Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Fitm2 is required for ER homeostasis and normal function of murine liver

ABSTRACT:

ORGANISM(S): Mus Musculus

TISSUE(S): Liver

PROVIDER: ST002303 | MetabolomicsWorkbench |

REPOSITORIES: MetabolomicsWorkbench

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	mwtab	Other

Items per page:

1 - 1 of 1

Similar Datasets

Fitm2 is required for ER homeostasis and normal function of murine liver.

Project description: Not available

| S-EPMC10027564 | biostudies-literature

Angiocrine Bmp2 signaling in murine liver controls normal iron homeostasis.

Project description: Not available

| S-EPMC5291964 | biostudies-literature

Fitm2 is required for ER homeostasis and normal function of murine liver

Project description:The ER-resident prote in fat-inducing transcript 2 (FIT2) catalyzes acyl-CoA cleavage in vitro, and in cells is required for endoplasmic reticulum (ER)homeostasis and normal lipid storage. The gene encoding FIT2 is essential for viability of mice and worms. Whether FIT2 acts as anacyl-CoA diphosphatase in vivo and how this activity affects liver, where the protein was discovered,is unknown. Here, we report that hepatocyte-specific Fitm2 knockout (FIT2-LKO) mice exhibited elevated acyl-CoA levels, ER stress, and signs of liver injury. FIT2-LKO mice had increased triglyceride (TG) content in liver when fed a chow diet, compared with control littermates due in part to impaired secretion of TG-rich lipoproteins and reduced capacity for fatty acid oxidation. Challenging FIT2-LKO mice with a high-fat diet to increase FIT2 acyl-CoA substrates worsened hepatic ER stress and liver injury, yet unexpectedly reversed the steatosis phenotype, similar to what is observed in FIT2-deficient cells loaded with fatty acids. Our findings show that FIT2 acts as anacyl-CoA diphosphatase in vivo and is crucial for normal hepatocyte function and ER homeostasis in murine liver

2023-05-10 | PXD033884 | Pride

Angiocrine Bmp2 signaling in murine liver controls normal iron homeostasis

Project description:Microvascular endothelial cells (EC) display a high degree of phenotypic and functional heterogeneity among different organs. Organ-specific EC control their tissue microenvironment by angiocrine factors in health and disease. Liver sinusoidal EC (LSEC) are uniquely differentiated to fulfil important organ-specific functions in development, under homeostatic conditions, and in regeneration and liver pathology. Recently, Bmp2 has been identified by us as an organ-specific angiokine derived from LSEC. To study angiocrine Bmp2 signaling in the liver, we conditionally deleted Bmp2 in LSEC using EC subtype-specific Stab2-Cre mice. Genetic inactivation of hepatic angiocrine Bmp2 signaling in Stab2-Cre;Bmp2fl/fl (Bmp2LSECKO) mice caused massive iron overload in the liver, and increased serum iron levels and iron deposition in several organs similar to classic hereditary hemochromatosis. Iron overload was mediated by decreased hepatic expression of hepcidin, a key regulator of iron homeostasis. Thus, angiocrine Bmp2 signaling within the hepatic vascular niche represents a constitutive pathway indispensable for iron homeostasis in vivo that is non-redundant with Bmp6. Notably, we demonstrate that organ-specific angiocrine signaling is essential not only for the homeostasis of the respective organ, but also for the homeostasis of the whole organism.

2017-01-31 | GSE90506 | GEO

Murine fetal liver TER119-negative erythroid precursors: Hipk1 or Hipk2 knockdown versus control

Project description:Expression profiling of fetal liver erythroid precursors after either Hipk1 or Hipk2 knockdown by shRNA versus control shRNA Two condition experiment, Hipk1 or Hipk2 knockdown versus control (shRNA against luciferase), two replicates each shRNA

2010-05-16 | E-GEOD-17106 | biostudies-arrayexpress

Normal Treg homeostasis and suppressive function require both FOXP1 and FOXP4.

Project description: Not available

| S-EPMC12487849 | biostudies-literature

Cell cyclin kinase inhibitor Cdkn2c regulates B cell homeostasis and function in the NZM2410-derived murine lupus susceptibility locus Sle2c1

Project description:Sle2c1 is an NZM2410-derived lupus susceptibility locus that induces an expansion of the B1a cell compartment. B1a cells have a repertoire enriched for autoreactivity, and an expansion of this B cell subset occurs in several mouse models of lupus. Here we showed that expression of Sle2c1 enhances NZB cellular phenotypes that have been associated with autoimmune pathogenesis. A combination of genetic mapping and candidate gene analysis presents Cdkn2c, a gene encoding for cyclin kinase inhibitor p18INK4c (p18), as the top candidate gene for inducing the Slec2c1 associated expansion of B1a cells. A novel SNP in the Cdkn2c promoter is associated with a significantly reduced Cdkn2c expression in the splenic B cells and B1a cells from Sle2c1-carrying mice, which leads to defective G1 cell cycle arrest in splenic B cells and increased proliferation of Pc B1a cells. As cell cycle is differentially regulated in B1a and B2 cells, these results suggest that Cdkn2c play a critical role in B1a cell self renewal, and that its impaired expression leads to an accumulation of these cells with high autoreactive potential. Total RNA from peritoneal cavity B cells (B1a) and splenic B cells (Bs) was isolated, with 4 biological replicates each. Gene expression data from C57BL/6 mice were compared with data from B6.Sle2c1 mice.

2010-07-24 | E-GEOD-23114 | biostudies-arrayexpress

Fecal Microbiome Data Distinguish Liver Recipients With Normal and Abnormal Liver Function From Healthy Controls.

Project description: Not available

| S-EPMC6619441 | biostudies-literature

Topical hesperidin improves epidermal permeability barrier function and epidermal differentiation in normal murine skin.

Project description: Not available

| S-EPMC3335754 | biostudies-literature

A disintegrin and metalloprotease 10 (ADAM10) is a central regulator of murine liver tissue homeostasis.

Project description: Not available

| S-EPMC4951223 | biostudies-literature