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

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. p/CIP was downregulated using two different siRNAs and total RNA was extracted and hybridized to a microarray. As control, wild type cells were transfected with pooled non specific siRNAs. The expression difference was calculated between the control wild-type cells and cells having p/CIP downregulation. The experiments were carried out at London Regional Genomic Centre (http://www.lrgc.ca/).

2013-08-21 | E-GEOD-50017 | biostudies-arrayexpress

Grimontia hollisae CIP 101886

Project description:Grimontia hollisae CIP 101886 genome sequencing project

| PRJNA40495 | ENA

Genome sequencing of prophage-free variants of the fast growing, Gram negative bacteria Vibrio natriegens ATCC 14048

Project description:After the wild type strain of Vibrio natriegens ATCC 14048 (BioSample Nr. NCBI: SAMN03178087) was cured from prophages (as described in the material and methods section), the genomes of the resulted strains dvnp1, dvnp2 and vnp12 were sequenced. As a control, the genome of the wild type strain was also prepared and used for sequencing. The aim of the sequencing was to verify the deleted regions and to screen the genome for new mutations.

2019-07-01 | E-MTAB-7875 | biostudies-arrayexpress

Cohnella sp. CIP 111063

Project description:Cohnella sp. CIP 111063, whole genome shotgun sequencing project

| PRJNA373949 | ENA