Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Non-muscle myosin heavy chain 9 maintains intestinal homeostasis by preventing epithelium necroptosis and colitis adenoma formation

ABSTRACT: Non-muscle myosin heavy chain 9 maintains intestinal homeostasis by preventing epithelium necroptosis and colitis adenoma formation

PROVIDER: PRJNA715738 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR14009392_1.fastq.gz	Fastqsanger.gz
	SRR14009392_2.fastq.gz	Fastqsanger.gz
	SRR14009393_1.fastq.gz	Fastqsanger.gz
	SRR14009393_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 4 of 4

Similar Datasets

Non-muscle myosin heavy chain 9 maintains intestinal homeostasis by preventing epithelium necroptosis and colitis adenoma formation

Project description:Non-muscle myosin IIA plays an important role in cell adhesion, cell migration and tissue architecture. We previously showed that low activity of the heavy chain of non-muscle myosin II Myh9 is beneficial to Lgr5+ intestinal stem cell maintenance. However, the function of Myh9 in adult mouse intestinal epithelium is largely unclear. In this study, we used the inducible Villin-creERT2 knockout approach to delete Myh9 in adult mouse intestinal epithelium and observed that homozygous deletion of Myh9 causes colitis-like morphologic changes in intestine, leads to a high sensitivity to dextran sulfate sodium and promotes the colitis related adenomas formation in colon. Myh9 deletion disturbs cell junctions and impairs intestinal lumen barrier integrity, promoting the necroptosis of epithelial cells. Consistently, these changes can be partially rescued by Ripk3 knockout. Our results indicate that Myh9 is required for the maintenance of intestinal epithelium integrity and the prevention of cell necroptosis.

2021-03-20 | GSE169225 | GEO

Non-muscle myosin heavy chain 9 maintains intestinal homeostasis by preventing epithelium necroptosis and colitis adenoma formation.

Project description:Non-muscle myosin IIA plays an important role in cell adhesion, cell migration, and tissue architecture. We previously showed that low activity of the heavy chain of non-muscle myosin II Myh9 is beneficial to LGR5+ intestinal stem cell maintenance. However, the function of Myh9 in adult mouse intestinal epithelium is largely unclear. In this study, we used the inducible Villin-creERT2 knockout approach to delete Myh9 in adult mouse intestinal epithelium and observed that homozygous deletion of Myh9 causes colitis-like morphologic changes in intestine, leads to a high sensitivity to dextran sulfate sodium and promotes colitis-related adenoma formation in the colon. Myh9 deletion disturbs cell junctions and impairs intestinal lumen barrier integrity, promoting the necroptosis of epithelial cells. Consistently, these changes can be partially rescued by Ripk3 knockout. Our results indicate that Myh9 is required for the maintenance of intestinal epithelium integrity and the prevention of cell necroptosis.

| S-EPMC8185465 | biostudies-literature

Myosin Heavy Chain-embryonic is a crucial regulator of skeletal muscle development and differentiation.

Project description:mRNA from 4 different muscles from control and Myosin heavy chain-embryonic knockout neonate mice were sequenced.

2020-03-08 | GSE100331 | GEO

Identification of myosin heavy chain post-translational modifications in patients with MHY mutations

Project description:Congenital myopathies are rare genetic muscle diseases notably due to mutations in the MYH2 gene. Here we assessed their myosin heavy chain post-translational modifications. For that, we purified beta/slow and type IIa myosin heavy chains from limb muscles of five patients and five healthy controls. We then ran a LC/MS analysis.

2023-01-30 | PXD039178 | Pride

Necroptosis of intestinal epithelial cells induces innate lymphoid cell-dependent lethal ileitis in preterm mice

Project description:CFLARs encodes short form of cellular FLICE-inhibitory protein that blocks apoptosis, but promotes necroptosis in vitro. Here, we generate transgenic mice expressing CFLARs on the X-chromosome, designated as XCFY or XCFX mice. All XCFY mice die perinatally due to severe ileitis, whereas XCFX mice appear to be normal and fertile. Intestinal epithelial cell (IEC)s of XCFY mice die by necroptosis that subsequently induces massive apoptosis of IECs. Deletion of Ripk3 or Mlkl that are essential for necroptosis rescues embryonic lethality of XCFY mice by preventing both apoptosis and necroptosis of IECs. Surprisingly, deletion of RORγt+ ILC3s or Il22 rescues embryonic lethality of CFLARs Tg mice by preventing apoptosis, but not necroptosis of IECs. Thus, necroptosis of IECs triggered by cFLIPs activates RORγt+ ILC3s, resulting in induction of lethal ileitis in preterm mice.

2019-06-21 | GSE120982 | GEO

CD47 promotes peripheral T cell survival by preventing dendritic cell–mediated T cell necroptosis

Project description:CD47 promotes peripheral T cell survival by preventing dendritic cell–mediated T cell necroptosis

| PRJNA931227 | ENA

Identification of a new mechanism for targeting myosin II heavy chain phosphorylation by Dictyostelium myosin heavy chain kinase B.

Project description:BackgroundHeavy chain phosphorylation plays a central role in regulating myosin II bipolar filament assembly in Dictyostelium, as well as in higher eukaryotic nonmuscle cells. Our previous work has demonstrated that the WD-repeat domain of Dictyostelium myosin II heavy chain kinase B (MHCK-B), unlike its counterpart in MHCK-A, is not absolutely required for targeting of the kinase to phosphorylate MHC. Thus, we tested the hypothesis that an asparagine-rich and structurally disordered region that is unique to MHCK-B can by itself function in substrate targeting.FindingsBiochemical assays comparing the activities of full-length MHCK-B, a truncation lacking only the WD-repeat domain (B-Delta-WD), and a truncation lacking both the N-rich region and the WD-repeat domain (B-Delta-N-WD) revealed that the N-rich region targets MHCK-B to phosphorylate MHC in a manner that leads to bipolar filament disassembly. This targeting is physiologically relevant since cellular over-expression of the B-Delta-WD truncation, but not the B-Delta-N-WD truncation, leads to dramatically reduced levels of myosin II filament assembly and associated defects in cytokinesis and multicellular development.ConclusionsThe results presented here demonstrate that an intrinsically unstructured, and asparagine-rich, region of a MHCK-B can mediate specific targeting of the kinase to phosphorylate myosin II heavy chain. This targeting involves a direct binding interaction with myosin II filaments. In terms of regulating myosin bipolar filament assembly, our results suggest that factors affecting the activity of this unique region of MHCK-B could allow for regulation of MHCK-B in a manner that is distinct from the other MHCKs in Dictyostelium.

| S-EPMC2838905 | biostudies-literature

Quantitative analysis of phosphoproteome in necroptosis reveals a role of TRIM28 phosphorylation in promoting necroptosis-induced cytokine production

Project description:Necroptosis is a form of regulated necrotic cell death which promotes inflammation. In cells undergoing necroptosis, the activated RIPK1 kinase mediates the formation of RIPK1/RIPK3/MLKL complex to promote MLKL oligomerization and execution of necroptosis. RIPK1 kinase activity also promotes cell-autonomous activation of proinflammatory cytokine production in necroptosis. However, the signaling pathways downstream of RIPK1 kinase in necroptosis and how RIPK1 kinase activation controls inflammatory response induced by necroptosis are still largely unknown. Here we quantitatively measured the temporal dynamics of over 7000 confident phosphosites during necroptosis using mass spectrometry. Our study defined a RIPK1-dependent phosphorylation pattern in late necroptosis that is associated with a proinflammatory component marked by p-S473 TRIM28. We show that the activation of p38 MAPK mediated by oligomerized MLKL promotes the phosphorylation of S473 TRIM28, which in turn mediates inflammation during late necroptosis. Taken together, our study illustrates a mechanism by which p38 MAPK may be activated by oligomerized MLKL to promote inflammation in necroptosis.

2021-04-01 | GSE171214 | GEO

Quantitative proteomics characterization of proteins modified by very long chain fatty acids (VLCFAs) under necroptosis

Project description:Necroptosis is a caspase-independent form of regulated cell death that is characterized by membrane permeabilization and rupture. This membrane rupture is responsible for the inflammatory properties of necroptosis and is critical for disease states involving this process. In efforts to understand how lipids might contribute to necroptosis, we previously showed that saturated very long chain fatty acids (VLCFAs) are functionally involved in this process, potentially through protein fatty acylation. Here we define the scope of protein acylation by saturated VLCFAs during necroptosis using a clickable lipid analog and IonStar quantitative proteomics.As a result, a total of 1672 proteins were quantified with high precision and no missing data across samples in the same condition. 1267 were detected with higher abundances in control cells and 405 were detected with higher abundance in necroptotic conditions.

2021-05-25 | PXD022527 | Pride

Ribonucleoprotein immunoprecipitation of myosin proteins and myosin-specific chaperones in fission yeast

Project description:Ribonucleoprotein immunoprecipitation microarray (RIp-chip) study using various myosin proteins and myosin-specific chaperones from the fission Schizosaccaromyces pombe

2010-03-01 | E-TABM-335 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data