Halo_CID
Ontology highlight
ABSTRACT:
INSTRUMENT(S): LTQ Orbitrap Elite
ORGANISM(S): Halobacterium Nrc-1
SUBMITTER:
PROVIDER: PAe004093 | PeptideAtlas |
REPOSITORIES: PeptideAtlas
Similar Datasets
Project description:Overall, this work describes the largest cohort of patients with RAG mutations and an associated phenotype consisting of combined immunodeficiency and granulomatous lesions and/or autoimmunity (CID-G/AI). By using multiple methods (microarray, ELISA and multiplex bead technology), we have consistently identified a distinctive signature of anti-cytokine antibodies in patients with RAG-dependent immunodeficiencies, especially in those with CID-G/AI and a history of severe viral infections. These autoantibodies were not detected in a large panel of patients with other forms of primary immunodeficiency, and may therefore represent a novel biomarker panel of this condition.
2015-07-08 | GSE70618 | GEO
Project description:Overall, this work describes the largest cohort of patients with RAG mutations and an associated phenotype consisting of combined immunodeficiency and granulomatous lesions and/or autoimmunity (CID-G/AI). By using multiple methods (microarray, ELISA and multiplex bead technology), we have consistently identified a distinctive signature of anti-cytokine antibodies in patients with RAG-dependent immunodeficiencies, especially in those with CID-G/AI and a history of severe viral infections. These autoantibodies were not detected in a large panel of patients with other forms of primary immunodeficiency, and may therefore represent a novel biomarker panel of this condition. Known autoantigens, cytokines, chemokines, growth factors and receptors were printed onto microarrays. All targets were printed in triplicate. Arrays were probed with diluted plasma and autoantibodies were detected with a AF647 conjugated anti-human IgG secondary.
2015-07-08 | E-GEOD-70618 | biostudies-arrayexpress
Project description:Compound CID 3538206 inhibits yeast TORC1 activity and functionally mimic rapamycin. We used microarrays to compare the global gene expression with the treatment of CID 3528206 and rapamycin.
2012-05-01 | GSE33320 | GEO
Project description:Compound CID 3538206 inhibits yeast TORC1 activity and functionally mimic rapamycin. We used microarrays to compare the global gene expression with the treatment of CID 3528206 and rapamycin. BY4741 yeast cells were treated with1% DMSO, 20 uM CID 3528206 and 200 nM rapamycin in duplicate for 3hrs. RNA extracted and labeled to probe yeast gene arrays
2012-04-30 | E-GEOD-33320 | biostudies-arrayexpress
Project description:A variety of high-throughput techniques are now available for constructing comprehensive gene regulatory networks in systems biology. In this study, we report a new statistical approach for facilitating in silico inference of regulatory network structure. The new measure of association, coefficient of intrinsic dependence (CID), is model-free and can be applied to both continuous and categorical distributions. When given two variables X and Y, CID answers whether Y is dependent on X by examining the conditional distribution of Y given X. In this paper, we apply CID to analyze the regulatory relationships between transcription factors (TFs) (X) and their downstream genes (Y) based on clinical data. More specifically, we use estrogen receptor alpha (ERalpha) as the variable X, and the analyses are based on 48 clinical breast cancer gene expression arrays (48A). RESULTS: The analytical utility of CID was evaluated in comparison with four commonly used statistical methods, Galton-Pearson's correlation coefficient (GPCC), Student's t-test (STT), coefficient of determination (CoD), and mutual information (MI). When being compared to GPCC, CoD, and MI, CID reveals its preferential ability to discover the regulatory association where distribution of the mRNA expression levels on X and Y does not fit linear models. On the other hand, when CID is used to measure the association of a continuous variable (Y) against a discrete variable (X), it shows similar performance as compared to STT, and appears to outperform CoD and MI. In addition, this study established a two-layer transcriptional regulatory network to exemplify the usage of CID, in combination with GPCC, in deciphering gene networks based on gene expression profiles from patient arrays. CONCLUSION: CID is shown to provide useful information for identifying associations between genes and transcription factors of interest in patient arrays. When coupled with the relationships detected by GPCC, the association predicted by CID are applicable to the construction of transcriptional regulatory networks. This study shows how information from different data sources and learning algorithms can be integrated to investigate whether relevant regulatory mechanisms identified in cell models can also be partially re-identified in clinical samples of breast cancers. AVAILABILITY: the implementation of CID in R codes can be freely downloaded from (http://homepage.ntu.edu.tw/~lyliu/BC/).
2009-07-10 | GSE17041 | GEO
Project description:The RNA polymerase II (RNApII) C-terminal domain (CTD)-interacting domain (CID) proteins are involved in two distinct termination pathways and recognize different phosphorylated forms of CTD. To investigate the role of differential CTDM-^VCID interactions in the choice of termination pathway, we altered the CTD-binding specificity of Nrd1 by domain swapping. ChIP-chip was performed to examine the effect of Nrd1 CID swapping on genome-wide RNA polymerase II (Rpb3 antibody, Neoclone) occupancy. Nrd1 with the CID from Rtt103 (Nrd1[CID-Rtt103]; strain YSB2445) causes read-through transcription at many genes, but can trigger termination where multiple Nrd1/Nab3-binding sites and serine 2 phosphorylated CTD co-exist.
2013-12-04 | E-MTAB-1626 | biostudies-arrayexpress
Project description:The centromere-specific Histone H3-variant CENH3 (also known as CENP-A) is considered to be an epigenetic mark for establishment and propagation of centromere identity. Pulse-induction of CENH3 (Drosophila CID) in Schneider S2 cells incorporates into noncentromeric regions and generates CID islands that resist clearing from chromosome arms for multiple cell generations. We demonstrate that CID islands represent functional ectopic kinetochores, which are non-randomly distributed on the chromosome and display a preferential localization near telomeres and pericentric heterochromatin in transcriptionally silent, intergenic chromatin domains. Although overexpression of heterochromatin protein 1 (HP1) or increasing Histone acetylation interferes with CID islands formation on a global scale, induction of a locally defined region of synthetic heterochromatin by targeting HP1-LacI fusions to stably integrated Lac Operator arrays produces a proximal hotspot for CID islands formation. These data suggest that the characteristics of regions bordering heterochromatin promote de novo kinetochore assembly and thereby contribute to centromere identity.
2011-07-15 | E-MTAB-652 | biostudies-arrayexpress