Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA192661 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We used microarrays to develop gene signatures for XBP1 and IRE1 in myeloma cells to explore the role of this UPR/differentiation pathway in proteasome inhibitor resistance. RPMI-8226 and JJN3 human myeloma cells were infected with lentivirus expressing non-targeted (NT) shRNA, shIRE1 or shXBP1 and processed for RNA extraction and hybridization on Affymetrix microarrays. Cells without lentiviral infection were processed as controls for gene expression changes related to the cellular response to lentivirus.
2013-03-09 | E-GEOD-44968 | biostudies-arrayexpress
Project description:We used microarrays to develop gene signatures for XBP1 and IRE1 in myeloma cells to explore the role of this UPR/differentiation pathway in proteasome inhibitor resistance.
2013-03-09 | GSE44968 | GEO
Project description:We developed a bioinformatics approach called the Read-Split-Walk (RSW) pipeline, and evaluated it using two Ire1? heterozygous and two Ire1?-null samples. The 26nt non-canonical splice site in Xbp1 was detected as the top hit by our RSW pipeline in heterozygous samples but not in the negative control Ire1? knockout samples. We compared the Xbp1 results from our approach with results using the alignment program BWA, STAR, Exonerate and the Unix “grep” command. We then applied our RSW pipeline to RNA-Seq data from the SKBR3 human breast cancer cell line. RSW reported a large number of non-canonical spliced regions for 108 genes in chromosome 17, which were identified by an independent study. Identification of non-canonical spliced regions for mouse MEF samples (two Ire1? heterozygous and two Ire1?-null samples)
2014-07-29 | E-GEOD-54631 | biostudies-arrayexpress
Project description:Multiple Myeloma (MM) arises through oncogenic transformation of immunoglobulin-secreting plasma cells. MM often co-opts the central endoplasmic-reticulum (ER)-stress mitigator, inositol-requiring enzyme 1 (IRE1), to sustain malignant growth. While certain MMs require enzymatic IRE1-dependent activation of the transcription factor XBP1s, others display a nonenzymatic IRE1 dependency that is not yet mechanistically understood. Here we identify interferon regulatory factor 4 (IRF4), which stimulates genes that promote immune-cell proliferation, as a key conduit for IRE1’s nonenzymatic control of cell-cycle progression in MM. IRE1 silencing increased inhibitory S114/S270 phosphorylation on IRF4, disrupting IRF4’s chromatin-binding and transcriptional activity. IRF4 knockdown recapitulated, whereas IRF4 repletion reversed the anti-proliferative phenotype of IRE1 silencing. Furthermore, phospho-deficient, but not phospho-mimetic, IRF4 mutants rescued proliferation under IRE1 silencing. Functional studies revealed that IRF4 engages the E2F1 and CDC25A genes and promotes CDK2 activation to drive cell-cycle progression. Our results advance mechanistic understanding of IRE1 and IRF4 in MM.
2025-02-04 | GSE288674 | GEO
Project description:Multiple Myeloma (MM) arises through oncogenic transformation of immunoglobulin-secreting plasma cells. MM often co-opts the central endoplasmic-reticulum (ER)-stress mitigator, inositol-requiring enzyme 1 (IRE1), to sustain malignant growth. While certain MMs require enzymatic IRE1-dependent activation of the transcription factor XBP1s, others display a nonenzymatic IRE1 dependency that is not yet mechanistically understood. Here we identify interferon regulatory factor 4 (IRF4), which stimulates genes that promote immune-cell proliferation, as a key conduit for IRE1’s nonenzymatic control of cell-cycle progression in MM. IRE1 silencing increased inhibitory S114/S270 phosphorylation on IRF4, disrupting IRF4’s chromatin-binding and transcriptional activity. IRF4 knockdown recapitulated, whereas IRF4 repletion reversed the anti-proliferative phenotype of IRE1 silencing. Furthermore, phospho-deficient, but not phospho-mimetic, IRF4 mutants rescued proliferation under IRE1 silencing. Functional studies revealed that IRF4 engages the E2F1 and CDC25A genes and promotes CDK2 activation to drive cell-cycle progression. Our results advance mechanistic understanding of IRE1 and IRF4 in MM.
2025-02-04 | GSE288671 | GEO
Project description:Multiple Myeloma (MM) arises through oncogenic transformation of immunoglobulin-secreting
plasma cells. MM often co-opts the endoplasmic-reticulum (ER) stress mitigator, inositol
requiring enzyme 1 (IRE1), to sustain malignant growth. While certain MMs require enzymatic
IRE1-dependent activation of the ER-homeostatic transcription factor XBP1s, others display
nonenzymatic dependency on IRE1 that is not yet mechanistically understood. Interferon
regulatory factor 4 (IRF4) stimulates gene programs that promote immune-cell proliferation and cell cycle control by IRE1 in MM. Here we show that IRF4 acts as a key conduit of nonenzymatic cell cycle control by IRE1 in MM. IRE1 silencing increased inhibitory phosphorylation of IRF4, disrupting its chromatin-binding activity and mRNA transcription. IRF4 knockdown recapitulated, whereas IRF4 repletion reversed the anti-proliferative phenotype of IRE1 silencing. Functional studies revealed that IRF4 engages the E2F1 and CDC25A genes and promotes CDK2 activation to drive cell cycle progression. Our results advance mechanistic understanding of IRE1 and IRF4 in MM.
| MSV000095907 | MassIVE
Project description:Gene expression profiling of immortalized human mesenchymal stem cells with hTERT/E6/E7 transfected MSCs. hTERT may change gene expression in MSCs. Goal was to determine the gene expressions of immortalized MSCs.
2010-09-25 | GSE24338 | GEO
Project description:Epigenetic silencing of the tumor suppressor RASSF4 favors multiple myeloma progression
| PRJNA335945 | ENA