Similar Datasets
Project description:RNA-Seq of wild type and Nfic-/- mice pancreata
| PRJNA523627 | ENA
Project description:In order to identify direct NFIC target genes, in the context of pancreatic homeostasis, ChIP-seq was performed using pancreata from 8-10 week-old wild type mice.
2023-05-24 | GSE181098 | GEO
Project description:Nuclear factor I-C belongs to a family of CTF binding transcription factor which is known for its role cellular differentiation. In our recent study we identified increased expression of NFIC in. AML samples as compared to normal haematpoitic stem and progenitor cells (HSPCs). We also found that overexpression of NFIC in cord blood derived HSPCs perturbed normal haematopoiesis by increasing monocyte production. Therefore in this analysis we aimed to identify the effect of NFIC overexpression in normal HSPCs at single cell level using single cell RNA (scRNA) sequencing. Cluster analysis based on the cellular and functional identities, identified eight clusters according to their terminal differentiation as monocytes, erythrocytes, dendritic cells (DC), megakaryocytes, neutrophils, megakaryocyte-erythroid progenitor cells, basophil/mast progenitor cells and eosinophils. We found that NFIC overexpressing CD34+ HSPCs had increased percentage of monocytes as compared to control. To understand the molecular basis of this, we focussed our analysis on monocytes to determine changes in mRNA expression following NFIC overexpression. We identified 164 and 88 significantly up-regulated and down-regulated genes, respectively (p<0.05, FDR<0.05) in NFIC overexpressing monocytes as compared to control. Pathway analysis identified enrichment in genes involved in mTOR signalling, cancer cell death and survival, energy metabolism pathways and oxidative phosphorylation. Therefore our scRNA suggested that NFIC play a role in monocytic growth development and its overexpression may lead to monocytic bias in normal haematopoiesis.
2023-01-04 | GSE200456 | GEO
Project description:This study aimed to perform transcriptome profiling of Nfic-/- and corresponding control tooth germ at root initiation stage to identify differentially expressed for key regulators of root development. Coordination between the Hertwig’s Epithelial Root Sheath (HERS) and apical papilla (AP) is crucial for proper root development process. The Hedgehog (Hh) signaling pathway and Nfic are both involved in tooth root development.
2017-08-29 | GSE69054 | GEO
Project description:The expression of IGF2BP2 in GCs from PCOS patients was detected using RT-qPCR and western blot. We captured IGF2BP2-interacting transcripts, global transcriptome together with alternative splicing by RNA immunoprecipitation sequencing (RIP-seq) and RNA sequencing (RNA-seq). KGN cells transfected with IGF2BP2 overexpressing plasmids and nuclear factor 1 C-type (NFIC) siRNAs, were applied to CCK-8, EdU and TUNEL assays. IGF2BP2 was highly expressed in GCs from PCOS patients. As a RBP, it preferentially bound to the 3’and 5’UTRs of mRNAs with GGAC motif and a newly found GAAG motif. The overexpression of IGF2BP2 changed the transcriptome profile of KGN cells. IGF2BP2 functioned to regulate alternative splicing events (ASEs) and promote cell proliferation through inhibiting exon skipping events of NFIC. In conclusion, we demonstrated that IGF2BP2 promotes granulosa cell proliferation via regulating alternative splicing of NFIC in PCOS. The findings help to better understand the roles of IGF2BP2 in the pathogenesis of PCOS.
2022-05-11 | GSE191023 | GEO
Project description:The expression of IGF2BP2 in GCs from PCOS patients was detected using RT-qPCR and western blot. We captured IGF2BP2-interacting transcripts, global transcriptome together with alternative splicing by RNA immunoprecipitation sequencing (RIP-seq) and RNA sequencing (RNA-seq). KGN cells transfected with IGF2BP2 overexpressing plasmids and nuclear factor 1 C-type (NFIC) siRNAs, were applied to CCK-8, EdU and TUNEL assays. IGF2BP2 was highly expressed in GCs from PCOS patients. As a RBP, it preferentially bound to the 3’and 5’UTRs of mRNAs with GGAC motif and a newly found GAAG motif. The overexpression of IGF2BP2 changed the transcriptome profile of KGN cells. IGF2BP2 functioned to regulate alternative splicing events (ASEs) and promote cell proliferation through inhibiting exon skipping events of NFIC. In conclusion, we demonstrated that IGF2BP2 promotes granulosa cell proliferation via regulating alternative splicing of NFIC in PCOS. The findings help to better understand the roles of IGF2BP2 in the pathogenesis of PCOS.
2022-05-11 | GSE191022 | GEO
Project description:NFIC overexpression perturbs normal haematopoeisis by promoting myeloid differentiaon
| PRJNA824534 | ENA
Project description:Genome-wide occupancy map of NFIC in mouse pancreas
| PRJNA750709 | ENA
Project description:Zfp92, a repressive KRAB domain-containing zinc-finger protein, was identified by Gene Co-expression Network analysis to be an interesting candidate gene involved in endocrine specification and maturation. We examined the role of Zfp92, a KRAB-ZFP that is highly expressed in pancreatic islets of adult mice, by analyzing global Zfp92 knockout (KO) mice. Adult Zfp92 KO animals exhibited only mild changes in glucose homeostasis and no change in islet structure, although, male KO mice exhibited decreased growth, and female KO mice exhibited increased body fat accumulation on a high fat diet. We found that Zfp92 regulates a subset of transposable elements as well as Mafb, a transcription factor involved in islet development.
2022-12-02 | E-MTAB-11637 | biostudies-arrayexpress
Project description:The NF-κB pathway is a master regulator of inflammatory processes and is implicated in insulin resistance and pancreatic beta cell dysfunction in the metabolic syndrome. While canonical NF-κB signaling is well studied, there is little information on the divergent non-canonical NF-κB pathway in the context of pancreatic islet dysfunction in diabetes. Here, we demonstrate that pharmacological activation of the non-canonical NF-κB inducing kinase (NIK) disrupts glucose homeostasis in zebrafish in vivo. Further, we identify NIK as a critical negative regulator of beta cell function as pharmacological NIK activation results in impaired glucose-stimulated insulin secretion in mouse and human islets. NIK levels are elevated in pancreatic islets isolated from diet-induced obese (DIO) mice, which exhibit increased processing of non-canonical NF-κB components p100 to p52, and accumulation of RelB. Tumor necrosis factor α (TNFα) and receptor activator of NF-κB ligand (RANKL), two ligands associated with diabetes, induce NIK in islets. Mice with constitutive beta cell intrinsic NIK activation present impaired insulin secretion with DIO. NIK activation triggers the non-canonical NF-κB transcriptional network to induce genes identified in human type 2 diabetes genome-wide association studies linked to beta cell failure. These studies reveal that NIK contributes a central mechanism for beta cell failure in diet-induced obesity. We identify a role for Nuclear Factor inducing κB (NIK) in pancreatic beta cell failure. NIK activation disrupts glucose homeostasis in zebrafish in vivo and impairs glucose-stimulated insulin secretion in mouse and human islets in vitro. NIK activation also perturbs beta cell insulin secretion in a diet-induced obesity mouse model. These studies reveal that NIK contributes a central mechanism for beta cell failure in obesity. To uncover the role of NIK in pancreatic beta cells, we performed a gene expression microarray analysis comparing pancreatic islets with constitutive beta cell intrinsicNIK activation from the 16 week old mice (beta cell specific TRAF2 and TRAF2 knockout mice) to their controls (n=3 per group).
2015-06-18 | E-GEOD-68317 | biostudies-arrayexpress