Defects in neutrophil number and survival are common to both hematologic disorders and chronic inflammatory diseases. At sites of inflammation, neutrophils respond to multiple signals that activate protein kinase A (PKA) signalling, which positively regulates neutrophil survival. We aimed to study the transcriptional responses to several stimuli in human neutrophils.
NR4A orphan nuclear receptor family members, NR4A2 and NR4A3, regulate neutrophil number and survival.
Specimen part
View SamplesGastric cancer is still one of the most common causes of cancer-related death worldwide, which is mainly attributable to late diagnosis and poor treatment options. Infection with H. pylori, different environmental factors and genetic alterations are known to influence the risk of developing gastric tumors. However, the molecular mechanisms involved in gastric carcinogenesis are still not fully understood, making it difficult to design targeted therapeutic approaches.
The stem cell factor SOX2 regulates the tumorigenic potential in human gastric cancer cells.
Specimen part, Cell line, Treatment, Time
View SamplesLong-lasting activation of T cells requires up-regulation of many genes, for example of transcription factors, cytoskeletal proteins and cell surface proteins encluding ion channels. An increase of ion channel density at the cell surface reflects the needs to manage increased Ca2+ influx into the activated T cell. Using oligonucleotide-based arrays we have surveyed changes in ion channel mRNA expression that occur upon T cell activation. We used Affymetrix Analysis to confirmate our data achieved by self-designed glass array analysis.
A truncation variant of the cation channel P2RX5 is upregulated during T cell activation.
No sample metadata fields
View SamplesWe profiled global gene expression for two separate lines of mouse embryonic fibroblasts and find that deletion of PKM2 and expression of PKM1 does not alter global gene expression profiles.
Pyruvate kinase isoform expression alters nucleotide synthesis to impact cell proliferation.
No sample metadata fields
View SamplesAgeing is the biggest risk factor to cardiovascular health and is associated with increased incidence of cardiovascular disease. Cellular senescence, a process driven in part by telomere shortening has been implicated in age-related cardiac dysfunction. However, the role of cellular senescence and its underlying mechanisms in slowly dividing/post-mitotic cardiomyocytes is not understood. Overall design: We quantify transcription via high throughput RNA sequencing in young (3 months) and old (20 months) mouse cardiomyocytes.
Length-independent telomere damage drives post-mitotic cardiomyocyte senescence.
Age, Cell line, Subject
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