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At least 109 records · Page 6Linked to original sources
PubMed2000

Proximal promoter of the surfactant protein D gene: regulatory roles of AP-1, forkhead box, and GT box binding proteins.

Surfactant protein D (SP-D) plays roles in pulmonary host defense and surfactant homeostasis and is increased following lung injury. Because AP-1 proteins regulate cellular responses to diverse environmental stimuli, we hypothesized that the conserved AP-1 motif (at -109) and flanking sequences in the human SP-D promoter contribute to the regulation of SP-D expression. The AP-1 sequence specifically bound to fra-1, junD, and junB in H441 lung adenocarcinoma nuclear extracts. Mutagenesis of the AP-1 motif in a chloramphenicol acetyltransferase reporter construct containing 285 base pairs of upstream sequence nearly abolished promoter activity, and co-transfection of junD significantly increased wild type but not mutant promoter activity. The sequence immediately downstream of the AP-1 element contained a binding site for HNF-3 (FOXA), and simultaneous mutation of this site (fox-d) and an upstream FoxA binding site (-277, fox-u) caused a 4-fold reduction in chloramphenicol acetyltransferase activity. Immediately upstream of the AP-1-binding site, we identified a GT box-containing positive regulatory element. Despite finding regions of limited homology to the thyroid transcription factor 1-binding site, SP-D promoter activity did not require thyroid transcription factor 1. Thus, transcriptional regulation of SP-D gene expression involves complex interactions with ubiquitous and lineage-dependent factors consistent with more generalized roles in innate immunity.

Amino Acid Motifs↗
PubMed1999

Box-counting dimension without boxes: computing D0 from average expansion rates.

We propose an efficient iterative scheme for calculating the box-counting (capacity) dimension of a chaotic attractor in terms of its average expansion rates. Similar to the Kaplan-Yorke conjecture for the information dimension, this scheme provides a connection between a geometric property of a strange set and its underlying dynamical properties. Our conjecture is demonstrated analytically with an exactly solvable two-dimensional hyperbolic map, and numerically with a more complicated higher-dimensional nonhyperbolic map.

Biophysical Phenomena↗
PubMed1996

Downstream box-anti-downstream box interactions are dispensable for translation initiation of leaderless mRNAs.

The downstream box (db) with complementarity to a segment in the penultimate stem of 16S rRNA has been suggested to serve as a recognition element for the ribosome. For some mRNAs, the db has been proposed to act synergistically with the Shine and Dalgarno sequence (SD), while for the leaderless lambda(cI) mRNA it has been suggested to substitute for the SD in translation initiation. To test whether the db-anti-db interaction is required for translation initiation, we have used three different leaderless transcripts, the lambda(cI), phage P2 gene V and Tn1721 tetR mRNA. Using primer extension inhibition analysis (toeprinting), we show that the db does not influence translation initiation complex formation in vitro. In an attempt to demonstrate the simultaneous interactions between the db and anti-db and between the anticodon of initiator tRNA and the start codon, respectively, chemical probing has been employed on cI translation initiation complexes. These studies did not reveal a protection of the bases comprising the putative db in cI. In addition, kinetic toeprinting experiments and in vivo expression studies with cI mRNA showed that the db is dispensable for the initial interaction between ribosome and cI mRNA in the pathway towards formation of the initiation complex.

Kinetics↗
PubMed2005

Signaling to the DEAD box--regulation of DEAD-box p68 RNA helicase by protein phosphorylations.

P68 nuclear RNA helicase is essential for normal cell growth. The protein plays a very important role in cell development and proliferation. However, the molecular mechanism by which the p68 functions in cell developmental program is not clear. We previously observed that bacterially expressed his-p68 was phosphorylated at multiple sites including serine/threonine and tyrosine [L. Yang, Z.R. Liu, Protein Expr. Purif., 35: 327]. Here we report that p68 RNA helicase is phosphorylated at tyrosine residue(s) in HeLa cells. Phosphorylation of p68 at threonine or tyrosine residues responds differently to tumor necrosis factor alpha (TNF-alpha)induced cell signal. Kinase inhibition and in vitro kinase assays demonstrate that p68 RNA helicase is a cellular target of p38 MAP kinase. Phosphorylation of p68 affects the ATPase and RNA unwinding activities of the protein. In addition, we demonstrate here that phosphorylation of p68 RNA helicase controls the function of the protein in the pre-mRNA splicing process. Interestingly, phosphorylation at different amino acid residues exhibits different regulatory effects. The data suggest that function(s) of p68 RNA helicase may be subjected to the regulation of multiple cell signal pathways.

DEAD-box RNA Helicases↗
PubMed2005

High functional overlap between MluI cell-cycle box binding factor and Swi4/6 cell-cycle box binding factor in the G1/S transcriptional program in Saccharomyces cerevisiae.

In budding yeast, many genes are induced early in the cell cycle. Induction of these genes has been predominantly attributed to two transcription factors, Swi4-Swi6 (SBF) and Mbp1-Swi6 (MBF). Swi4 and Mbp1 are related DNA-binding proteins with dissimilar target sequences. For most G1/S-regulated genes that we tested in a cdc20 block-release protocol for cell-cycle synchronization, removal of both Swi4 and Mbp1 was necessary and sufficient to essentially eliminate cell-cycle-regulated expression. Detectable SBF or MBF binding sites (SCBs or MCBs) in the promoters or available genome-wide promoter occupancy data do not consistently explain this functional overlap. The overlapping ability of these transcription factors to regulate many promoters with very similar cell-cycle kinetics may provide robustness to the G1/S transcriptional response, but poses a puzzle with respect to promoter-transcription factor specificity. In addition, for some genes, deletion of Mbp1 or Swi4 enhances transcription, suggesting that these factors can also function as transcriptional repressors. Finally, we observe residual G1/S transcriptional regulation in the absence of Swi4 and Mbp1.

Binding Sites↗