Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from liver of the KRAP deficient mice

ABSTRACT: KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule. KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia.

ORGANISM(S): Mus musculus

PROVIDER: GSE13583 | GEO | 2009/01/22

SECONDARY ACCESSION(S): PRJNA113937

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from BAT of the KRAP deficient mice

2009-01-22 | GSE13582 | GEO

Expression data from BAT and liver of the KRAP deficient mice

Project description:KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule. KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. This SuperSeries is composed of the SubSeries listed below.

2009-01-22 | GSE13585 | GEO

Transcription profiling of brown adipose tissue from KRAP deficient animals

Project description:KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule. KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. Experiment Overall Design: Total RNA was extracted from BAT of three pairs of littermates (KO1 vs. WT1, KO2 vs. WT2 and KO3 vs. WT3) fed normal chow.

2009-01-30 | E-GEOD-13582 | biostudies-arrayexpress

Transcription profiling of mous eliver of the KRAP deficient animals

Project description:KRAP (Ki-ras-induced actin-interacting protein) is a cytoskeleton-associated protein and a ubiquitous protein among tissues, originally identified as a cancer-related molecule. KRAP-deficient (KRAP-/-) mice show enhanced metabolic rate, decreased adiposity, improved glucose tolerance, hypoinsulinemia and hypoleptinemia. KRAP-/- mice are also protected against high-fat diet-induced obesity and insulin resistance despite of hyperphagia. Experiment Overall Design: Total RNA was extracted from livers of three pairs of littermates (KO1 vs. WT1, KO2 vs. WT2 and KO3 vs. WT3) fed normal chow.

2009-02-07 | E-GEOD-13583 | biostudies-arrayexpress

Transcription profiling of mouse liver and brown adipose tissue from KRAP deficient mice

2009-01-30 | E-GEOD-13585 | biostudies-arrayexpress

PTBP1 mediates Sertoli cell actin cytoskeleton organization through regulating alternative splicing of actin regulators

Project description:Spermatogenesis is a biological process within the testis that produces haploid spermatozoa for the continuity of species. Sertoli cells are somatic cells in the seminiferous epithelium that orchestrate spermatogenesis. Cyclic reorganization of Sertoli cell actin cytoskeleton is vital for spermatogenesis but the underlying mechanism remains largely unclear. Here we report that RNA-binding protein PTBP1 controls Sertoli cell actin cytoskeleton reorganization by programming alternative splicing of actin cytoskeleton regulators. This splicing control enables ectoplasmic specializations, the actin-based adhesion junctions, to maintain the blood-testis barrier and support spermatid transport and transformation. Of particular, we show that PTBP1 promotes actin bundle formation by repressing the inclusion of exon 14 of Tnik, a kinase present at the ectoplasmic specialization. Our results thus reveal a novel mechanism wherein Sertoli cell actin cytoskeleton dynamics is controlled post-transcriptionally by utilizing functionally distinct isoforms of actin regulatory proteins and PTBP1 is a key player in generating such isoforms.

2024-07-31 | GSE267924 | GEO

Characterization of T cells from the larval zebrafish tail via single-cell RNAseq

Project description:We report single-cell RNA sequencing of cells from the Tg(lck:GFP) larval zebrafish tail, to identify cell types expressing the marker and to identify gene candidates related to T cell migration behaviors. We identified 330 putative T cells and 131 putative epithelial cells. Differential expression analysis between the two groups revealed genes related to actin cytoskeleton remodeling associated with the T cells, in addition to canonical T and ubiquitous immune cell markers.

2020-05-13 | GSE137770 | GEO

E-GEOD-27077

Project description:Actin Cytoskeleton Integrates Auxin and Brassinosteroid Signaling in Plants.

2015-12-03 | E-GEOD-27077 | ExpressionAtlas

Large-scale genetic screens identify BET-1 as a cytoskeleton regulator promoting actin health and lifespan

Project description:The actin cytoskeleton is a three-dimensional scaffold of proteins that is a regulatory, energy-consuming material with dynamic properties shaping the structure and function of the cell. The proper function of actin is required for many cellular pathways, including cell division, autophagy, chaperone function, endocytosis, and exocytosis (1–5). The breakdown of these cellular processes manifests during aging and exposure to stress, which is in part due to the breakdown of the actin cytoskeleton (5–9). However, the regulatory mechanisms involved in preservation of cytoskeletal form and function are not well understood. Here, we performed a multi-pronged, cross-organismal screen combining a whole-genome CRISPR-Cas9 screen in human fibroblasts with in vivo C. elegans synthetic lethality screening. We identified the bromodomain protein, BET-1, as a key regulator promoting actin health and longevity. Interestingly, overexpression of bet-1 preserves actin health at late age and promotes lifespan and healthspan in C. elegans. These beneficial effects are through preservation of actin, downstream of the function of BET-1 as a transcriptional regulator. Together, our discovery attributes assigns a key role of BET-1 in cytoskeletal health, highlighting regulatory cellular networks promoting cytoskeletal homeostasis.

2023-06-01 | E-MTAB-12289 | biostudies-arrayexpress

Large-scale genetic screens identify BET-1 as a cytoskeleton regulator promoting actin health and lifespan

2023-06-01 | E-MTAB-11786 | biostudies-arrayexpress