ChIRP-seq of Hoxc4-au in epidydimal white adipose tissue (eWAT)-derived preadipocytes.
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE139172 | GEO | 2023/10/30
REPOSITORIES: GEO
Similar Datasets
Project description:ChIRP-seq of Hoxc4-au in epidydimal white adipose tissue (eWAT)-derived preadipocytes.
| PRJNA578693 | ENA
Project description:We found that overexpression of HOXC4 in mature adipocytes enhances thermogenesis. To investigate the binding sites of HOXC4 in the genome of brown adipocytes, we performed HOXC4 ChIP-seq experiments on differentiated primary brown adipocytes, which overexpressed HOXC4.
2025-01-22 | GSE266786 | GEO
Project description:At the molecular level, the mechanisms of action of Hox genes during hematopoiesis remain elusive. Although reports have described the implication of Hox genes in some molecular pathways in mice, the targets of HOX proteins in human hematopoietic cells are mostly unidentified. Since HOXB4 and HOXC4 are transcription factors encoded by paralogous genes that display similar effects on HSCs and progenitors, we presumed that HOXB4 and HOXC4 regulate the same target genes during human HSC expansion. This hypothesis was supported by the fact that HOXB4 and HOXC4 have similar molecular structure and similar roles and expression patterns during development. To identify early factors and signaling pathways involved in hematopoietic cell expansion consecutive to the action of HOXB4 or HOXC4, we performed a differential transcriptome analysis of RNAs from cord blood-derived CD34+ cells cultured for 24 hours in the presence of MS-5 cells engineered to secrete HOXB4 or HOXC4 proteins. MS-5/GFP cells were used as control in separate co-cultures to exclude nonspecific changes in gene expression that may be associated with the presence of lentivirus-transduced MS-5 cells. Human CD34+ cord blood (4.106) cells were co-cultured for 24 hours with irradiated EGFP-, HOXB4-, or HOXC4-transduced MS-5 cells. 12 arrays were analysed. Three competitive hybridizations to the arrays were performed in duplicate using each time two dye-swap following this experimental design: AVZ056 : CY5 (CD34+/MS5+HOXB4) / CY3 (CD34+/MS5+GFP) AVZ059 : CY5 (CD34+/MS5+GFP) / CY3 (CD34+/MS5+HOXB4) AVZ064 : CY5 (CD34+/MS5+GFP) / CY3 (CD34+/MS5+HOXB4) AVZ067 : CY5 (CD34+/MS5+HOXB4) / CY3 (CD34+/MS5+GFP) AVZ057 : CY5 (CD34+/MS5+GFP) / CY3 (CD34+/MS5+HOXC4) AVZ058 : CY5 (CD34+/MS5+HOXC4) / CY3 (CD34+/MS5+GFP) AVZ060 : CY5 (CD34+/MS5+HOXC4) / CY3 (CD34+/MS5+GFP) AVZ068 : CY5 (CD34+/MS5+GFP) / CY3 (CD34+/MS5+HOXC4) AVZ061 : CY5 (CD34+/MS5+HOXB4) / CY3 (CD34+/MS5+HOXC4) AVZ062 : CY5 (CD34+/MS5+HOXC4) / CY3 (CD34+/MS5+HOXB4) AVZ065 : CY5 (CD34+/MS5+HOXC4) / CY3 (CD34+/MS5+HOXB4) AVZ066 : CY5 (CD34+/MS5+HOXB4) / CY3 (CD34+/MS5+HOXC4)
2010-10-15 | E-GEOD-24379 | biostudies-arrayexpress
Project description:Aberrant expression of HOXC6 and HOXC4 is commonly detected in prostate cancer. The high expression of these transcription factors is associated with aggressive prostate cancer and can predict cancer recurrence after treatment. Thus, HOXC4 and HOXC6 are clinically relevant biomarkers of aggressive prostate cancer. However, the molecular mechanisms by which these HOXC genes contribute to prostate cancer is not yet understood. To begin to address the role of HOXC4 and HOXC6 in prostate cancer, we performed RNA-seq analyses before and after siRNA-mediated knockdown of HOXC4 and/or HOXC6 and also performed ChIP-seq to identify genomic binding sites for both of these transcription factors. Our studies demonstrate that HOXC4 and HOXC6 co-localize with HOXB13, FOXA1 and AR, three transcription factors previously shown to contribute to the development of prostate cancer. We suggest that the aberrantly upregulated HOXC4 and HOXC6 proteins may compete with HOXB13 for binding sites, thus altering the prostate transcriptome. This competition model may be applicable to many different human cancers that display increased expression of a HOX transcription factor.
2020-01-22 | GSE129951 | GEO
Project description:Current interventions for endometriosis mainly involve hormone therapies but have limited efficacy and unacceptable side effects, due to the lack of selectivity to distinguish between endometriosis and endometrial tissues. Elucidating the molecular mechanism underlying rapid growth of endometrial-like stromal cells, one of the main components of endometriotic lesions, will pave a path for more effective treatment of endometriosis. In the current study, we utilized transcriptome sequencing to compare the transcriptional profiles of endometrial-like stromal cells from endometriosis and endometrial tissues and demonstrated that Homeobox C4 (HOXC4) is preferentially expressed in endometriotic lesions. HOXC4 is indispensable for the proliferation of stromal cells from endometriosis, but not those from endometrial tissues. Mechanistically, HOXC4 acts as a transcription factor to promote the expression of Slit Guidance Ligand 2 (SLIT2) and thereby, increases the p38 MAPK activity via the SLIT2 receptor Roundabout Guidance Receptor 1 (ROBO1). Considering the essential role of the p38 MAPK activity in facilitating the development of ectopic endometrium, our findings strongly support the idea of HOXC4, as well as the SLIT2-ROBO1 axis, being as potential therapeutic targets for endometriosis.
2025-09-30 | GSE286315 | GEO
Project description:At the molecular level, the mechanisms of action of Hox genes during hematopoiesis remain elusive. Although reports have described the implication of Hox genes in some molecular pathways in mice, the targets of HOX proteins in human hematopoietic cells are mostly unidentified. Since HOXB4 and HOXC4 are transcription factors encoded by paralogous genes that display similar effects on HSCs and progenitors, we presumed that HOXB4 and HOXC4 regulate the same target genes during human HSC expansion. This hypothesis was supported by the fact that HOXB4 and HOXC4 have similar molecular structure and similar roles and expression patterns during development. To identify early factors and signaling pathways involved in hematopoietic cell expansion consecutive to the action of HOXB4 or HOXC4, we performed a differential transcriptome analysis of RNAs from cord blood-derived CD34+ cells cultured for 24 hours in the presence of MS-5 cells engineered to secrete HOXB4 or HOXC4 proteins. MS-5/GFP cells were used as control in separate co-cultures to exclude nonspecific changes in gene expression that may be associated with the presence of lentivirus-transduced MS-5 cells.
2010-10-15 | GSE24379 | GEO
Project description:KCNQOT1 ChIRP seq and perturbation epigentic profiles [ChIRP]
| PRJNA858014 | ENA
Project description:Gene expression change on weight cycling mice eWAT
2018-06-07 | GSE73345 | GEO
Project description:Response of Cupriavidus metallidurans CH34 to NaAuCl4, Au(I)-thiomalate, Au(I)-thiosulfate, KAuCN, (KCN as control)
2013-03-15 | GSE42199 | GEO
Project description:We employed ChIRP in combination with proteomic strategy to systematically discover HOTAIR-interacting proteins. Three independent biological replicates of ChIRP-MS experiment were performed, alongside negative controls.
2021-07-09 | PXD015546 | Pride