Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA280091 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To determine the biological effects of MPS1 inhibition (both by siRNA and Drug (NMSP715)) on signaling pathways in GBM cells (U251 &U87), we profiled the modulation of phosphorylated and non-phosphorylated proteins using RPPA Relative protein levels for each sample were determined by interpolation of each dilution curves from the standard curve antibody slide. All the data points were normalized for protein loading and transformed to a linear value. Linear values were transformed to Log2 value and then median‐centered for hierarchical cluster analysis.
2015-06-25 | E-GEOD-67502 | biostudies-arrayexpress
Project description:To determine the biological effects of MPS1 inhibition (both by siRNA and Drug (NMSP715)) on signaling pathways in GBM cells (U251 &U87), we profiled the modulation of phosphorylated and non-phosphorylated proteins using RPPA
2015-06-25 | GSE67502 | GEO
Project description:The calcitonin receptor (CTR) signaling axis has been implicated in growth regulation in Glioblastoma (GBM). This study examines the molecular and signaling effects of salmon calcitonin (sCT) treatment in GBM using proteomic, cellular, in vivo, and computational approaches. Reverse Phase Protein Array (RPPA) analysis was performed to assess changes in protein expression in glioma cells following sCT treatment and to identify signaling pathways associated with CTR activation. Complementary biochemical and functional assays were used to characterize CTR-mediated regulation of the Hippo pathway. CTR expression was found to be elevated in human and murine glioma stem-like cells in comparison to their differentiated counterparts, and intranasal sCT treatment lead to decrease in the GSC-initiated tumor growth in orthotopic mouse glioma model. In parallel, microsecond-scale all-atom molecular dynamics simulations were conducted to examine structural features of wild-type and patient-derived mutant CTR variants and their interactions with calcitonin and Gα subunits. Together, this work reveals mechanism of CT/CTR axis, therapeutic implications of sCT, and impact of structural alterations in patient-derived CTR variants in GBM.
2026-02-10 | GSE319121 | GEO
Project description:Gene expression changes were analyzed in U251 GBM cells after downregulation of MPS1 by RNA interference technology at different time points
2015-06-15 | GSE57091 | GEO
Project description:Gene expression changes were analyzed in U251 GBM cells after downregulation of MPS1 by RNA interference technology at different time points Microarray analysis was used to compare the mRNA expression profile of siMPS1 silenced U251 cells compared to siNegative (siNeg) and untransfected (Control) cells at 6, 24 and 48 hours post tranfection
2015-06-15 | E-GEOD-57091 | biostudies-arrayexpress
Project description:Chromobox protein homolog 7 (CBX7) can inhibit the progression of various tumors, but its impact on the stem cell-like properties of GBM cells remains unclear. Clinically, low levels of CBX7 are associated with poor prognosis and increased distant metastasis in GBM patients, and this low expression is caused by methylation of the CBX7 promoter. In this study, through bioinformatics analysis, we found that CBX7 is the most significantly downregulated member of the CBX family in GBM and is closely associated with the stem-like phenotype of GBM cells. Subsequent research showed that CBX7 promotes the degradation of myosin heavy chain 9 (MYH9) protein through the ubiquitin-proteasome pathway via the polycomb repressive complex (PRC1) and suppresses the stem-like phenotype of GBM cells by inhibiting the nuclear factor kappa-B (NF κB) signaling pathway. Furthermore, overexpression of MYH9 in GBM cells can reverse the inhibitory effects of CBX7 on migration, proliferation, invasion, and stemness of GBM cells. In summary, CBX7 acts as a tumor suppressor by inhibiting the stem cell-like characteristics of GBM. The CBX7-MYH9-NF-κB signaling axis may serve as a potential therapeutic target for GBM.
2024-12-08 | GSE283387 | GEO
Project description:Chemotaxis is used by free-living motile bacteria to swim towards nutrient sources or away from repellents, and to navigate the environment to locate niches optimal for growth and survival. Multiple chemotaxis systems have been identified in different bacterial species, including Azospirillum brasilense. In A. brasilense, chemotaxis is mediated by two distinct chemotaxis pathways, named Che1 and Che4, that physically interact to form mixed chemotaxis signaling arrays. Signaling from the Che1 and Che4 pathways control transient increases in swimming speed and swimming reversals, respectively, during chemotaxis. In A. brasilense, chemotaxis is tightly linked to energy metabolism with this coupling occurring through the sensory input of several energy-sensing chemoreceptors and through the control of chemoreceptor activity by the c-di-GMP second messenger. Previous work has demonstrated that chemotaxis in A. brasilense also affects unrelated cellular functions including cell-to-cell clumping and flocculation. However, the molecular mechanism for these effects is not known. Here, we identify additional effects of mutations abolishing Che1 (cheA1 mutant), Che4 (cheA4 mutant) or both Che1 and Che4 (cheA1/cheA4 mutant) function on nitrogen and carbon metabolism and use whole cell proteome and metabolome mass spectrometry to further characterize the interplay between chemotaxis and metabolism. We found that CheA1 mediates most changes in chemoreceptor arrays composition and also affects small molecules signaling while a mutant lacking CheA4 displays changes in nitrogen metabolism, including nitrate assimilation and nitrogen fixation. In contrast, the mutant lacking both CheA1 and CheA4, which lacks chemotaxis and does not form chemotaxis signaling arrays, displays distinct and non-overlapping changes that suggest the assembly of chemotaxis signaling arrays modulates energy and carbon metabolism. Together, the results suggest distinct roles for CheA1, CheA4 and chemotaxis signaling arrays in modulating chemotaxis and metabolism, likely through control of distinct global regulatory networks.
2020-08-25 | MSV000086008 | MassIVE