Dataset: Expression in HepG2 cells with overexpression of TMPRSS6 or its mutant version.

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. Experiment Overall Design: Triplicate per transfection with wildtype Tmprss6 cDNA, mutant version of Tmprss6 cDNA and empty vector as control, respectively. 36 hours post transfection, cells were harvested and subjected to RNA extraction.

Species:

human

Samples:

9

Source:

E-GEOD-10591

PubMed:

18451267

Updated:

Dec.12, 2014

Registered:

Aug.12, 2014