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Transcription profiling of human OCUBM cells trasfected with IGF1R

ABSTRACT: This SuperSeries is composed of the following subset Series:; GSE5224: Expression data from OCUBM cells trasfected with 12G FEZL; GSE5225: Expression data from OCUBM cells trasfected with IGF1R Experiment Overall Design: Refer to individual Series

ORGANISM(S): Homo sapiens

SUBMITTER: Mayumi Sugimoto

PROVIDER: E-GEOD-5231 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcription profiling of human breast cancer-derived OCUB-M cells transfected with expression vector encoding 12GFEZL

Project description:To investigate genes that might influence resistance to infection through IGF1R, we screened human breast cancer-derived OCUB-M cells transfected with expression vector encoding IGF1R using microarray analysis. Experiment Overall Design: OCUBM cells were transfected with/without IGF1R for RNA extraction and hybridization on Affymetrix microarrays.

2009-07-04 | E-GEOD-5225 | biostudies-arrayexpress

Transcription profiling of human breast cancer-derived OCUB-M cells transfected with expression vector encoding IGF1R

Project description:To identify genes that influence resistance to mastitis, we scanned; a whole genome of 181 susceptible and 297 resistant cows and revealed; significant linkage to Bos taurus autosomal chromosome (BTA) 21 with a; likelihood of odds (LOD) score of 28. Because FEZL is a transcription factor that influences resistance to mastitis, we compared LOD scores of BTA21 among cows carrying 12G/12G, 12G/13G, and 12G/13GFEZL to evaluate whether FEZL affects linkage in this chromosome. Cows carrying 13G/13GFEZL had the most significant linkage with a LOD score of 35, despite a decrease in the number of samples from 478 to 224. This finding suggested that the gene influencing resistance to mastitis on BTA21 might be controlled by FEZL. To investigate genes that might influence resistance to mastitis through FEZL, we screened human breast cancer-derived OCUB-M cells transfected with expression vector encoding 12GFEZL using microarray analysis. Experiment Overall Design: OCUBM cells were transfected with/without 12G FEZL for RNA extraction and hybridization on Affymetrix microarrays.

2009-07-04 | E-GEOD-5224 | biostudies-arrayexpress

Homo sapiens

Project description:Expression data from OCUBM cells trasfected with IGF1R

| PRJNA104293 | ENA

Transcription profiling of mouse ventricles of IGF1R, IGF1R-caPI3K, IGF1R-dnPI3K, caPI3K, dnPI3K transgenic female mice at 3 months of age vs. non transgenic littermate controls

Project description:IGF1 and IGF1 receptors (IGF1R) are present in the adult heart and have been shown to be essential for myocardial performance. Insulin-like growth factor 1 (IGF1) is produced in numerous tissues particularly by the liver in response to growth hormone stimulation and is an important factor in the regulation of post-natal growth and development. We have generated and characterized transgenic mice over-expressing the IGF1R. We crossed IGF1R transgenic mice with dominant negative (dn)PI3K (p110) and with constitutively active (ca)PI3K(p110) transgenic mice. Expression profiling was performed on the ventricles of IGF1R, IGF1R-caPI3K, IGF1R-dnPI3K, caPI3K, dnPI3K transgenic female mice at 3 months of age. Non-transgenic littermates were used as controls.

2007-09-29 | E-GEOD-1143 | biostudies-arrayexpress

Transcriptional analysis of tendons from mice with a tenocyte-specific deletion of IGF1R

Project description:We report RNA sequencing data from the plantaris tendons of adult male mice in the C57Bl/6 background that either have the IGF1 receptor (IGF1R) present in their tendons (Scx:IGF1R+) or mice in which IGF1R has been deleted in tenocytes expressing scleraxis (Scx:IGF1R-). Mice were created by crossing ScxCreERT2 mice with IGF1R flox/flox mice. Mice were treated with tamoxifen for 5 days to induce recombination at the IGF1R allele, and then subjected to a synergist ablation procedure in which the Achilles tendon is removed, resulting in compensatory growth of the plantaris tendon. Mice were analyzed either 7 or 14 days after synergist ablation. Control mice that did not undergo tamoxifen treatment or synergist ablation were also studied.

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Expression data from OCUBM cells trasfected with IGF1R

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Transcriptomic study on the effect of Igf1r deficiency in control and bleomycin-challenged mouse lungs.

Project description:Acute lung injury (ALI), ARDS and COVID-19 usually involve a “cytokine storm”. IGF1R (Insulin-like growth factor receptor 1) maintains lung homeostasis and is implicated in these pulmonary inflammatory diseases. In mice, widespread IGF1R deficiency was reported to counteract respiratory inflammation and alveolar damage after bleomycin (BLM)-induced ALI. To explore the molecular mechanisms mediated by Igf1r signaling after BLM challenge, we performed RNA-sequencing in lungs of IGF1R-deficient mice after BLM or saline (SAL) instillation. Transcriptomic analysis identified differentially expressed genes between BLM-challenged and SAL-treated control lungs, detecting biological processes and signaling pathways involved in ALI pathobiology. Igf1r depletion in BLM-challenged mice reversed large part of the transcriptional changes triggered by BLM, counteracting the transcriptomic profile of the inflammatory "cytokine storm". Data mining also identified changes in the expression of gene clusters with key roles in DNA damage, metabolic reprogramming, mitochondrial homeostasis, and epigenetics. Exploration of these functional groups, together with validation studies, provide new insights into the molecular mechanisms underlying the attenuating effect of Igf1r deficiency on ALI. These findings allow a more comprehensive view of IGF1R signaling at the transcriptional level, reinforcing its important role in promoting ALI and postulating it as a global epigenetic regulator in ARDS.

2024-11-01 | GSE274184 | GEO

Detect IGF1R function in postnatal bone marrow mesenchymal stem cell

Project description:1. IGF1R signaling pathway is highly enriched in P0.5 BMMSC compared to adult BMMSC; 2. Niche factors are highly expressed in PDGFRa+Sca1+ (PaS) cells. 3. Knockout IGF1R in Prx1+ BMMSC significantly impaired niche factors expression in P0.5 BMMSC.

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Transcription profiling of mouse CD8-IGF1R 3T3 cells and 3T3 Vector control treated for 24 h with vehicle or IGF1R inhibitor A-928605 reveals reversal of oncogene transformation and suppression of tumor growth by the novel IGF1R kinase inhibitor A-928605.

Project description:The insulin-like growth factor (IGF) axis is an important signaling pathway in the growth and survival of many cell types and has been implicated in multiple aspects of cancer progression from tumorigenesis to metastasis. The multiple roles of IGF signaling in cancer suggest that selective inhibition of the pathway might yield clinically effective therapeutics. Here we describe A-928605, a novel small molecule inhibitor of the receptor tyrosine kinase responsible for IGF signal transduction. This small molecule is able to abrogate activation of the pathway as shown by effects on the target and downstream effectors and is shown to be effective at inhibiting the proliferation of an oncogene addicted tumor model cell line (CD8-IGF1R 3T3) both in vitro and in vivo. Experiment Overall Design: CD8-IGF1R 3T3 cells and 3T3 Vector control treated for 24 h with vehicle or IGF1R inhibitor A-928605, all with 3 replicates.

2009-06-11 | E-GEOD-14024 | biostudies-arrayexpress

Decreased IGF1R Attenuates Senescence and Improves Function in Pancreatic beta-Cells

Project description:We previously reported that increased expression of IGF1R in mouse and human beta-cells is a marker of older beta-cells; however, its contribution to age-related dysfunction and cellular senescence remains to be determined. In this study, we explored the direct role of IGF1R in beta-cell function and senescence using inducible beta-cell specific IGF1R knockdown (betaIgf1rKD) mice. Adult betaIgf1rKD mice showed improved glucose clearance and glucose-induced insulin secretion, accompanied by decreased p21Cip1 protein expression in beta-cells. RNASeq of islets isolated from these betaIgf1rKD mice revealed restoration of 3 signaling pathways known to be downregulated by aging: sulfide oxidation, autophagy, and mTOR signaling. Additionally, deletion of IGF1R in mouse beta-cells increased transcription of genes important for maintaining beta-cell identity and function, such as Mafa, Nkx6.1, and Kcnj11, while decreasing senescence-related genes, such as Cdkn2a, Il1b, and Serpine 1. These results suggest that IGF1R signaling plays a causal role in aging-induced beta-cell dysfunction.

2023-06-19 | GSE229709 | GEO

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