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Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of mous eAID-silenced plasmacytoma J558 (BALB/c, H-2Ld)cell lines

ABSTRACT: To determine the potential mechanisms by which AID-elimination facilitate better J558 tumor rejection by P1CTL, we performed cDNA microarray analysis to compare AID-silenced J558 cells and their relative controls. Experiment Overall Design: The mouse Affymetrix Mouse Genechips 430-2.0 arrays were hybridized to RNA derived from control and AID-silenced J558 cells according to manufacturerâs directions. Two different pairs of cells (C4 vs AID 2.27 (a) and C5 vs AID 2.13 (b)) were used for RNA extraction and hybridization on Affymetrix microarrays.

ORGANISM(S): Mus musculus

SUBMITTER: Yi Xiao

PROVIDER: E-GEOD-19110 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from AID-silenced mouse plasmacytoma J558 (BALB/c, H-2Ld)cell lines

Project description:To determine the potential mechanisms by which AID-elimination facilitate better J558 tumor rejection by P1CTL, we performed cDNA microarray analysis to compare AID-silenced J558 cells and their relative controls.

2009-11-20 | GSE19110 | GEO

AD and FTLD model mouse, brain, Phosphoproteome

Project description:Using a high-end mass spectrometry, we screened phosphoproteins and phosphopeptides in five types of Alzheimer's disease (AD) mouse models (5xFAD, APP-tg, PS1-tg, PS2-tg and APP-KI) and four types of frontotemporal lobar degeneration (FTLD) mouse models(CHMP2B-KI, PGRN-KI, VCP-KI and TDP43-KI) at multiple time points (1, 3 and 6 months).

2021-09-07 | PXD027119 | Pride

A Cytoskeletal Protein Complex is Essential for Division of Intracellular Amastigotes of Leishmania mexicana (LAND-483 and LAND-536)

Project description:Previous studies in Leishmania mexicana have identified the cytoskeletal protein KHARON as being important for both flagellar trafficking of the glucose transporter GT1 and for successful cytokinesis and survival of infectious amastigote forms inside mammalian macrophages. KHARON is located in three distinct regions of the cytoskeleton: the base of the flagellum, the subpellicular microtubules, and the mitotic spindle. To deconvolve the different functions for KHARON, we have identified two partner proteins, KHAP1 and KHAP2, that associate with KHARON. KHAP1 is located only in the subpellicular microtubules, while KHAP2 is located at the subpellicular microtubules and the base of the flagellum. Both the KHAP1 and KHAP2 null mutants are unable to execute cytokinesis but are able to traffic GT1 to the flagellum. These results confirm that KHARON assembles into distinct functional complexes and that the subpellicular complex is essential for cytokinesis and viability of disease-causing amastigotes but not for flagellar membrane trafficking.

2020-08-17 | PXD019032 | Pride

MicroRNAs differentially expressed in MUC1 overexpressing cells

Project description:To determine if overexpression of MUC1 alters the microRNA profile of pancreatic cancer cells S2.013. Comparison of miRNAs differentially regulated in pancreatic cancer cell line S2.013 with and without MUC1 overexpression. MiRCURY LNA microarray was used to determine differential microRNA expression in one replicate of S2.013.Neo (control) cells compared to S2.013.MUC1 (experimental) cells. Confirmation with qRT-PCR was performed on a subset of microRNAs identified as differentially regulated between the two groups.

2013-08-10 | E-GEOD-48185 | biostudies-arrayexpress

miR-196a is able to restore the aggressive phenotype of Annexin A1 CRISPR/Cas9 knock-out pancreatic cancer cells

Project description:Annexin A1 (ANXA1) is a Ca2+-binding protein involved in pancreatic cancer (PC) progression. It is able to mediate cytoskeletal organization maintaining a malignant phenotype. ANXA1 Knock-Out (KO) MIA PaCa-2 cells partially lost their migratory and invasive capabilities and also the metastatization process is affected in vivo. Here, we investigated the microRNA (miRNA) profile in ANXA1 KO cells. The analysis of the modification in miRNA expression remarked the significant involvement of ANXA1 in PC progression. In this study, we focused on miR-196a which is a well known oncogenic factor in several tumour models and it appeared down-modulated in absence of ANXA1. Furthermore, both ANXA1 and miR-196a are able to trigger the mechanisms of the epithelial to mesenchymal transition (EMT). Our results show that the reintroduction of miR-196a through the mimic sequence restored the early aggressive phenotype of MIA PaCa-2. Then, ANXA1 seems to support the expression of miR-196a and its role. On the other hand, this miRNA is able to mediate some of protein functions in PC progression. This work elucidates the correlation between ANXA1 and specific miRNA sequences, particularly miR-196a, and provides new knowledge about the protein intracellular role.

2018-08-31 | E-MTAB-6599 | biostudies-arrayexpress

Transcription profiling by array of human Caco-2 cells with ATP8B1 knock down

Project description:To gain insights whether and if activation of the nuclear receptor FXR is involved in the disease ethiology of ATP8B1 deficiency, we contstructed a Caco-2 ATP8B1 knock down cell line and a Caco-2 empty vector control cell line. Furthermore we expect to gain new insights from transcriptional profiling of ATP8B1 deficient cells.

2010-12-31 | E-TABM-989 | biostudies-arrayexpress

Transcription profiling of human HUVEC T-cell (CD40L+) induced, anti-CD40-siRNA treated

Project description:The CD40-CD40L dyad seems to play a prominent role fostering the immune-inflammatory response triggered by endothelial cell (EC)-T cell interaction. To comprehensively delineate the involvement of CD40 (TNFRSF5) in EC activation, we combined RNAi-mediated CD40 knock-down with comparative genome-wide transcriptional profiling of EC in response to T cell. We report the initiation of a profound stress response in ECs upon CD40-CD40L engagement through early up-regulation, among others, of the major pro-inflammatory NFkB and MAPK/SAPK pathways and their associated transcription factors. Moreover, we have identified novel genes regulated through the CD40-CD40L interaction, and pathways previously unrecognized to be induced by CD40 signaling in ECs. Thus, we document a strong down-regulation of endothelial APLN by CD40-CD40L interaction, which could lead to vascular tone dysfunction in atherosclerotic lesions. Conversely, CD40-mediated up-regulation of the viral immune surveillance system, notably TLR3, IFIH1, RIG-I, and RNASEL, establishes a reverse link from adaptive to innate immunity in ECs. Moreover, systematic enrichment analysis substantiates endothelial CD40 involvement in the transcriptional regulation of gene networks associated with adhesion and motility, immunity, cell fate control, hemostasis and metabolism. Our study also highlights the potency and specificity of CD40 siRNA mediated inhibition, and the relevance of CD40 signaling pathways for anti-inflammatory therapeutic intervention. Experiment Overall Design: Time course experiment comparing endothelial gene expression profiling of CD40-silenced versus non-silenced cultured cells using RNA interference. Two independent experiments were performed where HUVECs were siRNA-transfected and co-cultured with Jurkat D1.1 for 4, 10, 16 h and harvested for RNA extraction. Technical dye swap duplicates were performed for each of the two biological replicates in all three time points.

2009-02-21 | E-GEOD-10601 | biostudies-arrayexpress

Transcriptome profiling of breast cancer cells with Insulin like growth factor binding protein 2 (IGFBP2) knockdown

Project description:The study was carried out to identify the genes regulated upon IGFBP2 modulation in breast cancer. This will help to understand the molecular targets and biological pathways targeted by IGFBP2 in breast cancer. C5 (Cy5) Vs. Vector(Cy3), C5 (Cy5) Vs. Vector(Cy3), C12 (Cy5) Vs. Vector(Cy3), C12 (Cy5) vs. Vector(Cy3)

2013-09-06 | E-GEOD-40682 | biostudies-arrayexpress

Transcriptional effects of CSB and the CSB-PGBD3 fusion protein in CSB-null UVSS1KO cells

Project description:Cockayne syndrome is a segmental progeria most often caused by mutations in the CSB gene encoding a SWI/SNF-like ATPase required for transcription-coupled DNA repair (TCR). Over 43 Mya before marmosets diverged from humans, a piggyBac3 (PGBD3) transposable element integrated into intron 5 of the CSB gene. As a result, primate CSB genes now generate both CSB protein and a conserved CSB-PGBD3 fusion protein in which the first 5 exons of CSB are alternatively spliced to the PGBD3 transposase. We show by microarray analysis that expression of the fusion protein alone in CSB-null UV-sensitive syndrome cells (UVSS1KO) cells induces an interferon-like response that resembles both the innate antiviral response and the prolonged interferon response normally maintained by unphosphorylated STAT1 (U-STAT1); moreover, as might be expected based on conservation of the fusion protein, this potentially cytotoxic interferon-like response is largely reversed by coexpression of functional CSB protein. Interestingly, expression of CSB and the CSB-PGBD3 fusion protein together, but neither alone, upregulates the insulin growth factor binding protein IGFBP5 and downregulates IGFBP7, suggesting that the fusion protein may also confer a metabolic advantage, perhaps in the presence of DNA damage. Finally, we show that the fusion protein binds in vitro to members of a dispersed family of 900 internally deleted piggyBac elements known as MER85s, providing a potential mechanism by which the fusion protein could exert widespread effects on gene expression. Our data suggest that the CSB-PGBD3 fusion protein is important in both health and disease, and could play a role in Cockayne syndrome. 12 samples total; 4 gene expression conditions in triplicate; 1 condition is a tag-only negative control

2014-03-20 | E-GEOD-56049 | biostudies-arrayexpress

Transcription profiling of human HEK cells transfected with the calcium regulated gene HcARG reveals HCaRG increases renal cell migration by a TGF-alpha autocrine loop mechanism

Project description:HEK293 cells were transfected with control plasmid (pcDNA1/Neo; Invitrogen) or with the plasmid encoding HCaRG by a standard calcium phosphate co-precipitation method. The clones expressing the highest levels of HCaRG, HCaRG clone 8 and 9 were used in this experiment, while clone transfected with vector alone, Neo clone, served as controls. Stable transfectants were synchronized and grown in the presence of 10% FBS for 48 h. Total RNAs were purified with the mini RNeasy kit (Qiagen).

2007-11-11 | E-GEOD-4737 | biostudies-arrayexpress

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