Project description:35 paired samples from initial diagnosis and first marrow relapse. Genes and pathways differentiating diagnosis and relapse were identified. Potential therapeutic targets were also identified. Keywords: paired
Project description:Ficolled AML-M0 sample gene expression profiles on Affymetrix HGU133Plus2.0 GeneChips. Acute myeloid leukemia (AML) classified as FAB-M0 is defined as a subtype with minimally differentiated morphology. Here we investigated by gene expression (GEP) profiling whether AML-M0 cases should be considered as one or more unique molecular subgroups that discriminates them from other AML patients. By applying GEP and subsequent unsupervised analysis of 35 AML-M0 samples and 253 previously reported AML cases, we demonstrate that AML-M0 cases express a unique signature. Hematological transcription regulators such as CEBPA, CEBPD, PU.1 and ETV6 and the differentiation associated gene MPO appeared strongly down-regulated, in line with the very primitive state of this type of leukemia. Moreover, AML M0 cases appeared to have a strong positive correlation with a previously defined immature AML subgroup with adverse prognosis. AML-M0 leukemias frequently carry loss-of-function RUNX-1 mutation and unsupervised analyses revealed a striking distinction between cases with and without mutations. RUNX1 mutant AML-M0 samples showed a distinct up-regulation of B-cell-related genes, e.g. members of the B-cell receptor complex, transcriptions regulators RUNX3, ETS2, IRF8 or PRDM1 and major histocompatibility complex class II genes. Importantly, expression of one single gene, i.e. BLNK, enabled prediction of RUNX1 mutations in AML-M0 with high accuracy. We propose that RUNX1 mutations in this subgroup of AML cause lineage infidelity, leading to aberrant co-expression of myeloid and B-lymphoid genes in the same cells.
Project description:modENCODE_submission_3213 This submission comes from a modENCODE project of Michael Snyder. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We are identifying the DNA binding sites for 300 transcription factors in C. elegans. Each transcription factor gene is tagged with the same GFP fusion protein, permitting validation of the gene's correct spatio-temporal expression pattern in transgenic animals. Chromatin immunoprecipitation on each strain is peformed using an anti-GFP antibody, and any bound DNA is deep-sequenced using Solexa GA2 technology. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-seq. BIOLOGICAL SOURCE: Strain: YL409(official name : YL409 genotype : unc-119(ed3) III; vrIs60 [pLIN-35::LIN-35:GFP:FLAG::DPL-1 3'-UTR genotype : unc-119 (+)]) outcross : 0 mutagen : None tags : GFP::3xFlag description : The LIN-35::GFP fusion protein is driven by its own lin-35 promoter. made_by : Michelle Kudron (Valerie Reinke's lab) ); Developmental Stage: fed L1; Genotype: unc-119(ed3) III; vrIs60 [pLIN-35::LIN-35:GFP:FLAG::DPL-1 3'-UTR; Sex: Hermaphrodite; EXPERIMENTAL FACTORS: Developmental Stage fed L1; Target gene lin-35; Strain YL409(official name : YL409 genotype : unc-119(ed3) III; vrIs60 [pLIN-35::LIN-35:GFP:FLAG::DPL-1 3'-UTR genotype : unc-119 (+)]) outcross : 0 mutagen : None tags : GFP::3xFlag description : The LIN-35::GFP fusion protein is driven by its own lin-35 promoter. made_by : Michelle Kudron (Valerie Reinke's lab) ); temp (temperature) 20 degree celsius
Project description:Disruptions of microbiota composition by factors such as genetics have been suggested to be critical contributing factors to the growth of the worldwide epidemics of chronic illness such as metabolic diseases. IL-35-producing regulatory B and T regulatory cells are critical regulators to these illnesses. Whether microbiota-derived metabolites can regulate these IL-35+ cells maintain elusive. Here, we found gut genetic factor Reg4 associated lactobacillus could promote the generation of IL-35+ B cells through producing 3-idoleacetic acid (IAA). HuREG4IEC tg mice had markedly accumulation of IL-35+ not only in adipose tissues but also in colon tissues; whereas significantly decreased IL-35+ cells in adipose tissues and colon tissues could be detected in Reg4 KO mice. On the mechanism, IAA-mediated IL35+ B cells was through PXR), RXR and CAR in the presence of LPS. PXR KO, CAR KO and NF-B KO mice impaired the generation of IAA- IL-35+B cells. Interestingly, lower levels of IAA and IL-35 were also detected in the peripheral blood of individuals with obesity. Thus, IAA is a factor to promote the generation of IL-35+B cells to impede the development of obesity.
Project description:modENCODE_submission_3602 This submission comes from a modENCODE project of Michael Snyder. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We are identifying the DNA binding sites for 300 transcription factors in C. elegans. Each transcription factor gene is tagged with the same GFP fusion protein, permitting validation of the gene's correct spatio-temporal expression pattern in transgenic animals. Chromatin immunoprecipitation on each strain is peformed using an anti-GFP antibody, and any bound DNA is deep-sequenced using Solexa GA2 technology. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-seq. BIOLOGICAL SOURCE: Strain: YL402(official name : YL402 genotype : unc-119(ed3) III; vrIs56[pPIE-1::LIN-35::GFP FLAG: LIN-35 3'-UTR genotype : unc-119 (+)] outcross : 0 mutagen : None tags : GFP::3xFlag description : The LIN-35::GFP fusion protein is driven by the pie-1 promoter. made_by : Michelle Kudron in Reinke lab ); Developmental Stage: Young adult; Genotype: unc-119(ed3) III; vrIs56[pPIE-1::LIN-35::GFP FLAG: LIN-35 3'-UTR; Sex: Hermaphrodite; EXPERIMENTAL FACTORS: Developmental Stage Young adult; Target gene lin-35; Strain YL402(official name : YL402 genotype : unc-119(ed3) III; vrIs56[pPIE-1::LIN-35::GFP FLAG: LIN-35 3'-UTR genotype : unc-119 (+)] outcross : 0 mutagen : None tags : GFP::3xFlag description : The LIN-35::GFP fusion protein is driven by the pie-1 promoter. made_by : Michelle Kudron in Reinke lab ); temp (temperature) 20 degree celsius
Project description:modENCODE_submission_3603 This submission comes from a modENCODE project of Michael Snyder. For full list of modENCODE projects, see http://www.genome.gov/26524648 Project Goal: We are identifying the DNA binding sites for 300 transcription factors in C. elegans. Each transcription factor gene is tagged with the same GFP fusion protein, permitting validation of the gene's correct spatio-temporal expression pattern in transgenic animals. Chromatin immunoprecipitation on each strain is peformed using an anti-GFP antibody, and any bound DNA is deep-sequenced using Solexa GA2 technology. For data usage terms and conditions, please refer to http://www.genome.gov/27528022 and http://www.genome.gov/Pages/Research/ENCODE/ENCODEDataReleasePolicyFinal2008.pdf EXPERIMENT TYPE: CHIP-seq. BIOLOGICAL SOURCE: Strain: YL398(official name : YL398 genotype : unc-119(ed3) III; vrIs55[pGES-1::LIN-35::GFP FLAG: LIN-35 3'-UTR genotype : unc-119 (+)] outcross : 0 mutagen : None tags : GFP::3xFlag description : The LIN-35::GFP fusion protein is driven by the ges-1 promoter and is expressed in the intestine. made_by : Michelle Kudron in Reinke lab ); Developmental Stage: fed L1; Genotype: unc-119(ed3) III; vrIs55[pGES-1::LIN-35::GFP FLAG: LIN-35 3'-UTR; Sex: Hermaphrodite; EXPERIMENTAL FACTORS: Developmental Stage fed L1; Target gene lin-35; Strain YL398(official name : YL398 genotype : unc-119(ed3) III; vrIs55[pGES-1::LIN-35::GFP FLAG: LIN-35 3'-UTR genotype : unc-119 (+)] outcross : 0 mutagen : None tags : GFP::3xFlag description : The LIN-35::GFP fusion protein is driven by the ges-1 promoter and is expressed in the intestine. made_by : Michelle Kudron in Reinke lab ); temp (temperature) 20 degree celsius