Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

INSTRUMENT(S): Orbitrap Exploris 480

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Forelimb Muscle

DISEASE(S): Congenital Myopathy

SUBMITTER: Michael Wierer

LAB HEAD: Julien Ochala

PROVIDER: PXD039178 | Pride | 2023-01-30

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	20210503_EXPL3_PRInLC1_PRI_P0022_R0155_S1.raw	Raw
	20210503_EXPL3_PRInLC1_PRI_P0022_R0155_S10.raw	Raw
	20210503_EXPL3_PRInLC1_PRI_P0022_R0155_S11.raw	Raw
	20210503_EXPL3_PRInLC1_PRI_P0022_R0155_S12.raw	Raw
	20210503_EXPL3_PRInLC1_PRI_P0022_R0155_S13.raw	Raw

Items per page:

1 - 5 of 22

Similar Datasets

Transcriptomic analysis of myosin IIa-deficient B cells

Project description:Myosin IIa-deficient follicular B cells have a hyperactivated phenotype. To identify what pathways are regulated by myosin IIa, we performed RNA-seq of coding RNA on flow cytometry sorted follicular B cells from CD23Cre+Myh9fl/fl and CD23Cre+Myh9wt/fl mice.

2018-04-14 | GSE113114 | GEO

Transcriptomic analysis of myosin IIa-deficient B cells

Project description:Transcriptomic analysis of myosin IIa-deficient B cells

| PRJNA450071 | ENA

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

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

Effects of lifelong exercise and age on transcriptome dynamics in MHC I and MHC IIa muscle fibers at baseline and in response to resistance exercise

Project description:RNA-Seq was used for the first time to investigate the effects of resistance exercise on transcriptome dynamics in slow myosin heavy chain (MHC) I and fast MHC IIa muscle fibers among 3 groups of men. Vastus lateralis muscle biopsies were obtained before and 4 hours after resistance exercise.

2024-01-08 | GSE235781 | GEO

Knocking out non-muscle myosin II in retinal ganglion cells promotes long-distance optic nerve regeneration (RNA-Seq I)

Project description:In addition to altered gene expression, pathological cytoskeletal dynamics in the axon are another key intrinsic barrier for axon regeneration in the central nervous system (CNS). Here we showed that knocking out myosin IIA/B in retinal ganglion cells alone either before or after optic nerve crush induced significant optic nerve regeneration. Combined Lin28a overexpression and myosin IIA/B knockout led to additive promoting effect and long-distance axon regeneration. Immunostaining, RNA sequencing and western blot analyses revealed that myosin II deletion did not affect known axon regeneration signaling pathways or the expression of regeneration associated genes. Instead, it abolished the retraction bulb formation and significantly enhanced the axon extension efficiency. The study provided clear evidence that directly targeting neuronal cytoskeleton was sufficient to induce significant CNS axon regeneration, and combining altered gene expression in the soma and modified cytoskeletal dynamics in the axon was a promising approach for long-distance CNS axon regeneration

2020-03-22 | GSE147328 | GEO

Knocking out non-muscle myosin II in retinal ganglion cells promotes long-distance optic nerve regeneration (RNA-Seq II)

2020-03-24 | GSE147400 | GEO

MYBPH, a novel transcriptional target of NKX2-1/TTF-1, inhibits ROCK1 and actomyosin assembly, and reduces cell motility and tumor metastasis

Project description:Cell migration driven by actomyosin filament assembly is a critical step in tumour invasion and metastasis. Herein, we report identification of myosin binding protein H (MYBPH) as a transcriptional target of NKX2-1 (also known as TTF-1 and TITF1), a lineage-survival oncogene in lung adenocarcinoma. MYBPH inhibits assembly competence-conferring phosphorylation of the myosin regulatory light chain (RLC) as well as activating phosphorylation of LIM domain kinase (LIMK). These are unexpectedly implemented through direct physical interaction of MYBPH with Rho kinase 1 (ROCK1) rather than with RLC. In addition, MYBPH is shown to directly bind with non-muscle myosin heavy chain IIA (NMHC IIA), resulting in inhibition of NMHC IIA assembly. Thus, MYBPH plays multi-facetted roles in negative regulation of actomyosin organization, which in turn reduces cell motility, invasion, and metastasis. Finally, we also show that MYBPH is epigenetically inactivated by promoter DNA methylation in a fraction of lung adenocarcinomas abundantly expressing NKX2-1, which appears to be in accordance with its deleterious function for lung adenocarcinoma invasion and metastasis, as well as with the paradoxical association of NKX2-1 expression with favourable prognosis in lung adenocarcinoma patients. Dye-swap experiment, vector control vs. transiently transfectanted with TTF-1 in HPL1D, immortalized human peripheral lung epithelial cell line.

2011-12-22 | E-GEOD-26721 | biostudies-arrayexpress

Borg5/Cdc42EP curbs Septin dependent stress fiber formation by antagonizing alpha Actinin 4 and Myosin IIA

Project description:The Borg5/Cdc42EP family comprises septin binding proteins, which are known to participate in septin-dependent stress fiber formation. We show here that epithelial Borg5/Cdc42Ep1 restrains stress fibers instead. Borg5 decorates septin filament-aligned thin F-actin filaments under the nucleus of MDCK cells, which in Borg5 depleted cells are replaced by thick stellate stress fibers. These associate with either cell-substratum- or cell-cell- adhesions, increasing tension on E-cadherin based junctions and causing MDCK cells to undergo collective streaming. We identified two known septin partners, Myosin-IIA and alpha Actinin 4 (ACTN4), among proteins that co isolated with Borg5 from MDCK lysates. We found that Borg5 binds Myosin-IIA and ACTN4 directly and negatively regulates their F-actin association. Since both septin partners along with Septins 2 and 9 were furthermore required for the Borg5 depletion-induced F actin phenotype, we propose that Borg5 prevents stellate stress fiber formation by counteracting septin dependent ACTN4 and Myosin IIA activities. The mass spectrometry raw files and search results for Borg 5 affinity purifications are deposited here.

| MSV000092958 | MassIVE

MYBPH, a novel transcriptional target of NKX2-1/TTF-1, inhibits ROCK1 and actomyosin assembly, and reduces cell motility and tumor metastasis

2011-12-22 | GSE26721 | GEO