Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomic Analysis of Foxc1-interacting proteins in HEK293T cells

ABSTRACT: Foxc1 has been identified to participate in regulating genes expression directly by binding their promoters as well as playing various roles in signal transduction within the cells. In this study, we found that, in F9 Embryonal Carcinoma cells, Foxc1 repressed the promoter’s transcription activity by binding the region of 1Kb upstream of Transcription Start Site within Nanog promoter.To understand more functions of Foxc1, streptavidin-biotin affinity purification combined with Liquid chromatography electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS) analysis was carried out.Bioinformatic analysis identified 360 proteins which may act as Foxc1 interactors.

INSTRUMENT(S): TripleTOF 5600

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Cell Culture

SUBMITTER: Hongni Xue

LAB HEAD: Zekun Guo

PROVIDER: PXD022178 | Pride | 2021-09-09

REPOSITORIES: pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	Biotin-Foxc1-proteinDetail.csv	Csv
	Biotin-Foxc1.mgf	Mgf
	Biotin-Foxc1.wiff.scan	Wiff
	Biotin-proteinDetail.csv	Csv
	Biotin.mgf	Mgf

Items per page:

1 - 5 of 6

Publications

FOXC1 Downregulates Nanog Expression by Recruiting HDAC2 to Its Promoter in F9 Cells Treated by Retinoic Acid.

Xue Hongni H Liu Fayang F Ai Zhiying Z Ke Jie J Yu Mengying M Chen Bingxue B Guo Zekun Z

International journal of molecular sciences 20210224 5

FOXC1, a transcription factor involved in cell differentiation and embryogenesis, is demonstrated to be a negative regulator of Nanog in this study. FOXC1 is up-regulated in retinoic acid-induced differentiation of F9 Embryonal Carcinoma (EC) cells; furthermore, FOXC1 specifically inhibits the core pluripotency factor Nanog by binding to the proximal promoter. Overexpression of FOXC1 in F9 or knockdown in 3T3 results in the down-regulation or up-regulation of Nanog mRNA and proteins, respectivel ...[more]

PMID: 33668324

Similar Datasets

A combined genomic approach unveils the transcriptional basis of heterogeneity of human pancreatic ductal adenocarcinoma [RNA-seq]

Project description:The histological grade of carcinomas describes the ability of tumor cells to organize differentiated epithelial structures and has prognostic impact. Molecular control of differentiation in normal and cancer cells relies on lineage-determining transcription factors (TFs) that activate the repertoire of cis-regulatory elements controlling cell type-specific transcriptional outputs. TF recruitment to cognate genomic DNA binding sites results in the deposition of histone marks characteristic of enhancers and other cis-regulatory elements. Here we integrated transcriptomics and genome-wide analysis of chromatin marks in human pancreatic ductal adenocarcinoma (PDAC) cells of different grade to identify first, and then experimentally validate the sequence-specific TFs controlling grade-specific gene expression. We identified a core set of TFs with a pervasive binding to the enhancer repertoire characteristic of differentiated PDACs and controlling different modules of the epithelial gene expression program. Defining the regulatory networks that control the maintenance of epithelial differentiation of PDAC cells will help determine the molecular basis of PDAC heterogeneity and progression. Poly(A) fraction of the total RNA from human pancreatic ductal adenocarcinoma cell lines was extracted and subjected to by multiparallel sequencing. Experiments were carried out in unmodified cells in duplicate, genome edited clonal CFPAC1 cells (2 KLF5-deleted CRISPR-Cas9 clones, 3 ELF3-deleted CRISPR-Cas9 clones and 2 wt clones) and CFPAC1 cells ectopically expressing ZEB1 or empty vector control (in duplicate).

2016-01-18 | E-GEOD-64558 | biostudies-arrayexpress

Definition of the fibroblast adhesome using multiplexed proximity biotinylation

Project description:Integrin adhesion complexes (IACs) bridge the extracellular matrix to the actin cytoskeleton and transduce signals in response to both chemical and mechanical cues. The composition, interactions, stoichiometry and topological organisation of proteins within IACs are not fully understood. To address this gap, we used multiplexed proximity biotinylation (BioID) to generate an in situ, proximity-dependent adhesome. Integration of the interactomes of 16 IAC-associated baits revealed a network of 147 proteins with 361 proximity interactions. Candidates with underappreciated roles in adhesion were identified, in addition to established IAC components. Bioinformatic analysis revealed five clusters of IAC baits that link to common groups of prey, and which therefore may represent functional modules. The five clusters, and their spatial associations, are consistent with current models of IAC interaction networks and stratification. This study provides a resource to examine proximal relationships within IACs on a global level.

2020-06-01 | PXD017241 | Pride

A combined genomic approach unveils the transcriptional basis of heterogeneity of human pancreatic ductal adenocarcinoma.

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-01-18 | E-GEOD-64560 | biostudies-arrayexpress

CircBIRC6-2 inhibits transmissible gastroenteritis virus induced mitochondrial permeability transition pore opening by its encoding protein

Project description:Transmissible gastroenteritis virus (TGEV), a member of coronavirus, is the pathogen of TGE. We previously found 123 circular RNAs (circRNAs) were differential expression during activation of mitochondrial permeability transition in porcine intestinal epithelial cells-jejunum 2 cell line (IPEC-J2) in response to TGEV infection. Mitochondrial permeability transition pore (mPTP) is a transmembrane pore of mitochondria and plays a key role in MPT. mPTP abnormal opening causes MPT. Therefore, we postulated that circRNAs might be related to mPTP abnormal opening induced by TGEV. In this study, we found that circBIRC6-2 could inhibit the mPTP abnormal opening induced by TGEV. Interestingly, circBIRC6-2 encodes protein BIRC6-236aa. An open reading frame (ORF) and internal ribosomal entrance site (IRES) of circBIRC6-2 were identified. We also found that BIRC6-236aa rather than circBIRC6-2 inhibited the mPTP opening by overexpression of circBIRC6-2 related vectors. We obtained 91 proteins that interacted with BIRC6-236aa using immunoprecipitation-mass spectrometry (IP-MS). The interaction between voltage-dependent anion-selective channel protein 1 (VDAC1) and BIRC6-236aa was demonstrated through co-immunoprecipitation (Co-IP). Moreover, BIRC6-236aa could inhibit the formation of VDAC1 and Cyclophilin D (CypD) complexes. Overall, these results indicated that BIRC6-236aa antagonized mPTP opening by interacting with VDAC1 to weaken the extent of interaction between VDAC1 and CypD.

2022-10-13 | PXD029055 | Pride

Decoding the signalling profile of hematopoietic progenitor kinase 1 (HPK1) in innate immunity: a proteomic approach

Project description:The fine-tuned spatiotemporal response of leukocytes to external stimuli is a hallmark of the immune system. Sensing of stimuli occurs through cell surface receptors, which transmit signals into the cell. Signaling via β2 integrins, B cell, and T cell receptors involve similar pathways. However, the activation of the same signaling molecule can result in opposing cell effector functions. One such example is the hematopoietic progenitor kinase 1 (HPK1), which negatively regulates activation of B and T cells but in contrast enforces neutrophil activation upon β2 integrin receptor engagement. Whether this difference is determined by specific interacting proteins might be disclosed by decoding the binding partners of HPK1. In the adaptive immune system, the interactome of HPK1 has already been described, whereas it is unknown in innate immune cells. Therefore, we set out to identify interacting proteins of HPK1 in the myeloid system. Neutrophil-like differentiated HL-60 cells were exposed to immobilized fibrinogen and either stimulated with Mn2+ to allow β2 integrin-mediated adhesion or left unstimulated for control. Co-immunoprecipitation experiments followed by mass spectrometry led to the identification of 116 proteins interacting with HPK1 in total. Here, 58 proteins were found only in unstimulated cells and 39 proteins only in Mn2+-stimulated adherent cells. From these results we constructed the interacting network of HPK1 with signaling, cytoskeleton-associated, transmembrane, adapter, and other proteins. Taken together, our study provides comprehensive insights into the HPK1 interactome in innate immune cells paving the way to a deeper understanding of the complex signaling profile of HPK1 in leukocytes.

2022-02-10 | PXD021136 | Pride

ZMYND11-MBTD1 induces leukemogenesis through hijacking NuA4/TIP60 acetyltransferase complex and a PWWP-mediated chromatin association mechanism

Project description:Recurring chromosomal translocation t(10;17)(p15;q21) present in a subset of human acute myeloid leukemia (AML) patients creates an aberrant fusion gene termed ZMYND11-MBTD1 (ZM); however, its function remains undetermined. Here, we show that ZM confers primary murine hematopoietic stem/progenitor cells indefinite self-renewal capability ex vivo and causes AML in vivo. Genomics profilings reveal that ZM directly binds to and maintains high expression of pro-leukemic genes including Hoxa, Meis1, Myb, Myc and Sox4. Mechanistically, ZM recruits NuA4/Tip60 histone acetyltransferase complex to cis-regulatory elements, sustaining an active chromatin state enriched in histone acetylation and devoid of repressive histone marks. Systematic mutagenesis of ZM demonstrates essential requirements of Tip60 interaction and an H3K36me3-binding PWWP domain for oncogenesis. Inhibitor of histone acetylation-‘reading’ bromodomain proteins, which act downstream of ZM, is efficacious in treating ZM-induced AML. Collectively, this study demonstrates AML-causing effects of ZM, examines its gene-regulatory roles, and reports an attractive mechanism-guided therapeutic strategy.

2021-01-21 | PXD023702 | Pride

Characterization of PARP-6 function in knock out mice and patients with developmental delay

Project description:PARP-6, a member of a family of enzymes (17 in humans) known as poly-ADP- ribose polymerases (PARPs), is a neuronally enriched PARP. While previous studies from our group show that PARP-6 is a regulator of dendrite morphogenesis in hippocampal neurons, its function in the nervous system in vivo is poorly understood. Here, we describe the generation of a PARP-6 loss-of-function mouse model for examining the function of PARP-6 during neurodevelopment in vivo. Using CRISPR-Cas9 mutagenesis, we generated a mouse line that expresses a PARP-6 truncated variant (PARP-6TR) in place of PARP-6WT. Unlike PARP-6WT, PARP-6TR is devoid of catalytic activity. Homozygous PARP-6TR do not exhibit obvious neuromorphological defects during development, but nevertheless die perinatally. This suggests that PARP-6 catalytic activity is important for postnatal survival. We also report PARP-6 mutations in six patients with several neurodevelopmental disorders, including microencephaly, intellectual disabilities, and epilepsy. The most severe mutation in PARP-6 (C563R) results in the loss of catalytic activity. Expression of the PARP-6C563R mutant in hippocampal neurons decreases dendrite morphogeneis. Taken together, these results suggest that PARP-6 is an essential gene in mice, and the loss of PARP-6 catalytic activity has detrimental effects on neuronal function in humans.

2021-07-21 | PXD025386 | Pride

Reconstructing the RUNX2 transcriptional hierarchy in thyroid cancer using a multi-layered network- based approach

Project description:The aim of this experiment was to identify the RUNX2-dependent transcriptional program in thyroid cancer. To this end TPC1 cell line was infected with dCas9-KRAB and sgRNA targeting RUNX2 distal promoter or a non-targeting sgRNA as control. RNA was collected 10 days after infection and changes in gene expression were evaluated by mRNA-seq. Three replicates were analyzed.

2023-10-20 | E-MTAB-11049 | biostudies-arrayexpress

A Long Noncoding RNA Acts as a Tumor Suppressor in Esophageal Squamous Cell Carcinoma

Project description:Many long noncoding transcripts are involved in cancer progression. Here, we utilized high-throughput microarray to compare the transcriptome alterations between the KYSE30 cells overexpressing an empty vector and Epist, thus identified 95 and 99 down-regulated and up-regulated genes, respectively. Expression levels of several previously reported genes implicated in cancer development and progression were altered, such as DDIT3, GATA6, UPP1, FAT3. These genes are involved in tumorigenesis through diverse mechanisms. The present study reveals that Epist functions as a tumor suppressor in Esophageal Squamous Cell Carcinoma. KYSE30 cells overexpressing an empty vector were compared to KYSE30 cells overexpressing Epist. Three biological replicates of each condition were analysed on Agilent microarray.

2015-01-09 | E-GEOD-64792 | biostudies-arrayexpress

Gene expression analyses in IRF8-induced monocyte differentiation

Project description:To understand the differentiation program in monocyte/macrophage differentiation, we performed ChIP-seq for IRF8 and H3K4me1 together with gene expression profiling during IRF8-induced monocyte differentiation. Both promoter-proximal and -distal binding of IRF8 associated with induction of the genes especially those related to monocytes/macrophages and immunity. DNA motif analysis for cis-regulatory elements of indirect IRF8 target genes predicted KLF4, essential for Ly6C+ monocyte development, to be a downstream transcription factor regulating the indirect target gene expression. Introduction of KLF4 into an Irf8-/- myeloid progenitor cell line induced a subset of IRF8 target genes and partially induced monocyte/macrophage differentiation. Together, this study revealed the genome-wide behavior of IRF8 and the IRF8-KLF4 axis during monocyte differentiation. Gene expressions in monocyte-like cells differentiated by IRF8 or KLF4 were measured at day 4 after retroviral transductions to myeloid progenitor cell line, Tot2. Two independent experiments were performed.

2013-01-24 | E-GEOD-38810 | biostudies-arrayexpress