Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A proteomic analysis of WASH complex subunit 3 deficiency in adult heart.

ABSTRACT: The WASH complex is primarily responsible for the activation of actin branching on endosomes, regulating vesicle trafficking across intracellular organelles. As one of the core subunits of the WASH complex, the function of washc3 remains largely unknown. In this study, we performed proteomic analysis of washc3 mutant, focusing specifically on the adult heart.

INSTRUMENT(S):

ORGANISM(S): Danio Rerio (zebrafish) (brachydanio Rerio)

SUBMITTER: Marcin Luzarowski

LAB HEAD: Marcin Luzarowski

PROVIDER: PXD062550 | Pride | 2026-03-09

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	24-93-PRIDE-SampleList.xlsx	Xlsx
	Q25-24-93-01-12zebrafish.msf	Msf
	Q25-24-93-01.raw	Raw
	Q25-24-93-02.raw	Raw
	Q25-24-93-04.raw	Raw

Items per page:

1 - 5 of 11

Publications

WASHC3 knockout disrupts mitochondrial protein homeostasis and energy metabolism in cardiomyocytes.

Kim Sujin S Park Deung-Dae DD Glazier Amelia A Rottbauer Wolfgang W Just Steffen S

Frontiers in cardiovascular medicine 20260212

<h4>Introduction</h4>The WASH complex regulates endosomal actin dynamics and vesicular trafficking and is essential for neuronal integrity and motor function. Although variants in WASHC4, WASHC5, and WASHC3 are linked to neurodevelopmental abnormalities, the role of WASHC3 beyond the nervous system, particularly in cardiac mitochondrial regulation, remains unclear.<h4>Methods</h4>We modeled WASHC3 loss of function in zebrafish and human cardiomyocytes. Washc3 was suppressed in zebrafish embryos ...[more]

PMID: 41768586

Similar Datasets

Rapid reprogramming of epigenetic and transcriptional profiles in mammalian culture systems

Project description:Comparison of the methylation profile of mouse embryonic fibroblasts (MEFs) before and during adaptation to cell culture conditions. Matched expression data is deposited under accession: E-MTAB-3172

2014-12-17 | E-MTAB-3176 | biostudies-arrayexpress

Rapid reprogramming of epigenetic and transcriptional profiles in mammalian culture systems

Project description:5-hmC profiling of mouse embryonic fibroblasts before and during adaptation to cell culture conditions using hMeDIP-chip

2014-12-17 | E-MTAB-3177 | biostudies-arrayexpress

Climate sensitivity of Equatorial Pacific nutrient limitation

Project description:Projected responses of ocean net primary productivity (NPP) to climate change are highly uncertain. The climate sensitivity of phytoplankton nutrient limitation in the low-latitude Pacific plays a crucial role, but field measurements are insufficient to provide suitable constraints. Here we quantify two decades of nutrient limitation in the Equatorial Pacific with satellite observations. Using field nutrient addition experiments, proteomics, and above-water hyperspectral radiometry, we demonstrate that physiological responses of phytoplankton to iron limitation led to ~3-fold increases in chlorophyll-normalized phytoplankton fluorescence. Extension to the >18-year satellite fluorescence record showed that Equatorial Pacific iron limitation was robust to changes in physical forcing through multiple El Niño–Southern Oscillation cycles, despite coherent fluctuations in limitation strength. In contrast, these iron limitation changes were overestimated 2-fold by a state-of-the-art climate model. Such synoptic constraints provide a powerful new approach for benchmarking the realism of model NPP projections to climate changes.

2023-06-26 | PXD030610 | Pride

Consequences of loss of spinophilin on striatal mGluR5 phosphorylation and interactome

Project description:Constitutive knockout of the obsessive-compulsive disorder-associated protein, SAPAP3, results in repetitive motor dysfunction, such as excessive grooming, caused by increased mGluR5 activity in striatal medium spiny neurons (MSNs). However, signaling mechanisms that mediate mGluR5-dependent grooming dysfunction are not fully understood. Here, we investigate the function of the striatal signaling hub protein, spinophilin, in regulating mGluR5 phosphorylation and protein interactions, which may predict spinophilin’s role in regulating mGluR5-dependent grooming dysfunction.

2022-12-14 | PXD034053 | Pride

IP of 5-methylcytosine (5-mc) enriched DNA fragments from control and mice with non-acoholic steatohepatitis (NASH) related hepatocellular carcinoma (HCC)

Project description:Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease); we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation; whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent with this reduced Tet1 protein levels are observed in mouse liver tumour lesions. As in human, DNA methylation changes at CGIs do not appear to be direct drivers of hepatocellular carcinoma progression in mice. Instead dynamic changes in H3K27me3 promoter deposition are strongly associated with tumour-specific activation and repression of transcription. Our data suggests that loss of promoter associated 5hmC in diverse liver tumours licences DNA methylation reprogramming at silent CGIs during cancer progression. 5-mc is a well establisehd epigenetic mark typically related to gene silencing events. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5mC in both control mouse livers as well as in liver tumours of high fat diet exposed mice who have progressed through NASH. Samples: 5mC profiles in livers of 2 control and 2 NASH driven HCC samples

2016-05-17 | E-GEOD-77725 | biostudies-arrayexpress

IP of 5-methylcytosine (5-mc) enriched DNA fragments from control, PB treated mouse livers, resulting Ctnnb1 mutated PB liver tumours and PB minus Ha-Ras mutate liver tumour

Project description:Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease); we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation; whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent with this reduced Tet1 protein levels are observed in mouse liver tumour lesions. As in human, DNA methylation changes at CGIs do not appear to be direct drivers of hepatocellular carcinoma progression in mice. Instead dynamic changes in H3K27me3 promoter deposition are strongly associated with tumour-specific activation and repression of transcription. Our data suggests that loss of promoter associated 5hmC in diverse liver tumours licences DNA methylation reprogramming at silent CGIs during cancer progression. 5-mc is a well establisehd epigenetic mark typically related to gene silencing events. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5mC in both control mouse livers as well as in the livers of 12 week PB treated mice. We also profile 5mC in liver tumours arising in the presence of long term PB exposure (35 week: resulting in Ctnnb1 mutated tumours) to a Ha-Ras liver tumour which arose without PB. Samples: 2 control and 2 PB exposed mouse livers, 3 liver tumours resulting from long term PB exposrue and 1 liver tumour arising without PB

2016-05-17 | E-GEOD-77727 | biostudies-arrayexpress

IP of 5-hydroxymethylcytosine (5-hmC) enriched DNA fragments from control ,PB treated mouse livers , resulting Ctnnb1 mutated PB liver tumours and PB minus Ha-Ras mutate liver tumour

Project description:Through the analysis of mouse liver tumours promoted by distinct routes (DEN exposure alone, DEN exposure plus non-genotoxic insult with phenobarbital and non-alcoholic fatty liver disease); we report that the cancer associated hyper-methylated CGI events in mice are also predicated by silent promoters that are enriched for both the DNA modification 5-hydroxymethylcytosine (5hmC) and the histone modification H3K27me3 in normal liver. During cancer progression these CGIs undergo hypo-hydroxymethylation, prior to subsequent hyper-methylation; whilst retaining H3K27me3. A similar loss of promoter-core 5hmC is observed in Tet1 deficient mouse livers indicating that reduced Tet1 binding at CGIs may be responsible for the epigenetic dysregulation observed during hepatocarcinogenesis. Consistent with this reduced Tet1 protein levels are observed in mouse liver tumour lesions. As in human, DNA methylation changes at CGIs do not appear to be direct drivers of hepatocellular carcinoma progression in mice. Instead dynamic changes in H3K27me3 promoter deposition are strongly associated with tumour-specific activation and repression of transcription. Our data suggests that loss of promoter associated 5hmC in diverse liver tumours licences DNA methylation reprogramming at silent CGIs during cancer progression. 5-hmC is a novel epigenetic mark derived from oxidation of methylcytosine. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5hmC in both control mouse livers as well as in the livers of 12 week PB treated mice. We also profile 5hmC in liver tumours arising in the presence of long term PB exposure (35 week: resulting in Ctnnb1 mutated tumours) to a Ha-Ras liver tumour which arose without PB. Samples: 5hmC profiles in 2 control and 2 PB exposed mouse livers, 3 liver tumours resulting from long term PB exposrue and 1 liver tumour arising without PB

2016-05-17 | E-GEOD-77726 | biostudies-arrayexpress

Hydroxymethyl DNA-IP of genomic DNA for many different normal human tissues

Project description:5-hmC is a novel epigenetic mark derived from oxidation of methylcytosine. We profile this mark in several normal human tissues 5-hmC patterns are highly tissue specific and enriched in the body of transcribed genes 5-hmC patterns are highly tissue specific and enriched in the body of transcribed genes comparison of six normal human tissue types

2011-11-18 | E-GEOD-33219 | biostudies-arrayexpress

IP of 5-methylcytosine (5-hmC) enriched DNA fragments from control and PB treated mouse livers (1 day)

Project description:5-hmC is an epigenetic modification of the DNA base cytosine with roles in gene silencing events, imprinting and X inactivation. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5hmC in both control mouse livers as well as in the livers of 1 day PB treated mice. 5hmC is largely found to reside in the bodies of active genes and promoter levels are perturbed upon PB induced gene activation events. 5-hmC is assocated with promoters fo silent genes. Upon PB exposire a handfull of genes are induced which reveal decreases in promoter 5hmC levels comparison of 5-hmC profiles in 5 control and 5 PB exposed mouse livers (dose: 1day PB)

2012-11-10 | E-GEOD-41395 | biostudies-arrayexpress

IP of 5-methylcytosine (5-mC) enriched DNA fragments from control and PB treated mouse livers (1 day)

Project description:5-mC is an epigenetic modification of the DNA base cytosine with roles in gene silencing events, imprinting and X inactivation. Phenobarbital (PB) is a well studied non-genotoxic carcinogen with roles in epigenetic perturbation. We profile 5mC in both control mouse livers as well as in the livers of 1 day PB treated mice. 5mC is largely found to reside in the bodies of active genes and promoter levels are perturbed upon PB induced gene activation events. 5-mC is assocated with promoters fo silent genes. Upon PB exposire a handfull of genes are induced which reveal decreases in promoter 5mC levels comparison of 5-mC profiles in 5 control and 5 PB exposed mouse livers (dose: 1day PB)

2012-11-10 | E-GEOD-41396 | biostudies-arrayexpress