Comparison of the Streptococcus pneumoniae D39 copY-stop mutant compared to D39 wild type in CDM without added copper One condition design comparision of two strains including a dye swap
Comparison of the Streptococcus pneumoniae D39 strain with 0mM compared to 0.05 mM in CDM Two condition design comparision of one strains including a dye swap
This SuperSeries is composed of the following subset Series: GSE30413: High low copper GSE30414: copY Mutant compared to D39 wild-type Refer to individual Series
Transcriptional profiling of genes recoverd by STOP2-complementation in the stop1-mutant (STOP2 expression is repressed in the stop1-mutant). The roots were exposed to Al and low pH stressed conditions, then genes recovered expression were analyzed. Goal is identifying the genes can be actevated the...
In order to explore molecules whose expression is controlled by Slc39a13, we investigated gene expression profiling of primary osteoblast isolated from wild-type and Slc39a13 knockout mice. Keywords: knockout vs wild-type wild-type vs Slc39a13 knockout
Medulloblastoma (MB) is the most common malignant brain tumor in children, among whom overexpression or amplification of MYC oncogenes has been associated with poor clinical outcome. Although the MYC functions during normal development and oncogenesis in various systems have been extensively investi...
The Saccharomyces cerevisiae TRAMP4 and TRAMP5 complexes, which consist of the poly(A) polymerase Trf4 or Trf5, respectively, the zinc knuckle proteins Air1 or Air2, and the RNA helicase Mtr4, play a critical role in nuclear RNA surveillance. Although it is known to enhance the nuclease activity of ...
Three-week-old DEX-AZF1, DEX-AZF2, and vector control plants were treated 10 µM DEX solution for 24 h. Two-week-old ProAZF2:AZF2 and vector control plants were treated with water as control or 200 mM NaCl for 5 h.
Ataxin 1 (Atxn1) is a protein of unknown function associated with cerebellar neurodegeneration in spinocerebellar ataxia type 1 (SCA1). SCA1 is caused by an expanded polyglutamine within Atxn1 by gain-of-function mechanisms. Lack of Atxn1 in mice triggers motor deficits in the absence of neurodegene...
