Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

ER-phagy regulates ER dynamics during myogenesis (3)

ABSTRACT: Proteomic landscape of primary murine myoblasts and differentiated myotubes

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Culture

SUBMITTER: Paolo Grumati

LAB HEAD: Paolo Grumati

PROVIDER: PXD050893 | Pride | 2024-12-27

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	2022-6-24_MS_PG_mMyoblasts_D0_1.raw	Raw
	2022-6-24_MS_PG_mMyoblasts_D0_2.raw	Raw
	2022-6-24_MS_PG_mMyoblasts_D0_3.raw	Raw
	2022-6-24_MS_PG_mMyoblasts_D10DM_1.raw	Raw
	2022-6-24_MS_PG_mMyoblasts_D10DM_2.raw	Raw

Items per page:

1 - 5 of 10

Similar Datasets

ER-phagy regulates ER dynamics during myogenesis (1)

Project description:Proteomic profile of C2C12 myoblasts and differentiated myotubes

2024-12-27 | PXD050867 | Pride

ER-phagy regulates ER dynamics during myogenesis

Project description:Proteomic landscape of human myoblasts and differentiated myotubes

2024-12-27 | PXD050898 | Pride

ER-phagy regulates ER dynamics during myogenesis (2)

Project description:Proteomic landscape of Fam134b knockout myoblasts and myotubes

2024-12-27 | PXD050874 | Pride

ER-phagy regulates ER dynamics during myogenesis (4)

Project description:IP-MS interactome of FAM134B1 and FAM134B2 in C2C12 cells differentiated into myotubes

2024-12-27 | PXD050899 | Pride

ER-phagy regulates ER dynamics during myogenesis (5)

Project description:IP-MS interactome of FAM134B1 and FAM134B2 complexes (bimolecular complementation affinity purification (BiCAP) system)

2024-12-27 | PXD050902 | Pride

ER-phagy regulates ER dynamics during myogenesis (7)

Project description:Proteomic landscape of Fam134b knockout C2C12 reconstituted with hFAM134B1 or hFAM134B2

2024-12-27 | PXD050907 | Pride

ER-phagy regulates ER dynamics during myogenesis (6)

Project description:Lysosomal isolation and mass spectrometry analysis from wild-type C2C12 myotubes and Fam134bknockout C2C12 myotubes

2024-12-27 | PXD050903 | Pride

Fam134c and Fam134b shape axonal endoplasmic reticulum architecture in vivo.

Project description:Endoplasmic reticulum (ER) remodeling is vital for cellular organization. ER-phagy, a selective autophagy targeting ER, plays an important role in maintaining ER morphology and function. The FAM134 protein family, including FAM134A, FAM134B, and FAM134C, mediates ER-phagy. While FAM134B mutations are linked to hereditary sensory and autonomic neuropathy in humans, the physiological role of the other FAM134 proteins remains unknown. To address this, we investigated the roles of FAM134 proteins using single and combined knockouts (KOs) in mice. Single KO in young mice showed no major phenotypes, however, combined Fam134b and Fam134c deletion (Fam134b/cdKO), but not the combination including Fam134a deletion, led to rapid neuromuscular and somatosensory degeneration, resulting in premature death. Fam134b/cdKO mice show rapid loss of motor and sensory axons in the peripheral nervous system. Long axons from Fam134b/cdKO mice exhibited expanded tubular ER with a transverse ladder-like appearance, whereas no obvious abnormalities were observed in cortical ER. Our study unveils critical roles of FAM134C and FAM134B in the formation of tubular ER network in axons of both motor and sensory neurons.

2024-06-24 | PXD050983 | Pride

Delivery of MFF through mitochondria-derived vesicles regulates melanosome maturation

Project description:Melanosomes are lysosome-associated organelles that produce and accumulate melanin. Their biogenesis begins with the trafficking of melanogenic proteins from the endo-lysosomal system into non-pigmented vacuoles derived from endosomes. Subsequently, melanosome maturation proceeds with the export and recycling of non-required cargo, through tubular carriers and vesicular fission derived from melanosome membranes. Although constriction events have been observed at melanosome membranes, the mechanisms underlying their fission remain unclear. We found that MFF is delivered to melanosomes by mitochondria-derived vesicles (MDVs) and that it is located at melanosome membrane fission sites. Downregulation of MFF leads to an increase in the size of early melanosomes, accumulation of intracellular melanin, and increased melanosome lumen catabolism. In melanocytes, MFF interactome highlighted its interplay with a complex network of cytoskeletal factors. Inhibition of actin nucleation is indeed sufficient to restore the effects on melanosome size. Our data show for the first time that MDVs-mediated MFF trafficking to melanosomes is necessary for their membrane remodeling and fission, promoting the transition from early to mature stage melanosomes.

2026-05-25 | PXD051372 | Pride

Brown Adipose Tissue undergoes pathological perturbations and shapes C2C12 myoblast homeostasis in the SOD1-G93A mouse model of Amyotrophic Lateral Sclerosis.

Project description:Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by the selective loss of motor neurons. While the contribution of peripheral organs remains incompletely understood, recent evidence suggests that brown adipose tissue (BAT) and its secreted extracellular vesicles (EVs) could play a role in diseased context as ALS. In this study, we employed a multi-omics approach, including RNA sequencing and proteomics, to investigate the alterations in BAT and its EVs in the SOD1-G93A mouse model of ALS. Our results revealed significant changes in the proteomic and transcriptomic profiles of BAT from SOD1-G93A mice, highlighting ALS-related features such as mitochondrial dysfunction and impaired differentiation capacity. Specifically, primary brown adipocytes (PBAs) from SOD1-G93A mice exhibited differentiation impairment, respiratory defects, and alterations in mitochondrial dynamics. Furthermore, the BAT-derived EVs from SOD1-G93A mice displayed distinct changes in size distribution and cargo content, which negatively impacted the differentiation and homeostasis of C2C12 murine myoblasts, as well as induced atrophy in C2C12-derived myotubes. These findings suggest that BAT undergoes pathological perturbations in ALS, contributing to skeletal muscle degeneration through the secretion of dysfunctional EVs. This study provides novel insights into the role of BAT in ALS pathogenesis and highlights potential therapeutic targets for mitigating muscle wasting in ALS patients.

2025-02-03 | PXD054147 | Pride

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