Rvb2p/Tih2p, the yeast RuvB-like protein, essential for cell growth.

In Saccharomyces cerevisiae, two highly conserved proteins, Rvb1p/Tih1p and Rvb2p/Tih2p, have been demonstrated to be major components of the chromatin-remodeling INO80 complex. The mammalian orthologues of these two proteins have been shown to physically associate with the TATA-binding protein (TBP) in vitro but not clearly in vivo. Here we show that yeast proteins interact with TBP under both conditions. To assess the functional importance of these interactions, we examined the effect of mutating both TIH2/RVB2 and SPT15, which encodes TBP, on yeast cell growth. Intriguingly, only those spt15 mutations that affected the ability of TBP to bind to the TATA box caused synthetic growth defects in a tih2-ts160 background. This suggests that Tih2p might be important in recruiting TBP to the promoter. A DNA microarray technique was used to identify genes differentially expressed in the tih2-ts160 strain grown at the restrictive temperature. Only 34 genes were significantly and reproducibly affected; some up-regulated and others down-regulated. We compared the transcription of several of these Tih2p target genes in both wild type and various mutant backgrounds. We found that the transcription of some genes depends on functions possessed by both Tih2p and TBP and that these functions are substantially impaired in the spt15/tih2-ts160 double mutants that confer synthetic growth defects.

Adenosine Triphosphatases↗