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GeneChip Array (genechip + array)

Distribution by Scientific Domains
Life Sciences71%
Medical Sciences28%

Selected Abstracts

Linkage Validation of RP25 Using the 10K GeneChip Array and Further Refinement of the Locus by New Linked Families

ANNALS OF HUMAN GENETICS, Issue 4 2008
I. Barragán
Summary Retinitis pigmentosa (RP) is a clinically and genetically heterogeneous group of retinal dystrophies, characterised by rod photoreceptor cell degeneration with autosomal recessive RP (arRP) as the commonest form worldwide. To date, a total of 26 loci have been reported for arRP, each having a prevalence of 1,5%, except for the RP25 locus which was identified as the genetic cause of 14% of arRP cases in Spain. In order to validate the original linkage of RP25, we undertook a total genome scan using the 10K GeneChip mapping array on three of the previously linked families. The data obtained supported the initial findings of linkage. Additionally, linkage analysis in 18 newly ascertained arRP families was performed using microsatellite markers spanning the chromosome 6p12.1-q15 interval. Five out of the 18 families showed suggestive evidence of linkage to RP25, hence supporting the high prevalence of this locus in the Spanish population. Furthermore, the finding of a crossover in one of these families is likely to have refined the disease interval from the original 16 cM to only a 2.67 cM region between D6S257 and D6S1557. [source]

Reduced alpha adrenergic mediated contraction of renal preglomerular blood vessels as a function of gender and aging

JOURNAL OF CELLULAR BIOCHEMISTRY, Issue 4 2005
John C. Passmore
Abstract As human males age, a decline in baroreflex-mediated elevation of blood pressure occurs due, at least in part, to a reduction in alpha-1 adrenergic vasoconstrictor function. Alpha adrenergic constriction is mediated by guanosine triphosphate binding Protein (G Protein) coupled signaling pathways. Alpha-1 A/C, B, and D adrenergic receptor expressions, measured by GeneChip array, are not reduced during aging in renal blood vessels of male or female rats. Alpha-1 A GeneChip expression is greater, at all ages studied, in females than in males. Prazosin binding by alpha-1 adrenergic receptors is greater in young adult female rats than in young adult male rats; however, it is reduced with aging in both male and female rats. G alpha q GeneChip expression declines while expression of adrenergic receptor kinase (GRK2) and tyrosine phosphatases (TyrP) increase with aging in male rats. The declines in alpha-1 adrenergic receptor binding and G alpha q expression and also the increases in GRK2 and TyrP expression likely relate to the age-related decline of vasoconstriction in male rats. The information that the expression of alpha-1 A adrenergic receptors is greater in female rats and (GRK2) expression does not increase during aging could relate to the gender differences in vasoconstrictor function with aging. Gene therapy to ameliorate the age-related decline in renal function could possibly reduce the need for renal dialysis. Signaling pathways such as those reviewed herein may provide an outline of the molecular pathways needed to move toward successful renal gene therapy for aging individuals. J. Cell. Biochem. © 2005 Wiley-Liss, Inc. [source]

Microarray analysis of gene expression associated with extrapulmonary dissemination of tuberculosis

RESPIROLOGY, Issue 5 2006
Deog Kyeom KIM
Objective: Although extrapulmonary organs are involved in 20% of patients with tuberculosis, the host genetic factors associated with the extrapulmonary dissemination of tuberculosis are not yet known. The aim of this study was to identify the host genetic factors associated with the extrapulmonary dissemination of tuberculosis by comparing gene expression profiles of patients who had recovered from extrapulmonary tuberculosis and those who had recovered from pulmonary tuberculosis. Methods: Five patients from each group were enrolled. Total RNA was extracted from peripheral blood mononuclear cells that had been incubated for 48 h with whole lysate of Mycobacterium tuberculosis (H37Rv, 0.5 µg/mL). Gene expression profiles were acquired using the GeneChip® array and its applied systems. Gene expression profiles from five patients with previous extrapulmonary tuberculosis and one pooled control sample from five patients with previous pulmonary tuberculosis were analysed and compared. Genes that were expressed concordantly in more than 80% of arrays and that showed more than twofold changes in at least one array among samples from patients who had recovered from extrapulmonary tuberculosis were identified. Results: Compared with the control sample, the expression of 16 genes, including those for tumour necrosis factor (TNF)-, and cathepsin W, was increased, and the expression of 45 genes including that for TNF-receptor superfamily member 7 (TNFRSF7), was decreased in the extrapulmonary tuberculosis patients. The altered expression of the TNF-,, cathepsin W and TNFRSF7 genes was confirmed by quantitative RT-PCR. Conclusions: Altered expression of the genes for TNF-,, cathepsin W and TNFRSF7 may be risk factors for the extrapulmonary dissemination of tuberculosis in humans. [source]

Identification of a novel cis -acting element conferring sulfur deficiency response in Arabidopsis roots

THE PLANT JOURNAL, Issue 3 2005
Akiko Maruyama-Nakashita
Summary SULTR1;1 high-affinity sulfate transporter is highly regulated in the epidermis and cortex of Arabidopsis roots responding to sulfur deficiency (,S). We identified a novel cis -acting element involved in the ,S-inducible expression of sulfur-responsive genes in Arabidopsis. The promoter region of SULTR1;1 was dissected for deletion and gain-of-function analysis using luciferase (LUC) reporter gene in transgenic Arabidopsis. The 16-bp sulfur-responsive element (SURE) from ,2777 to ,2762 of SULTR1;1 promoter was sufficient and necessary for the ,S-responsive expression, which was reversed when supplied with cysteine and glutathione (GSH). The SURE sequence contained an auxin response factor (ARF) binding sequence (GAGACA). However, SURE was not responsive to naphthalene acetic acid, indicating its specific function in the sulfur response. The base substitution analysis indicated the significance of a 5-bp sequence (GAGAC) within the conserved ARF binding site as a core element for the ,S response. Microarray analysis of early ,S response in Arabidopsis roots indicated the presence of SURE core sequences in the promoter regions of ,S-inducible genes on a full genome GeneChip array. It is suggested that SURE core sequences may commonly regulate the expression of a gene set required for adaptation to the ,S environment. [source]

Identification of cold-inducible downstream genes of the Arabidopsis DREB1A/CBF3 transcriptional factor using two microarray systems

THE PLANT JOURNAL, Issue 6 2004
Kyonoshin Maruyama
Summary The transcriptional factor DREB/CBF (dehydration-responsive element/C-repeat-binding) specifically interacts with the dehydration-responsive element (DRE)/C-repeat (CRT) cis -acting element (A/GCCGAC) and controls the expression of many stress-inducible genes in Arabidopsis. Transgenic plants overexpressing DREB1A showed activated expression of many stress-inducible genes and improved tolerance to not only drought, salinity, and freezing but also growth retardation. We searched for downstream genes in transgenic plants overexpressing DREB1A using the full-length cDNA microarray and Affymetrix GeneChip array. We confirmed candidate genes selected by array analyses using RNA gel blot and identified 38 genes as the DREB1A downstream genes, including 20 unreported new downstream genes. Many of the products of these genes were proteins known to function against stress and were probably responsible for the stress tolerance of the transgenic plants. The downstream genes also included genes for protein factors involved in further regulation of signal transduction and gene expression in response to stress. The identified genes were classified into direct downstream genes of DREB1A and the others based on their expression patterns in response to cold stress. We also searched for conserved sequences in the promoter regions of the direct downstream genes and found A/GCCGACNT in their promoter regions from ,51 to ,450 as a consensus DRE. The recombinant DREB1A protein bound to A/GCCGACNT more efficiently than to A/GCCGACNA/G/C. [source]

Molecular characterization of Treponema denticola infection-induced bone and soft tissue transcriptional profiles

MOLECULAR ORAL MICROBIOLOGY, Issue 4 2010
V. Bakthavatchalu
Summary Treponema denticola is associated with subgingival biofilms in adult periodontitis and with acute necrotizing ulcerative gingivitis. However, the molecular mechanisms by which T. denticola impacts periodontal inflammation and alveolar bone resorption remain unclear. Here, we examined changes in the host transcriptional profiles during a T. denticola infection using a murine calvarial model of inflammation and bone resorption. T. denticola was injected into the subcutaneous soft tissue over the calvaria of BALB/c mice for 3 days, after which the soft tissues and the calvarial bones were excised. RNA was isolated and analysed for transcript profiling using Murine GeneChip® arrays. Following T. denticola infection, 2905 and 1234 genes in the infected calvarial bones and soft tissues, respectively, were differentially expressed (P , 0.05). Biological pathways significantly impacted by T. denticola infection in calvarial bone and calvarial tissue included leukocyte transendothelial migration, cell adhesion (immune system) molecules, cell cycle, extracellular matrix,receptor interaction, focal adhesion, B-cell receptor signaling and transforming growth factor-, signaling pathways resulting in proinflammatory, chemotactic effects, and T-cell stimulation. In conclusion, localized T. denticola infection differentially induces transcription of a broad array of host genes, the profiles of which differed between inflamed calvarial bone and soft tissues. [source]

Developmental gene expression profiling of mammalian, fetal orofacial tissue

BIRTH DEFECTS RESEARCH, Issue 12 2004
Partha Mukhopadhyay
Abstract BACKGROUND The embryonic orofacial region is an excellent developmental paradigm that has revealed the centrality of numerous genes encoding proteins with diverse and important biological functions in embryonic growth and morphogenesis. DNA microarray technology presents an efficient means of acquiring novel and valuable information regarding the expression, regulation, and function of a panoply of genes involved in mammalian orofacial development. METHODS To identify differentially expressed genes during mammalian orofacial ontogenesis, the transcript profiles of GD-12, GD-13, and GD-14 murine orofacial tissue were compared utilizing GeneChip arrays from Affymetrix. Changes in gene expression were verified by TaqMan quantitative real-time PCR. Cluster analysis of the microarray data was done with the GeneCluster 2.0 Data Mining Tool and the GeneSpring software. RESULTS Expression of >50% of the ,12,000 genes and expressed sequence tags examined in this study was detected in GD-12, GD-13, and GD-14 murine orofacial tissues and the expression of several hundred genes was up- and downregulated in the developing orofacial tissue from GD-12 to GD-13, as well as from GD-13 to GD-14. Such differential gene expression represents changes in the expression of genes encoding growth factors and signaling molecules; transcription factors; and proteins involved in epithelial-mesenchymal interactions, extracellular matrix synthesis, cell adhesion, proliferation, differentiation, and apoptosis. Following cluster analysis of the microarray data, eight distinct patterns of gene expression during murine orofacial ontogenesis were selected for graphic presentation of gene expression patterns. CONCLUSIONS This gene expression profiling study identifies a number of potentially unique developmental participants and serves as a valuable aid in deciphering the complex molecular mechanisms crucial for mammalian orofacial development. Supplementary material for this article can be found at http://www.mrw.interscience.wiley.com/suppmat/1542-0752/suppmat/2004/70/v70.mukhopadhyay.html Birth Defects Research (Part A), 2004. © 2004 Wiley-Liss, Inc. [source]