Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA105655 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A Krüppel-like factor 9 (Klf9) regulated network in HEC-1-A endometrial carcinoma cells encompassing adhesion proteins, steroid- and menstrual cycle-regulated proteins of the uterine endometrium, novel membrane proteins, and nuclear receptors
2009-06-23 | GSE11855 | GEO
Project description:Endometriosis is characterized by progesterone resistance and is associated with infertility. Krüppel-like Factor 9 (KLF9) is a progesterone receptor (PGR)-interacting protein, and mice null for Klf9 are subfertile. Whether loss of KLF9 contributes to progesterone resistance of eutopic endometrium of women with endometriosis is unclear. The aim of this study was to investigate KLF9 and PGR co-regulation of human endometrial stromal cell (HESC) transcriptome network.
2012-04-04 | GSE31683 | GEO
Project description:Endometriosis is characterized by progesterone resistance and is associated with infertility. KrM-CM-<ppel-like Factor 9 (KLF9) is a progesterone receptor (PGR)-interacting protein, and mice null for Klf9 are subfertile. Whether loss of KLF9 contributes to progesterone resistance of eutopic endometrium of women with endometriosis is unclear. The aim of this study was to investigate KLF9 and PGR co-regulation of human endometrial stromal cell (HESC) transcriptome network. Microarray gene expression analysis was conducted in decidualizing HESC by silencing the expression of KLF9 and PGR, alone or in combination by a siRNA approach, to identify additional KLF9 and PGR co-regulated genes and signaling networks/pathways. HESC also treated with 8-bromo-cAMP, 17M-CM-^_-estradiol, and medroxyprogesterone acetate (cAME) to mimic stromal progression from a proliferative to a differentiated state.
2012-04-03 | E-GEOD-31683 | biostudies-arrayexpress
Project description:Krüppel-like factor 9 (Klf9), a zinc-finger transcription factor, is implicated in the control of cell proliferation, cell differentiation and cell fate in brain and uterus. Using Klf9 null mutant mice, we have investigated the involvement of Klf9 in small intestine crypt-villus cell renewal and lineage determination. We report the predominant expression of Klf9 gene in small intestine smooth muscle (muscularis externa). Jejunums null for Klf9 have shorter villi, reduced crypt stem/transit cell proliferation, and altered lineage determination as indicated by decreased and increased numbers of Goblet and Paneth cells, respectively. A stimulatory role for Klf9 in villus cell migration was demonstrated by BrdU labeling. Results suggest that Klf9 controls the elaboration, from small intestine smooth muscle, of molecular mediator(s) of crypt cell proliferation and lineage determination, and of villus cell migration. Keywords: Genetic modification
2006-12-08 | GSE6443 | GEO
Project description:This study identifies an unknown role for KLF9 signaling in normal uterine development, which is decreased in a mouse model of resistance to thyroid hormone (RTHa), resulting in infertility through ectopic IL-33 expression produced by abnormally differentiated, KLF9-deficient endometrial cells. Utilizing a combination of genetically engineered mouse models, histopathology, spatial transcriptomics, and pharmacological inhibitors, we revealed that infertility in RTHa results from abnormal endometrial differentiation mediated by KLF9 suppression. These abnormally differentiated endometrial cells were the source of ectopic IL-33 overexpression. Increased endometrial IL-33 led to T-cell infiltration, destruction of glands, and endometrial fibrosis, which culminated in infertility. This study uncovers a link between TRa1 and KLF9 signaling for normal endometrial differentiation, reveals a mechanism for ectopic uterine IL-33 in female fertility, and provides new insights on the impact of hypothyroidism in female reproduction.
2024-08-29 | GSE273927 | GEO
Project description:ChIP-seq of endometrial cancer cell lines Ishikawa (Ish) and Hec1a (Hec) cells
2019-12-01 | GSE100789 | GEO
Project description:Kruppel-like factor-9 (KLF9), a member of the large KLF transcription factor family, has emerged as a regulator of oncogenesis, cell differentiation and neural development; however, the molecular basis for KLF9M-bM-^@M-^Ys diverse contextual functions remains unclear. This study focuses on the functions of KLF9 in human glioblastoma stem-like cells. We establish for the first time a genome-wide map of KLF9-regulated targets in human glioblastoma stem-like cells, and show that KLF9 functions as a transcriptional repressor and thereby regulates multiple signaling pathways involved in oncogenesis and stem cell regulation. A detailed analysis of one such pathway, integrin signaling, shows that the capacity of KLF9 to inhibit glioblastoma cell stemness and tumorigenicity requires ITGA6 repression. These findings enhance our understanding of the transcriptional networks underlying cancer cell stemness and differentiation, and identify KLF9-regulated molecular targets applicable to cancer therapeutics. Two cell lines were used as biological replicates. Each cell line has one KLF9 induction sample and one control sample.
2014-10-10 | E-GEOD-62212 | biostudies-arrayexpress
Project description:Kruppel-like factor-9 (KLF9), a member of the large KLF transcription factor family, has emerged as a regulator of oncogenesis, cell differentiation and neural development; however, the molecular basis for KLF9M-bM-^@M-^Ys diverse contextual functions remains unclear. This study focuses on the functions of KLF9 in human glioblastoma stem-like cells. We establish for the first time a genome-wide map of KLF9-regulated targets in human glioblastoma stem-like cells, and show that KLF9 functions as a transcriptional repressor and thereby regulates multiple signaling pathways involved in oncogenesis and stem cell regulation. A detailed analysis of one such pathway, integrin signaling, shows that the capacity of KLF9 to inhibit glioblastoma cell stemness and tumorigenicity requires ITGA6 repression. These findings enhance our understanding of the transcriptional networks underlying cancer cell stemness and differentiation, and identify KLF9-regulated molecular targets applicable to cancer therapeutics. Two cell lines were used as biological replicates. Each cell line have one KLF9 ChIP-enriched DNA sample and one input genomic DNA sample.
2014-10-10 | E-GEOD-62211 | biostudies-arrayexpress
Project description:Krüppel-like factor 9 (Klf9) is a ubiquitously expressed transcription factor that is a feedforward regulator of multiple stress-responsive and endocrine signaling pathways. We previously described how loss of Klf9 function affects the transcriptome of zebrafish larvae sampled at a single time point 5 days post-fertilization (dpf). However, klf9 expression oscillates diurnally, and the time point that was sampled corresponded to its expression nadir. To determine if klf9-/- function varies with time of day, we performed bulk RNA-seq on 5 dpf zebrafish embryos sampled at three timepoints encompassing the predawn peak and midmorning nadir of klf9 expression. We found that while the major effects of the klf9-/- mutation that we reported previously are robust to time of day, the mutation has additional effects that manifest only at the predawn time point. We used a published single-cell atlas of zebrafish development to map the effects of the klf9-/- mutation onto different cell types and found that the mutation increased representation of genes associated with digestive organs (liver, pancreas, and intestine) and decreased representation of genes associated with differentiating neurons, blood, and somites. Measurements from confocally-imaged larvae suggest that overrepresentation of liver genes in klf9-/- mutants is due to development of enlarged livers.
2023-02-01 | GSE218687 | GEO
Project description:Kruppel-like factor-9 (KLF9), a member of the large KLF transcription factor family, has emerged as a regulator of oncogenesis, cell differentiation and neural development; however, the molecular basis for KLF9’s diverse contextual functions remains unclear. This study focuses on the functions of KLF9 in human glioblastoma stem-like cells. We establish for the first time a genome-wide map of KLF9-regulated targets in human glioblastoma stem-like cells, and show that KLF9 functions as a transcriptional repressor and thereby regulates multiple signaling pathways involved in oncogenesis and stem cell regulation. A detailed analysis of one such pathway, integrin signaling, shows that the capacity of KLF9 to inhibit glioblastoma cell stemness and tumorigenicity requires ITGA6 repression. These findings enhance our understanding of the transcriptional networks underlying cancer cell stemness and differentiation, and identify KLF9-regulated molecular targets applicable to cancer therapeutics.
2014-10-10 | GSE62212 | GEO