Heat stress is one of the most prominent and deleterious environmental threads affecting plant growth and development. Upon high temperatures, plants launch specialized gene expression programs that promote stress protection and survival. These programs involve global and specific changes at the transcriptional and translational levels. However the coordination of these processes and their specific role in the establishment of the heat stress response is not fully elucidated.
Analysis of genome-wide changes in the translatome of Arabidopsis seedlings subjected to heat stress.
Specimen part
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The transcription factor GATA6 enables self-renewal of colon adenoma stem cells by repressing BMP gene expression.
Specimen part, Cell line
View SamplesAberrant activation of WNT signaling and loss of BMP signals represent the two main alterations leading to the initiation of colorectal cancer (CRC). Here we screen for genes required for maintaining the tumor stem cell phenotype and identify the zinc-finger transcription factor GATA6 as key regulator of the WNT and BMP pathways in CRC. GATA6 directly drives the expression of LGR5 in adenoma stem cells while it restricts BMP signaling to differentiated tumor cells. Genetic deletion of Gata6 in mouse colon adenomas increases the levels of BMP factors, which signal to block self-renewal of tumor stem cells. In human tumors, GATA6 competes with beta-catenin/TCF4 for binding to a distal regulatory region of the BMP4 locus that has been previously linked to increased susceptibility to develop CRC. Hence, GATA6 creates a permissive environment for tumor stem cell expansion by controlling the major signaling pathways that influence CRC initiation.
The transcription factor GATA6 enables self-renewal of colon adenoma stem cells by repressing BMP gene expression.
Specimen part, Cell line
View SamplesAberrant activation of WNT signaling and loss of BMP signals represent the two main alterations leading to the initiation of colorectal cancer (CRC). Here we screen for genes required for maintaining the tumor stem cell phenotype and identify the zinc-finger transcription factor GATA6 as key regulator of the WNT and BMP pathways in CRC. GATA6 directly drives the expression of LGR5 in adenoma stem cells while it restricts BMP signaling to differentiated tumor cells. Genetic deletion of Gata6 in mouse colon adenomas increases the levels of BMP factors, which signal to block self-renewal of tumor stem cells. In human tumors, GATA6 competes with beta-catenin/TCF4 for binding to a distal regulatory region of the BMP4 locus that has been previously linked to increased susceptibility to develop CRC. Hence, GATA6 creates a permissive environment for tumor stem cell expansion by controlling the major signaling pathways that influence CRC initiation.
The transcription factor GATA6 enables self-renewal of colon adenoma stem cells by repressing BMP gene expression.
Specimen part, Cell line
View SamplesCryptosporidium hominis and parvum primarily infect intestinal epithelial cells, which, in turn, play a key role in activating and communicating with the host immune system. To determinate which genes are regulated during early infection of non-transformed human epithelial cells, human ileal mucosa was removed (from surgical specimens), placed on collagen membranes, and cultured as explants. Explant cultures were infected with C. parvum, C. hominis, or control culture medium. After 24 hrs, RNA was extracted and analyzed using Affmetrix GeneChip microarrays. Among the more prominent genes with regulated expression was Osteoprotegerin (OPG), which was increased in all of the explants at 24 hrs and further up-regulated 1.58 fold by C. parvum and 2.54 fold by C. hominis infection compared with uninfected explants. Using real time PCR, we confirmed a 3.14 and 3.79 fold increase in OPG mRNA after infection with C. parvum and C. hominis respectively.
Cryptosporidium infection of human intestinal epithelial cells increases expression of osteoprotegerin: a novel mechanism for evasion of host defenses.
No sample metadata fields
View SamplesmRNA profiling of mouse kidney preglomerular arterioles comparing wild type arterioles vs.arterioles from mice having deletion of RBP-J in cells of the renin lineage
Recombination signal binding protein for Ig-κJ region regulates juxtaglomerular cell phenotype by activating the myo-endocrine program and suppressing ectopic gene expression.
Sex, Age
View Samples18 different population of cells in different developmental stages in hematopoietic hierarchy have been purifyed by FACS analyses from wild type C57Bl6 mice and subjected to Micrroarray Affymetrix mouse 430.2 platform
CCAAT/enhancer binding protein alpha (C/EBP(alpha))-induced transdifferentiation of pre-B cells into macrophages involves no overt retrodifferentiation.
No sample metadata fields
View SamplesEarlier work has shown that pre-B cells can be converted into macrophages by the transcription factor C/EBP? at very high frequencies. Using this system we have now performed a systematic analysis of the question whether during transdifferentiation the cells transiently reactivate progenitor restricted genes or even retrodifferentiate. A transcriptome analysis of transdifferentiating cells showed that most genes are continuously up or downregulated, acquiring a macrophage phenotype within 5 days. In addition, we observed the transient reactivation of a subset of immature myeloid markers, as well as low levels of the progenitor markers Kit and Flt3 and a few lineage inappropriate genes. However, we were unable to observe the re-expression of cell surface marker combinations that characterize hematopoietic stem and progenitor cells (HSPCs), including c-Kit and Flt3. This was the case even when C/EBPalpha was activated in pre-B cells under culture conditions that favor HSPC growth or when the transcription factor was activated in a time limited fashion. Together, our findings are consistent with the notion that the conversion from pre-B cells to macrophages is mostly direct and does not involve overt retrodifferentiation.
CCAAT/enhancer binding protein alpha (C/EBP(alpha))-induced transdifferentiation of pre-B cells into macrophages involves no overt retrodifferentiation.
Specimen part, Time
View SamplesCyanide is stoichiometrically produced as a co-product of the ethylene biosynthesis pathway, and it is detoxified by the b-cyanoalanine synthase enzyme. The molecular and phenotypical analysis of T-DNA insertional mutants of the mitochondrial b-cyanoalanine synthase CYS-C1 suggests that discrete accumulation of cyanide is not toxic for the plant and does not alter mitochondrial respiration rates, but does act as a strong inhibitor of root hair development. The cys-c1 null allele is defective in root hair formation and accumulates cyanide in root tissues. The root hair defect is phenocopied in wild type plants by the exogenous addition of cyanide to the growth medium and is reversed by the addition of hydroxocobalamin. Hydroxocobalamin not only recovers the root phenotype of the mutant, but also the formation of ROS at the initial step of the root hair tip. Transcriptional profile analysis of the cys-c1 mutant reveals that cyanide accumulation acts as a repressor signal for several genes encoding enzymes involved in cell wall rebuilding and the formation of the root hair tip, as well as genes involved in ethylene signaling and metabolism. Our results demonstrate that mitochondrial b-cyanoalanine synthase activity is essential to maintain a low level of cyanide for proper root hair development.
Mitochondrial beta-cyanoalanine synthase is essential for root hair formation in Arabidopsis thaliana.
Specimen part
View SamplesTF1a AML cell line was selected for in vitro modelling of dormancy in AML. TF1-a were subjected to AML-niche-mimicking in vitro conditioning by culture with TGFB1 and the mTOR inhibitor rapamycin. Also TF1a cells were in vitro cultured with prolonged sublethal doses of Etoposide.
A molecular signature of dormancy in CD34<sup>+</sup>CD38<sup>-</sup> acute myeloid leukaemia cells.
Specimen part
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