GEO DataSets

Analysis of liver from Tmprss6 knockouts (KO) and iron-deficient WT littermates treated with LPS to induce acute inflammation. Tmprss6 KOs are iron-deficient with high levels of hepcidin, a key iron regulator. Results provide insight into molecular basis of the Tmprss6 KO inflammatory response.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 genotype/variation, 2 growth protocol, 2 stress sets

Platform:

GPL6887

Series:

GSE46287

12 Samples

Download data

(Submitter supplied) Tmprss6 is the master inhibitor of hepcidin and its inactivation causes iron refractory iron deficiency anemia both in human and in mice. Mice with iron deficiency anemia (IDA)-low hepcidin show a pro-inflammatory response that is blunted in iron deficienct-high hepcidin Tmprss6 null mice. We investigated the transcriptional response associated with chronic hepcidin overexpression by comparing whole genome transcription profiling of the liver of Tmprss6 KO mice and IDA animals, irrespective of iron deficiency.

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS5271

Platform:

GPL6887

12 Samples

Download data: TXT

(Submitter supplied) TMPRSS6 is a type II transmembrane serine protease and is revealed by our work to be part of a low-iron sensing pathway. When animal gets iron deficient, TMPRSS6 is required to shut off hepcidin gene, so as to allow iron to be uptaken from GI tract. The mutant mouse, which was generated by ENU mutagenesis, has developed microcytic anemia. The phenotype is caused by a splicing error in Tmprss6 gene. However, the mechanism of TMPRSS6 effect remains elusive. To gain further insight into the molecular components of the TMPRSS6 signaling pathway, we overexpressed either TMPRSS6 or its mutant version of protein in human liver carcinoma cell line HepG2 cells, and compared the transcription status betweem these two treatments. Keywords: genetic modification

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

9 Samples

Download data: CEL, EXP

(Submitter supplied) Matriptase-2 (Tmprss6), a recently described member of the TTSP family, is an essential regulator of iron homeostasis. Tmprss6-/- mice display an overt phenotype of alopecia and a severe iron deficiency anemia. These hematological alterations found in Tmprss6-/- mice are accompanied by a marked up-regulation of hepcidin, a negative regulator of iron export into plasma.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

2 Samples

Download data: CEL

(Submitter supplied) Iron is an essential trace element whose absorption is usually tightly regulated in the duodenum. HFE-related hereditary hemochromatosis (HH) is characterized by abnormally low expression of the iron-regulatory hormone, hepcidin, which results in increased iron absorption. The liver is crucial for iron homeostasis as it is the main production site of hepcidin. The aim of this study was to explore and compare the genome-wide transcriptome response to Hfe deficiency and dietary iron overload in murine liver and duodenum.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6105

19 Samples

Download data: TXT

(Submitter supplied) Hfe disruption in the mouse leads to experimental hemochromatosis by a mechanism which remains elusive. Evidence for at least five modifier genes has been obtained. These account for the higher iron load of Hfe-deficient D2 mice compared to B6 mice. Gene expression profling was used to clarify the mechanism of Hfe action and to identify potential modifier genes. Keywords: response to genetic modification

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL1261

24 Samples

Download data: CEL, CHP, EXP