Project description:To identify the downstream gene of p63, STAT3 and PPARg signling Total RNA from p63 knock down UC14 and STAT3 knockdown Scaber cells were compared to control cells. Also Total RNA from Rosiglitazone treated UC7 cells were compared to untreated control.
Project description:RNA-Seq data of human colorectal cancer cell line SW837 transfected with siRNA against STAT3 (siSTAT3) or control RNA (siCtrl), untreated or treated with Hyper-IL-6 (Hy-IL-6)
Project description:p63 ChIP-SEQ in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS and in a p63 deficient claudin-low subtype breast cancer cell line, MDA-MB-231 p63 ChIP-SEQ on MCFDCIS and MDA-MB-231 cell lines
Project description:The placenta plays a crucial role in pregnancy success. deltaNp63alpha (p63), a transcription factor from the TP53 family, is highly expressed in villous cytotrophoblasts (CTBs), the epithelial stem cells of the human placenta, and has been shown to be involved in CTB maintenance and differentiation. In this study, we set out to identify mechanism(s) of action of p63, by identifying its downstream targets. We evaluate gene expression changes following overexpression and knockdown of p63 in the JEG3 choriocarcinoma cell line, using microarray-based RNA profiling. We identify High temperature requirement A4 (HTRA4), a placenta-specific serine protease involved in trophoblast differentiation and altered in preeclampsia, as a gene reciprocally regulated by p63, and characterize its expression in primary human placental tissues by RNAseq (PMID 34540826; GSE173372) and in situ hybridization. Forced overexpression of deltaNp63alpha in JEG-3 was obtained by pCMV lentiviral vector infection (empty vector used as control). ) The pLKO.1-based non-targeting scramble and p63-specific short hairpin (shRNA) lentiviral plasmids were used for gene knock-down. Vectors were previously described in Li et al Am J Pathol. 2014 PMID: 25307348.
Project description:p63 ChIP-SEQ in a p63 expressing basal-subtype breast cancer cell line, MCFDCIS and in a p63 deficient claudin-low subtype breast cancer cell line, MDA-MB-231
Project description:Overexpression in IL6 in MCF10A vs. WT, MCF10A.ErbB2* with/without shRNA targeting STAT3 Overexpression in IL6 in MCF10A vs. WT, MCF10A.ErbB* with/without shSTAT3, duplicates, two STAT3 shRNAs
Project description:To identify downstream targets of Jak/Stat3 pathways without being distracted by differentiation signalings from MEK/ERK pathway, we exploited a engineered B6 cells, which stably stably expressing a chimeric receptor (GRgp-Y118F). The chimeric receptor can induce the phosphorylation of Stat3 by GCSF without activating the MEK/ERK pathway. To mimic the effect of GCSF, the chimeric B6 cells were also treated with LIF plus a selective MEK chemical inhibitor, PD0325901, to induce LIF/Jak/Stat3 but MEK/ERK pathways. mESCs starved in serum free growth medium for 6hrs were treated with GCSF or with LIF plus PD0325901 for 1hr, after which total RNA was extracted for analysis.
Project description:We report here genome wide identification of p63 binding sites in cycling neonatal foreskin keratinocytes using high throughput sequencing of ChIP enriched DNA. Analysis of gene ontology, database mining with integration with publicly available data, reveals a role for p63 in transcriptional regulation of multiple genes genetically linked to cleft palate. In addition, we identify AP-2α, a transcription factor which, when mutated, also results in craniofacial clefting syndrome, as a co-regulator of p63 responsive genes. Examination of p63 binding sites in neonatal foreskin keratinocytes