Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA173550 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE40323: KLF7 KO vs WT HSPC expression array GSE40324: HSC expression array GSE40327: KLF7 overexpression in HSPCs expression array Refer to individual Series
2012-08-24 | E-GEOD-40331 | ArrayExpress
Project description:Increased expression of Kruppel like factor 7 (KLF7) is an independent predictor of poor outcome in pediatric acute lymphoblastic leukemia. The contribution of KLF7 to hematopoiesis has not been previously described. Herein, we characterized the effect on murine hematopoiesis of the loss of KLF7 and enforced expression of KLF7. Long-term multilineage engraftment of Klf7-/- cells was comparable to control cells, and self-renewal, as assessed by serial transplantation, was not affected. Enforced expression of KLF7 results in a marked suppression of myeloid progenitor cell growth and a loss of short- and long-term repopulating activity. Interestingly, enforced expression of KLF7, while resulting in multi-lineage growth suppression that extended to hematopoietic stem cells and common lymphoid progenitors, spared T cells and enhanced the survival of early thymocytes. RNA expression profiling of KLF7-overexpressing hematopoietic progenitors identified several potential target genes mediating these effects. Notably, the known KLF7 target Cdkn1a (p21Cip1/Waf1) was not induced by KLF7, and loss of CDKN1A does not rescue the repopulating defect. These results suggest that KLF7 is not required for normal hematopoietic stem and progenitor (HSPC) function, but increased expression, as seen in a subset of lymphoid leukemia, inhibits myeloid cell proliferation and promotes early thymocyte survival. KLF7 overexpression in HSPCs expression array: Lin- c-Kit+ Sca-1+ cells transduced with a KLF7 expressing or control (empty vector) lentivirus. Expression profiles of KLF7 overexpressing vs controls HSPCs. Cells were harvested 72 hrs post-transduction to compare expression profiles of control vs KLF7 overexpressing HSPCs
2012-08-24 | E-GEOD-40327 | ArrayExpress
Project description:Kruppel-like transcription factor 7 (KLF7) is a negative regulator of adipogenesis, however, its precise mechanism is poorly understood. Our previous KLF7 ChIP-seq analysis showed that one of the KLF7 binding peaks was present upstream of GATA binding protein 3 (GATA3) in chicken preadipocytes. In the present study, we identified GATA3 as a target of KLF7. Overexpression analysis showed KLF7 markedly enhanced the endogenous expression of GATA3 in the immortalized chicken preadipcyte cell line (ICP2), and the luciferase reporter assay showed that KLF7 overexpression increased the reporter gene activity of the cloned upstream region (-5285/-4336 relative to the translation initiation codon ATG) of GATA3 in ICP2 and DF1 cells, and mutation of the putative KLF7 binding site abolished the promotive effect of KLF7 overexpression on the reporter gene activity of the cloned GATA3 upstream region. ChIP-qPCR further demonstrated that KLF7 directly bound to the GATA3 upstream region. Gene expression analysis showed that GATA3 mRNA expression in abdominal adipose tissue was significantly higher in lean chicken line than in the fat line at 2, 3, and 6 weeks of age. In addition, GATA3 mRNA expression markedly decreased during the preadipocyte differentiation. Furthermore, a functional study showed that GATA3 overexpression inhibited the differentiation of the ICP2 cells. Taken together, our results demonstrated that KLF7 inhibits chicken adipogenesis, at least in part through direct upregulation of GATA3.
2020-01-01 | S-EPMC7298121 | BioStudies
Project description:Axon regeneration in the central nervous system normally fails, in part because of a developmental decline in the intrinsic ability of CNS projection neurons to extend axons. Members of the KLF family of transcription factors regulate regenerative potential in developing CNS neurons. Expression of one family member, KLF7, is down-regulated developmentally, and overexpression of KLF7 in cortical neurons in vitro promotes axonal growth. To circumvent difficulties in achieving high neuronal expression of exogenous KLF7, we created a chimera with the VP16 transactivation domain, which displayed enhanced neuronal expression compared with the native protein while maintaining transcriptional activation and growth promotion in vitro. Overexpression of VP16-KLF7 overcame the developmental loss of regenerative ability in cortical slice cultures. Adult corticospinal tract (CST) neurons failed to up-regulate KLF7 in response to axon injury, and overexpression of VP16-KLF7 in vivo promoted both sprouting and regenerative axon growth in the CST of adult mice. These findings identify a unique means of promoting CST axon regeneration in vivo by reengineering a developmentally down-regulated, growth-promoting transcription factor.
1000-01-01 | S-EPMC3358880 | BioStudies
Project description:BACKGROUND:Malignant brain tumors have been a serious threat to human health worldwide. This study aims to investigate the role of miR-136-3p in glioma development. METHODS:Hematoxylin-eosin staining (H&E) staining was used to determine the pathologic alterations of glioma tissues. Quantitative real-time PCR (qRT-PCR) analysis and GEO2R analysis was performed to examine the expression of miRNAs and genes. Western blot was applied to detect the protein expression. Cell counting kit-8 (CCK-8) and colony formation were used to analyze the glioma cell growth. Trans-well assay was used to determine the cell migration. Annexin V-FITC/PI staining was conducted to determine the cell apoptosis of transfected glioma cells. The dual-luciferase reporter assay was carried out to confirm the binding sites of miR-136-3p on 3' untranslated regions (3' UTR) of Kruppel-like factor 7 (KLF7). Tumor-bearing experiment in nude mice was performed to comprehensively investigate the role of miR-136-3p/KLF7 axis in gliomas. RESULTS:Firstly, the results showed that miR-136-3p was decreased in glioma tissues compared with adjacent tissues. Overexpression of miR-136-3p significantly inhibited cell growth of LN-229 and U251 by decreasing expression of Cyclin A1 and PCNA (proliferating cell nuclear antigen), and it suppressed glioma cell migration by downregulating N-cadherin and elevating E-cadherin levels, and it also promotes glioma cell apoptosis by promoting Bcl2-associated X (Bax) expression but suppressing Bcl-2 expression. Furthermore, we observed that KLF7 was a direct target of miR-136-3p, and KLF7 was negatively regulated by miR-136-3p in glioma cells. Finally, overexpression of KLF7 partly blocked miR-136-3p-induced inhibition of tumor growth in vitro and in vivo. CONCLUSIONS:Targeting miR-136-3p/KLF7 axis might be a novel manner to counter against gliomas.
2020-01-01 | S-EPMC7367243 | BioStudies
Project description:This experiment is one of a series of experiments on interspecific recombinant congenic strain (IRCS) mice that aimed to identify novel genes involved in male or female hyporfertility by comparing characteristics of the sperm, number of offspring, quality of implantation etc. in C57B6/J and IRCS mice. <br>The goal of this experiment was to understand the basis of female hypofertility/embryonic resorption in a mouse model of congenic strains. The IRCS strain used in this experiment is the 66H Ch13 mouse. This strain was derived by introgression of a ~6 Mb fragment of mus spretus origin inside the genome of Mus musculus (C57B6/J) (L'hôte et al, Bioessays, 2010. PMID:20091755 ) Previous ultrasonographic analysis of this line revealed an increased rate of embryonic resorption compared to the C57B6/J parent (Laissue et al, Int. J . Dev. Biol, 2009 PMID: 19488966 ). <br>In this experiment we measured gene expression in the tissues that are relevant for implantation and early development, i.e. the uterus and the placenta, in C57B6/J and 66H Chr13 mice at 12 days post-coïtus with C57B6/J males. Pools of RNA from four mice per sample were obtained and analysed using a Nimblegen mouse expression array.
2016-10-14 | E-MTAB-4643 | BioStudies
Project description:The ability, propensity and need to mount an immune response vary both among individuals and within a single individual over time.A wide array of parameters has been found to influence immune state in carefully controlled experiments, but we understand much less about which of these parameters are important in determining immune state in wild populations.Diet can influence immune responses, for example when nutrient availability is limited. We therefore predict that natural dietary variation will play a role in modulating immune state, but this has never been tested.We measured carbon and nitrogen stable isotope ratios in an island population of house mice Mus musculus domesticus as an indication of dietary variation, and the expression of a range of immune-related genes to represent immune state.After accounting for potential confounding influences such as age, sex and helminth load, we found a significant association between carbon isotope ratio and levels of immune activity in the mesenteric lymph nodes, particularly in relation to the inflammatory response.This association demonstrates the important interplay between diet and an animal's response to immune challenges, and therefore potentially its susceptibility to disease. A plain language summary is available for this article.
2019-01-01 | S-EPMC6767599 | BioStudies
Project description:Increased expression of Kruppel-like factor 7 (KLF7) is an independent predictor of poor outcome in pediatric acute lymphoblastic leukemia. The contribution of KLF7 to hematopoiesis has not been previously described. Herein, we characterized the effect on murine hematopoiesis of the loss of KLF7 and enforced expression of KLF7. Long-term multilineage engraftment of Klf7(-/-) cells was comparable with control cells, and self-renewal, as assessed by serial transplantation, was not affected. Enforced expression of KLF7 results in a marked suppression of myeloid progenitor cell growth and a loss of short- and long-term repopulating activity. Interestingly, enforced expression of KLF7, although resulting in multilineage growth suppression that extended to hematopoietic stem cells and common lymphoid progenitors, spared T cells and enhanced the survival of early thymocytes. RNA expression profiling of KLF7-overexpressing hematopoietic progenitors identified several potential target genes mediating these effects. Notably, the known KLF7 target Cdkn1a (p21(Cip1/Waf1)) was not induced by KLF7, and loss of CDKN1A does not rescue the repopulating defect. These results suggest that KLF7 is not required for normal hematopoietic stem and progenitor function, but increased expression, as seen in a subset of lymphoid leukemia, inhibits myeloid cell proliferation and promotes early thymocyte survival.
2012-01-01 | S-EPMC3471512 | BioStudies
Project description:BACKGROUND:Identification of protein-protein interactions is an important first step to understand living systems. High-throughput experimental approaches have accumulated large amount of information on protein-protein interactions in human and other model organisms. Such interaction information has been successfully transferred to other species, in which the experimental data are limited. However, the annotation transfer method could yield false positive interologs due to the lack of conservation of interactions when applied to phylogenetically distant organisms. RESULTS:To address this issue, we used phylogenetic profile method to filter false positives in interologs based on the notion that evolutionary conserved interactions show similar patterns of occurrence along the genomes. The approach was applied to Mus musculus, in which the experimentally identified interactions are limited. We first inferred the protein-protein interactions in Mus musculus by using two approaches: i) identifying mouse orthologs of interacting proteins (interologs) based on the experimental protein-protein interaction data from other organisms; and ii) analyzing frequency of mouse ortholog co-occurrence in predicted operons of bacteria. We then filtered possible false-positives in the predicted interactions using the phylogenetic profiles. We found that this filtering method significantly increased the frequency of interacting protein-pairs coexpressed in the same cells/tissues in gene expression omnibus (GEO) database as well as the frequency of interacting protein-pairs shared the similar Gene Ontology (GO) terms for biological processes and cellular localizations. The data supports the notion that phylogenetic profile helps to reduce the number of false positives in interologs. CONCLUSION:We have developed protein-protein interaction database in mouse, which contains 41109 interologs. We have also developed a web interface to facilitate the use of database http://lgsun.grc.nia.nih.gov/mppi/.
2008-01-01 | S-EPMC2571111 | BioStudies