Similar Datasets
Project description:ChIP-seq for V5 in the mammary tissues of Elf5-V5 mice
| PRJNA489868 | ENA
Project description:Carboxy-terminally tagged MOZ (Flag-V5-BIO tagged) was detected by ChIP-seq using anti-V5 antibody (Sigma, A7345) to precipitate chromatin associated with MOZ
2019-07-23 | GSE134607 | GEO
Project description:Elf5, an epithelial-specific Ets transcription factor, plays a crucial role in the pregnancy-associated development of the mammary gland. However, the molecular mechanisms employed by Elf5 to exert its effects on the mammary gland are largely unknown. Transcript profiling was used to investigate the transcriptional changes that occur as a result of Elf5 haploinsufficiency. We show that the development of the Elf5+/- gland is delayed at a transcriptional and morphological level, due to the delayed increase in Elf5 protein in these glands. We also identify a number of potential Elf5 target genes, including Mucin 4, whose expression, is directly regulated by the binding of Elf5 to an Ets-binding site within its promoter. We identify novel transcriptional targets of Elf5 and show that Muc4 is a direct target of Elf5, further elucidating the mechanisms through which Elf5 regulates proliferation and differentiation in the mammary gland.
2010-09-27 | GSE23373 | GEO
Project description:We developed conditional knockout mice where the transcription factor Elf5 (also called ESE-2) is deleted in the mammary glands. Loss of Elf5 results in block in alveologenesis and epithelial differentiation defects. Mammary gland samples from Elf5 knockout and wild type animals were analyzed for global transcriptome changes.
2012-09-01 | GSE32103 | GEO
Project description:Elf5, an epithelial-specific Ets transcription factor, plays a crucial role in the pregnancy-associated development of the mammary gland. However, the molecular mechanisms employed by Elf5 to exert its effects on the mammary gland are largely unknown. Transcript profiling was used to investigate the transcriptional changes that occur as a result of Elf5 haploinsufficiency. We show that the development of the Elf5+/- gland is delayed at a transcriptional and morphological level, due to the delayed increase in Elf5 protein in these glands. We also identify a number of potential Elf5 target genes, including Mucin 4, whose expression, is directly regulated by the binding of Elf5 to an Ets-binding site within its promoter. We identify novel transcriptional targets of Elf5 and show that Muc4 is a direct target of Elf5, further elucidating the mechanisms through which Elf5 regulates proliferation and differentiation in the mammary gland. We used Compugen 22,000 oligo arrays from the Adelaide Microarray Centre to determine the transcriptional effects of the loss of one Elf5 allele on mammary gland development. We examined Elf5+/+ and Elf5+/- mammary glands over 5 timepoints of mammary gland development in three experiments. Each experiment used the pooled RNA of 2 mice, resulting in a total of 6 individual mice at each timepoint per genotype. Replica 1 of each condition was labelled with the one fluorophore, and replicas 2 and 3 with the other fluorophore. A common reference design was used for this experiment. RNA extracted from eight pooled 17.5dpc C57BL/6 mouse embryos was used as the reference sample. In total, we performed 30 micraoarray hybridisations, examining 5 timepoints of mammary gland development in 2 genotypes (Elf5+/+ and Elf5+/-). This experiment was repeated with a total of three biological replicates.
2010-09-26 | E-GEOD-23373 | biostudies-arrayexpress
Project description:ChIP-Seq analysis of V5-tagged budding yeast Rif1
| PRJEB67558 | ENA
Project description:Genomic locations of V5-tagged budding yeast Rif1 (including wilt-type and designer mutants) were analysed by ChIP-Seq. Mutants tested were rif1-7A and rif1-7E, in which Ser/Thr residues in the cluster of SQ/TQ sites were mutated to Ala or Glu, respectively. We also tested tested rif1-∆594, in which the C-terminal 594 amino acids were deleted.
2023-11-19 | E-MTAB-13452 | biostudies-arrayexpress
Project description:We developed conditional knockout mice where the transcription factor Elf5 (also called ESE-2) is deleted in the mammary glands. Loss of Elf5 results in block in alveologenesis and epithelial differentiation defects. Mammary gland samples from Elf5 knockout and wild type animals were analyzed for global transcriptome changes. We used microarrays to performing transcriptional profiling of Elf5KO and control mammary glands at Lac1 (Lactation day 1)
2012-09-01 | E-GEOD-32103 | biostudies-arrayexpress
Project description:The data generated here shows increased interferon gamma gene signatures in Elf5- tumor cells in C3-T; Elf5-GFP reporter mice tumors
2020-02-15 | GSE122180 | GEO
Project description:E74-like ETS transcription factor 5 (ELF5) is one of three epithelial ETS family transcription factors. The ELF5 gene maps to chr11p13 where it is located adjacent to another epithelial ETS factor gene, ETS homologous factor (EHF). This genomic interval is associated with lung disease. The functions of ELF5 in the airway epithelium are not well studied, in large part due to a lack of cellular models expressing the gene. Using scRNA-seq data from primary human bronchial (HBE) and nasal (HNE) epithelial cells we show ELF5 expression in subsets of ciliated and secretory cells, implicating a role for this factor in the airway epithelium. Next, we generate cistrome and transcriptome data for ELF5 in another epithelial cell type with abundant ELF5, and use bioinformatic tools to reveal the potential functions of this factor in the airway epithelium. ELF5 has a strong repressive function in epithelial cells, where it has a profound impact on organization of the extracellular matrix. Activation of ELF5 expression in primary HBE cells using CRISPRa enhanced transepithelial resistance (TER) and wound repair. These results illustrate an important role for ELF5 in maintaining airway epithelial integrity, which is critical to lung health. Furthermore, ELF5 can act independently from EHF and exhibits opposite effects in the airway epithelium.
2026-05-04 | GSE173880 | GEO