Disease relevance of Gene Expression

• Furthermore, knockdown of FoxA1 expression blocks the association of ER with chromatin and estrogen-induced gene expression demonstrating the necessity of FoxA1 in mediating an estrogen response in breast cancer cells [1].
• Stochastic gene expression in a lentiviral positive-feedback loop: HIV-1 Tat fluctuations drive phenotypic diversity [2].
• High levels of MRP gene expression in patients with neuroblastoma correlate strongly with poor outcome [3].
• Bacillus subtilis glutamine synthetase controls gene expression through a protein-protein interaction with transcription factor TnrA [4].
• Wilms' tumor 1 and Dax-1 modulate the orphan nuclear receptor SF-1 in sex-specific gene expression [5].

Psychiatry related information on Gene Expression

• Previous studies with mice deleted for the Dbp gene have established that DBP participates in the regulation of several clock outputs, including locomotor activity, sleep distribution, and liver gene expression [6].
• Mutations in the DRA X box that disrupt the binding of this factor result in a lower level of gene expression, as does the presence of Id (a trans-dominant regulatory protein that negatively regulates helix-loop-helix proteins) [7].
• Dopamine D1 and D2 receptor gene expression in the striatum in Huntington's disease [8].
• The mismatch between elevated glucocorticoids and maintained 5-HT2C receptor and increased GR gene expression in the hippocampus provides a new model to dissect mechanisms that may underlie affective and eating disorders [9].
• Aberrant GAP-43 gene expression in Alzheimer's disease [10].

High impact information on Gene Expression

• Although chemically unrelated, CsA and FK-506 affect a similar subset of calcium-associated signaling events involved in the regulation of lymphokine gene expression, activation-driven T-cell death and exocytosis [11].
• Presentation of immunoregulatory signals to transformed B cells can profoundly influence their proliferation, morphology, differentiation, gene expression, and immunoglobulin synthesis [12].
• Through these regulatory mechanisms, IP3R modulates diverse cellular functions, which include, but are not limited to, contraction/excitation, secretion, gene expression, and cellular growth [13].
• Below we describe these recent advances, which highlight the important role of the RNA polymerase II elongation complex in regulation of eukaryotic gene expression [14].
• We further examine the evidence for independent signaling by PGHS-1 and PGHS-2, and the complex mechanisms for regulation of PGHS-2 gene expression [15].

Chemical compound and disease context of Gene Expression

• We now report that a human retinoic acid receptor expressed from cloned complementary DNA or the endogenous retinoic acid receptor present in F9 teratocarcinoma cells can activate gene expression from promoters fused to a natural or synthetic thyroid hormone response element [16].
• Adipsin is a serine protease that is secreted by adipocytes into the bloodstream; it is deficient in several animal models of obesity, representing a striking example of defective gene expression in this disorder [17].
• Chloramphenicol acetyltransferase gene expression was cis-activated by a region of the Ia A alpha k gene in a B lymphoma line, but not in a myeloma line [18].
• Compensatory ahpC gene expression in isoniazid-resistant Mycobacterium tuberculosis [19].
• DCoH, the dimerization cofactor of hepatocyte nuclear factor-1, stimulates gene expression by associating with specific DNA binding proteins and also catalyzes the dehydration of the biopterin cofactor of phenylalanine hydroxylase [20].

Biological context of Gene Expression

• Evidence indicates that ethanol affects hormone- and neurotransmitter-activated signal transduction, leading to short-term changes in regulation of cellular functions and long-term changes in gene expression [21].
• Ligands for some of these receptors have been recently identified, showing that products of lipid metabolism such as fatty acids, prostaglandins, or cholesterol derivatives can regulate gene expression by binding to nuclear receptors [22].
• In this issue of Cell, the effect of H1 downregulation on gene expression is examined [23].
• Indeed, cells lacking SRB2 and cells lacking a large portion of the CTD exhibit the same set of conditional growth phenotypes and exhibit very similar defects in gene expression in vivo [24].
• CREB phosphorylation and dephosphorylation: a Ca(2+)- and stimulus duration-dependent switch for hippocampal gene expression [25].

Anatomical context of Gene Expression

• Analysis of the genetic controls governing the SP-B gene has led to the definition of DNA-protein interactions that determine respiratory epithelial cell gene expression in general [26].
• Osteoblast differentiation is a multistep series of events modulated by an integrated cascade of gene expression that initially supports proliferation and the sequential expression of genes associated with the biosynthesis, organization, and mineralization of the bone extracellular matrix [27].
• Acetylcholine receptor gene expression at the developing neuromuscular junction [28].
• Generalized misexpression activates later programs of tracheal gene expression and branching, resulting in massive networks of branches. bnl encodes a homolog of mammalian fibroblast growth factors (FGFs) and appears to function as a ligand for the breathless receptor tyrosine kinase, an FGF receptor homolog expressed on developing tracheal cells [29].
• Transgenic expression of Galgt2 directed to vascular endothelial cells reproduces the low VWF phenotype, confirming this switch in lineage-specific gene expression as the likely molecular mechanism for Mvwf [30].

Associations of Gene Expression with chemical compounds

• Major factors that increase PEPCK-C gene expression include cyclic AMP, glucocorticoids, and thyroid hormone, whereas insulin inhibits this process [31].
• The purpose of this review is to describe the components of the cyclic AMP response unit and to analyze how these components cooperate to induce target gene expression in response to hormonal stimulation [32].
• In vitro, beta-cells display loss of control of insulin gene expression by glucose and impaired GSIS with a loss of first phase but preserved second phase of secretion, while the secretory response to non-glucidic nutrients or to D-glyceraldehyde is normal [33].
• We propose that the T3 receptor binds to estrogen response elements in a transcriptionally inactive form and competes for estrogen receptor binding, resulting in a net decrease in gene expression [34].
• Control of globin gene expression by steroid hormones in differentiating Friend leukemia cells [35].

Gene context of Gene Expression

• These proteins also activate MAP kinase (MAPK) cascades that regulate gene expression [36].
• Whereas some p38alpha(-/-) embryos die between embryonic days 11.5 and 12.5, those that develop past this stage have normal morphology but are anemic owing to failed definitive erythropoiesis, caused by diminished erythropoietin (Epo) gene expression [37].
• Levels of MRP gene expression were significantly higher in tumors with N-myc amplification than in tumors without such amplification (P < 0.001) [3].
• Spatial regulation of Antennapedia and bithorax gene expression by the Polycomb locus in Drosophila [38].
• RESULTS: Permutation analysis of multivariate classification functions established that the gene-expression profiles of tumors with BRCA1 mutations, tumors with BRCA2 mutations, and sporadic tumors differed significantly from each other [39].

Analytical, diagnostic and therapeutic context of Gene Expression

• Indeed, mutant LAMR1 caused specific changes to gene expression in cardiomyocytes, as detected by gene chip analysis [40].
• Microarray analysis of gene expression in mice with mutations in Acads indicates overexpression of Glo1 (encoding glyoxylase 1), a gene involved in the detoxification of metabolic by-products [41].
• The mechanism by which prolactin, a peptide hormone, regulates casein gene expression has been studied in mammary gland organ culture [42].
• Through systematic DNA footprinting of the TNF (encoding tumour necrosis factor, TNF) promoter region, we have identified a single nucleotide polymorphism (SNP) that causes the helix-turn-helix transcription factor OCT-1 to bind to a novel region of complex protein-DNA interactions and alters gene expression in human monocytes [43].
• Human CCAAT displacement protein (CDP), a putative repressor of developmentally regulated gene expression, was purified from HeLa cells by DNA binding-site affinity chromatography. cDNA encoding CDP was obtained by immunoscreening a lambda gt11 library with antibody raised against purified protein [44].

References