Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TfRc Dependent Gene Expression in Embryonic Renal Cells

ABSTRACT: We investigated the ability of transferrin receptor1 (TfRc) knockout cells to populate different domains of the developing kidney by using a chimeric approach. The TfRc cells developed into all segments of the developing nephron, but there was a relative exclusion from the ureteric bud and a positive bias towards the stromal compartment. Here we conducted a microarray analysis of differential gene expression between TfRc deficient and wild type (wt) cells in chimeric embryonic kidneys derived from embryos created by blastocyst injection of wt blastocysts with TfRc-/- green fluorescent protein-expressing (GFP+) embryonic stem cells. Keywords: cell type comparison, genetic modification, iron signaling

ORGANISM(S): Mus musculus

PROVIDER: GSE7396 | GEO | 2008/08/01

SECONDARY ACCESSION(S): PRJNA97885

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Transcription profiling of mouse TfRc deficient and wild type renalcells in chimeric embryonic kidneys derived from embryos created by blastocyst injection

Project description:We investigated the ability of transferrin receptor1 (TfRc) knockout cells to populate different domains of the developing kidney by using a chimeric approach. The TfRc cells developed into all segments of the developing nephron, but there was a relative exclusion from the ureteric bud and a positive bias towards the stromal compartment. Here we conducted a microarray analysis of differential gene expression between TfRc deficient and wild type (wt) cells in chimeric embryonic kidneys derived from embryos created by blastocyst injection of wt blastocysts with TfRc-/- green fluorescent protein-expressing (GFP+) embryonic stem cells. Experiment Overall Design: Following blastocyst injection of 3-5 TfRc-/- GFP+ embryonic stem cells in wt blstocysts, we harvested the chimeric kidney at day E15.5 and separated the TfRc-/- GFP+ cell population from wt GFP- cell population by using fluorescence activated cell sorting. Biotinlyated cRNA was prepared from the isolated cells and hybridized to Mouse Genome 430 2.0 Arrays (Affymetrix) according to standard protocols.

2008-10-18 | E-GEOD-7396 | biostudies-arrayexpress

Effect of R22W mutation in TFRC gene on gene expression in PBMCs

Project description:TFRC, also known as CD71, regulates the uptake of transferrin-bound iron into cells through receptor-mediated endocytosis. In a patient with a combined immunodeficiency, we identified a homozygous missense mutation in TFRC gene leading to R22W amino acid change in the cytoplasmic tail of the receptor. This mutation impairs the endocytosis of TFRC, which results in profound aberrations in the immune system.

2024-01-31 | GSE243237 | GEO

Targeting circRNA TFRC in bladder cancer alleviates urinary tract infections by reducing erythroid progenitor cells

Project description:the same population of EPCs was detected in bladder cancer patients. The EPCs, whose function could be reversed via anti-CD71 treatment, were induced by the circRNA TFRC (circular RNA derived from the transferrin receptor mRNA; cTFRC) in bladder cancer exosomes.

2021-09-27 | GSE171000 | GEO

Impact of Tfrc deficiency on gut microbiome [16s rRNA-seq]

Project description:Iron metabolism is pivotal for cell fitness in the mammalian host. However, its role in group 3 innate lymphoid cells (ILC3s) is unknown. Here we show that transferrin receptor CD71-mediated iron metabolism cell-intrinsically controls ILC3 maintenance, cytokine production and host protection against Citrobacter rodentium infection, and metabolically affects mitochondrial respiration by switching of oxidative phosphorylation toward glycolysis. Iron deprivation or Tfrc deficiency reduces the expression and/or activity of the aryl hydrocarbon receptor (Ahr), a ligand-dependent transcription factor and a key ILC3 regulator. Furthermore, consistent with its role in generation of Ahr ligand, microbiome exerts a negative impact on CD71 expression in an Ahr-dependent manner. Genetic ablation or activation of Ahr in ILC3s leads to CD71 upregulation or downregulation, respectively, suggesting an active suppression of CD71 by Ahr. Iron overload partially restores defective ILC3 compartment in the small intestine of Ahr-deficient mice, representing compensatory action of CD71 upregulation during Ahr deficiency. Mechanistically, Ahr directly binds to the promoter region of the Tfrc locus to inhibit Tfrc transcription. These data collectively demonstrate an under-appreciated role of the Ahr-CD71-iron axis in regulation of ILC3 maintenance and function.

2023-07-10 | GSE222620 | GEO

Stutzerimonas kunmingensis strain:TFRC-KFRI-1

Project description:Stutzerimonas kunmingensis strain:TFRC-KFRI-1 Genome sequencing

| PRJNA1147901 | ENA

Gene expression profiles of an E10.5 ureteric duct cell (GUDMAP Series_id: 40)

Project description:The long term objective is to create an encyclopedia of the expression levels of all genes in multiple components of the developing kidney. The central thesis is straightforward. The combination of fluorescent activated cell sorting (FACS) plus microarray analysis offers a powerful, efficient and effective method for the creation of a global gene expression atlas of the developing kidney. Microarrays with essentially complete genome coverage can be used to quantitate expression levels of every gene in FACS isolated components of the developing kidney. The ensuing rapid read-out provides an expression atlas that is more sensitive, more economical and more complete than would be possible by in situ hybridizations alone. HoxB7-GFP transgenic mice were utilized to isolate the ureteric duct cells from E10.5 embryonic kidneys. The ureteric duct cells were isolated from embryos using microdissection, trypsin treatment and FACS. The RNA was isolated from purified ureteric duct cells and the gene expression profiles were determined by microarrays.

2010-05-27 | E-GEOD-21584 | biostudies-arrayexpress

Gene expression profiles of E10.5 ureteric bud cells. (GUDMAP Series_id: 39)

Project description:The long term objective is to create an encyclopedia of the expression levels of all genes in multiple components of the developing kidney. The central thesis is straightforward. The combination of fluorescent activated cell sorting (FACS) plus microarray analysis offers a powerful, efficient and effective method for the creation of a global gene expression atlas of the developing kidney. Microarrays with essentially complete genome coverage can be used to quantitate expression levels of every gene in FACS isolated components of the developing kidney. The ensuing rapid read-out provides an expression atlas that is more sensitive, more economical and more complete than would be possible by in situ hybridizations alone. HoxB7-GFP transgenic mice were utilized to isolate the ureteric bud cells from E10.5 embryonic kidneys. The ureteric bud cells were isolated from embryos using microdissection, trypsin treatment and FACS. The RNA was isolated from purified ureteric bud cells and the gene expression profiles were determined by microarrays.

2010-05-27 | E-GEOD-21558 | biostudies-arrayexpress

CCT3 drives sorafenib resistance by inhibiting TFRC-mediated iron uptake in HCC

Project description:Sorafenib is commonly utilized in the management of advanced hepatocellular carcinoma (HCC). However, its efficacy in extending patients' survival is hindered by the development of drug resistance. By employing protein posttranslational modification (PTM) omics, including acetylome, phosphoproteome, and ubiquitinome, in conjunction with genome-wide CRISPR/Cas9 knockout library screening, we have successfully identified chaperonin containing TCP1 subunit 3 (CCT3) as a key factor contributing to sorafenib resistance. Furthermore, we observed a reduction in the ubiquitination of CCT3 at lysine 21 (K21) subsequent to sorafenib treatment. This study provides evidence that CCT3 hinders the recycling of transferrin receptor protein 1 (TFRC) by interacting with alpha-actinin-4 (ACTN4), which is influenced by K6-linked ubiquitination on K21. Depleting CCT3 increased the susceptibility of cells to sorafenib-induced ferroptosis, while reintroducing CCT3 through transfection restored resistance to ferroptosis. Additionally, impairing ACTN4 or TFRC depletion compromised CCT3's ability to inhibit sorafenib-induced ferroptosis. In summary, targeting CCT3 presents a potential strategy for overcoming sorafenib resistance in HCC.

2023-09-21 | PXD045576 |

A missense mutation in TFRC, encoding transferrin receptor 1, causes combined immunodeficiency (Family B)

Project description:Affymetrix 6.0 SNP data for haplotype comparison of patients from two different families sharing the same homozygous mutation in TFRC, to determine if the families were related to each other Peripheral blood was used for patients who had no history of hematopoietic stem cell transplant (HSCT). Fibroblasts cell lines were used as a source of DNA for the individual who received HSCT. Genomic DNA from 3 subjects (2 from Family A, 1 from Family B in duplicate) was genotyped at 909,622 single nucleotide polymorphisms (SNPs) on the Genome-Wide Human SNP 6.0 Array (Affymetrix).

2015-11-25 | E-GEOD-75349 | biostudies-arrayexpress

A missense mutation in TFRC, encoding transferrin receptor 1, causes combined immunodeficiency (Family B)

2015-11-25 | GSE75349 | GEO