Project description:RNA-seq of Mycobacteriophage Island3 infection of Mycolicibacterium smegmatis mc2155, Mycolicibacterium smegmatis mc2155(Butters), and Mycolicibacterium smegmatis mc2155(Buttersgp57r) to assess the impact of Butters lysogen and specifically Buttersgp57r on transcript levels of island3 during infection.

2022-12-24 | GSE221406 | GEO

Mycolicibacterium aurum strain:NCT 10437 | isolate:tree

Project description:Mycolicibacterium aurum strain:NCT 10437 | isolate:tree Genome sequencing

| PRJNA543719 | ENA

Mycolicibacterium mageritense DSM 44476 = CIP 104973

Project description:Mycolicibacterium mageritense DSM 44476 = CIP 104973 Genome sequencing

| PRJNA170464 | ENA

p/CIP gene regulation in mouse embryonic stem cells

Project description:p/CIP binds to many nuclear receptors and plays a major role in hormone dependent transcription of genes. Recently, p/CIP was shown to affect mouse stem cell pluripotency. Microarray gene expression analysis was conducted to assess the role of p/CIP in mouse embryonic stem cells.

2013-08-21 | GSE50017 | GEO

CIP, a cardioprotective factor, inhibits the transition from cardiac hypertrophy to heart failure

Project description:Heart failure is characterized by the inability of the heart to pump effectively and generate proper blood circulation to meet the body's needs; it is a devastating condition that affects more than 100 million people globally. In spite of this, little is known about the mechanisms regulating the transition from cardiac hypertrophy to heart failure. Previously, we identified a cardiomyocyte-enriched gene, CIP, which regulates cardiac homeostasis under pathological stimulation. Here, we show that the cardiac transcriptional factor GATA4 binds the promotor of CIP gene and regulates its expression. We further determined that both CIP mRNA and protein decrease in diseased human hearts. In a mouse model, induced cardiac-specific overexpression of CIP after the establishment of cardiac hypertrophy protects the heart by inhibiting disease progression toward heart failure. Transcriptome analyses revealed that the IGF, mTORC2 and TGFβ signaling pathways mediate the inhibitory function of CIP on pathologic cardiac remodeling. Our study demonstrates GATA4 as an upstream regulator of CIP gene expression in cardiomyocytes, as well as the clinical significance of CIP expression in human heart disease. More importantly, our investigation suggests CIP is a key regulator of the transition from cardiac hypertrophy to heart failure. The ability of CIP to intervene in the onset of heart failure suggests a novel therapeutic avenue of investigation forthe prevention of heart disease progression.

2022-03-05 | GSE194149 | GEO

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