Mouse proteome pofiler array from AP and NP group.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE252915 | GEO | 2025/06/04
REPOSITORIES: GEO
Similar Datasets
Project description:Mouse proteome pofiler array from AP and NP group.
| PRJNA1063239 | ENA
Project description:Background: Negative-pressure wound therapy has become widely available in modern chronic wound cares. Accelerated keratinocyte (HaCaT cell) movements and decreased E-cadherin expressions induced by the applied negative pressure gradient of 125 mmHg (NP) have been reported in previous studies. However, the molecular mechanism for E-cadherin regulations under NP remains unexplored. We highlighted the signal transduction involved in NP-induced E-cadherin regulation for keratinocytes in the study. Results: Microarray results showed that catenin 1 (CTNND1) gene, the gene encoding the p120-catenin (p120ctn) in cell-cell junctions, was significantly (p = 0.0005) upregulated in HaCaT cells under NP for 12 hours in comparison with those at ambient pressure (AP). Cell fractionations and immunoblotting data showed that NP increased p120ctn phosphorylation, and resulted in p120ctn translocation from the plasma membrane to the cytoplasm. Fluorescent stains suggested that NP diminished the co-localization of p120ctn and E-cadherin on the plasma membrane. Similar phenomenon was also observed in the cells with overexpressed p120ctn at NP. Interestingly, overexpression of dN- p120ctn, a deletion mutant of p120ctn without the N-terminal phosphorylation sites, restored the adherens junctions (AJ) at NP. Knockdown of p120ctn with lentiviral small hairpin RNA not only diminished E-cadherin expressions but also accelerated cell movement at AP. Conclusions: Phosphorylation of p120ctn is endowed to respond rapidly to NP and contributes to the AJ disassembly. This NP-induced E-cadherin downregulation can possibly accelerate wound-healing process. Conclusions: Phosphorylation of p120ctn is endowed to respond rapidly to NP and contributes to the AJ disassembly. This NP-induced E-cadherin downregulation can possibly accelerate wound-healing process. HaCaT cells under negative pressure (NP) gradient of 125 mmHg for 12 hours in comparison with those at ambient pressure (AP) were tested for RNA extraction and hybridization on Affymetrix microarrays. The experiments have been biological replicated three times. The differential expression gene between NP and AP were selected and validated with qPCR method.
2015-12-31 | E-GEOD-70512 | biostudies-arrayexpress
Project description:Background: Negative-pressure wound therapy has become widely available in modern chronic wound cares. Accelerated keratinocyte (HaCaT cell) movements and decreased E-cadherin expressions induced by the applied negative pressure gradient of 125 mmHg (NP) have been reported in previous studies. However, the molecular mechanism for E-cadherin regulations under NP remains unexplored. We highlighted the signal transduction involved in NP-induced E-cadherin regulation for keratinocytes in the study. Results: Microarray results showed that catenin 1 (CTNND1) gene, the gene encoding the p120-catenin (p120ctn) in cell-cell junctions, was significantly (p = 0.0005) upregulated in HaCaT cells under NP for 12 hours in comparison with those at ambient pressure (AP). Cell fractionations and immunoblotting data showed that NP increased p120ctn phosphorylation, and resulted in p120ctn translocation from the plasma membrane to the cytoplasm. Fluorescent stains suggested that NP diminished the co-localization of p120ctn and E-cadherin on the plasma membrane. Similar phenomenon was also observed in the cells with overexpressed p120ctn at NP. Interestingly, overexpression of dN- p120ctn, a deletion mutant of p120ctn without the N-terminal phosphorylation sites, restored the adherens junctions (AJ) at NP. Knockdown of p120ctn with lentiviral small hairpin RNA not only diminished E-cadherin expressions but also accelerated cell movement at AP. Conclusions: Phosphorylation of p120ctn is endowed to respond rapidly to NP and contributes to the AJ disassembly. This NP-induced E-cadherin downregulation can possibly accelerate wound-healing process. Conclusions: Phosphorylation of p120ctn is endowed to respond rapidly to NP and contributes to the AJ disassembly. This NP-induced E-cadherin downregulation can possibly accelerate wound-healing process.
2015-12-31 | GSE70512 | GEO
Project description:Pancreatic cancer-derived cells NP-18 underwent four rounds of treatment with increasing doses of an adenoviral vector encoding TK enzyme and GCV. Surviving cells were termed NP-18AR and displayed decreased sensitivity to treatment. This experiment analyses the transcriptomic effect of TK/GCV treatment on NP-18AR as compared to that of NP-18 cells. Two-condition experiment, where response to treatment in naïve cells (NP-18) was compared to response to treatment in previously treated resistant cells (NP-18AR). Biological replicates: samples from 3 independently generated and independently treated NP-18AR lines (NP-18AR1, NP-18AR2 and NP-18AR3) were hibridized with 3 independently treated samples of NP-18 cells. A total of 9 hybridizations were performed, 2 for NP-18AR1 (including 1 dye-swap), 4 for NP-18AR2 (including 2 dye swaps) and 3 for NP-18AR3 (including 1 dye-swap).
2010-07-16 | E-GEOD-17137 | biostudies-arrayexpress
Project description:Pancreatic cancer-derived cells NP-18 underwent four rounds of treatment with increasing doses of an adenoviral vector encoding TK enzyme and GCV. Surviving cells were termed NP-18AR and displayed decreased sensitivity to treatment. This experiment analyses the transcriptomic effect of TK/GCV treatment on NP-18AR as compared to that of NP-18 cells.
2010-07-16 | GSE17137 | GEO
Project description:A diet rich in nucleic acids and protamin protein, termed as nucleoprotein was used for the study. Mice were fed with NP diets for 4 weeks followed by removal of the liver and spleen. Total RNA extracted from livers and spleens was pooled in each group (low NP or LNP-control, and 1.2% NP-treatment, diets), prior to DNA microarray analysis (Agilent mouse whole genome 4 x 44K). Results revealed 1373 & 3386 up (>1.5 fold)- and down (<0.75 fold)-regulated genes in the liver, and 252 & 1838 up- and down-regulated genes in the spleen, respectively following 1.2%NP diet. Analysis of genes related to NP diets will be discussed. To investigate the effect of NP, we added S-nuclegen® at a concentration of 1.2% into CLEA basic purified diet (CLEA JAPAN, Inc., Tokyo, Japan) known to include nucleic acids (NAs) at much lower amounts than standard diet. By HPLC analysis CLEA basic purified diet (low NP), and 1.2% NP diet included 0.03%, and 0.5% NAs, respectively. Male C57BL/6J mice (13 weeks) were fed with NP diet for 4 weeks. The liver and spleen were removed and deep frozen in liquid nitrogen. Whole blood was also sampled from these mice, and frozen in liquid nitrogen. Total RNA extracted from livers and spleens was pooled in each group (control, lowNP or LNP; and treatment, 1.2%NP), prior to DNA microarray analysis (Agilent mouse whole genome 4 x 44K).
2011-04-13 | E-GEOD-28505 | biostudies-arrayexpress
Project description:The combined effects of NP and MBP were much more toxic than NP or MBP exposed alone. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes and miRNAs after treated with 0.1μM NP, 0.1mM MBP, 0.1μM NP+0.1mM MBP and solvent control.
2016-06-09 | GSE83105 | GEO
Project description:The physiological function of the intervertebral disc (IVD) depends on the cellular and molecular composition of the nucleus pulposus (NP), which plays a key role in managing the mechanical loading of the IVD.We conducted single-cell RNA sequencing (scRNA-seq) analysis to better characterize the NP cells, particularly the Shh-tdTom+ NP cells, in the adult Shh-CreER; Rosa26tdTomato mice.
2025-02-15 | GSE255488 | GEO
Project description:This phase I trial is studying the best dose of 3-AP and the side effects of giving 3-AP together with gemcitabine in treating patients with advanced solid tumors or lymphoma. Drugs used in chemotherapy, such as 3-AP and gemcitabine (GEM), work in different ways to stop the growth of cancer cells, either by killing the cells or by stopping them from dividing. 3-AP may help gemcitabine kill more cancer cells by making the cells more sensitive to the drug. 3-AP may also stop the growth of tumor cells by blocking some of the enzymes needed for cell growth.
| 2026481 | ecrin-mdr-crc