Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Equine gluteal muscle LC-MSMS: Thoroughbred

ABSTRACT: Recurrent exertional rhabdomyolysis (RER) develops in 5-10% of Thoroughbred racehorses. High-stress environments, nervous temperament, and diet influence the presentation of RER. RER-susceptibility is associated with alterations in intramuscular Ca2+ regulation with detrimental effects on mitochondria. Our study aims to determine underlying molecular drivers influencing RER-susceptibility by comparing the muscle proteome of control, RER-susceptible, and RER horses treated with dantrolene. Animals used in this study were Thoroughbred mares in race training between episodes of RER.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Equus Caballus (horse)

TISSUE(S): Gluteal Muscle, Skeletal Muscle Tissue

SUBMITTER: Stephanie Valberg

LAB HEAD: Stephanie Valberg

PROVIDER: PXD020100 | Pride | 2021-01-07

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	RER_Thoroughbred_Melissa_20180817_merged.mzid.gz	Mzid
	RER_Thoroughbred_Melissa_20180817_merged.mzid_hf2018090412.MGF	Mzid
	RER_Thoroughbred_Melissa_20180817_merged.mzid_hf2018090413.MGF	Mzid
	RER_Thoroughbred_Melissa_20180817_merged.sf3	Other
	ScaffoldQuantML_Report_RER_Thoroughbred_20180817_merged.sqml	Other

Items per page:

1 - 5 of 9

Similar Datasets

Multi-omics characterization of recurrent exertional rhabdomyolysis in Standardbred horses

Project description:During an episode of acute rhabdomyolysis, a microarray study identified differential expression of calcium-regulatory, mitochondrial and metabolic genes in gluteal muscle of Standardbreds. Whether this represents expression related to acute myodegeneration or a specific molecular signature of susceptibility to recurrent exertional rhabdomyolysis (RER) is currently unknown. We compared gluteal muscle histopathology, gene/protein expression and antioxidant concentrations between Standardbreds with a history of, but not currently experiencing rhabdomyolysis, and race-trained controls to derive a molecular susceptibility profile.

2023-03-11 | PXD026121 | Pride

Gene Expression differences between replication error deficient and proficient colorectal cancers: the dominant role of deletions in 3âUTR poly T sequences

Project description:16 replication error proficient (RER-/MSI-) and 14 replication error deficient (RER+/MSI+) colorectal cancer cell lines Replication error deficient (RER+) colorectal cancers are a distinct subset of colorectal cancers, characterised by inactivation of the DNA mismatch repair system. They are typically pseudodiploid, accumulate mutations in repetitive sequences as a result of their mismatch repair deficiency, and have distinct pathologies. Regulatory sequences controlling all aspects of mRNA processing, including especially message stability are found in the 3âUTR sequence of most genes. The relevant sequences are typically A/U rich elements and/or U repeats. Microarray analysis of 14 RER+ (deficient) and 16 RER- (proficient) colorectal cancer (CRC) cell lines confirms a striking difference in expression profiles. Analysis of the incidence of mononucleotide repeat sequences in the 3âUTRs, 5âUTRs and coding sequences of those genes most differentially expressed in RER+ versus â cell lines has shown that much of this differential expression can be explained by the occurrence of a massive enrichment of genes with 3âUTR T repeats longer than 11 base pairs in the most differentially expressed genes. This enrichment was confirmed by analysis of two published consensus sets of RER differentially expressed probe sets for a large number of primary colorectal cancers. Sequence analysis of the 3âUTRs of a selection of the most differentially expressed genes shows that they all contain deletions in these repeats in all RER+ cell lines studied. These data strongly imply that deregulation of mRNA stability through accumulation of mutations in repetitive regulatory 3âUTR sequences underlies the striking difference in expression profiles between RER+ and RER- colorectal cancers. 16 replication error proficient (RER-/MSI-) and 14 replication error deficient (RER+/MSI+) colorectal cancer cell lines.

2010-10-19 | E-GEOD-24795 | biostudies-arrayexpress

Gene Expression differences between replication error deficient and proficient colorectal cancers: the dominant role of deletions in 3’UTR poly T sequences

Project description:16 replication error proficient (RER-/MSI-) and 14 replication error deficient (RER+/MSI+) colorectal cancer cell lines Replication error deficient (RER+) colorectal cancers are a distinct subset of colorectal cancers, characterised by inactivation of the DNA mismatch repair system. They are typically pseudodiploid, accumulate mutations in repetitive sequences as a result of their mismatch repair deficiency, and have distinct pathologies. Regulatory sequences controlling all aspects of mRNA processing, including especially message stability are found in the 3’UTR sequence of most genes. The relevant sequences are typically A/U rich elements and/or U repeats. Microarray analysis of 14 RER+ (deficient) and 16 RER- (proficient) colorectal cancer (CRC) cell lines confirms a striking difference in expression profiles. Analysis of the incidence of mononucleotide repeat sequences in the 3’UTRs, 5’UTRs and coding sequences of those genes most differentially expressed in RER+ versus – cell lines has shown that much of this differential expression can be explained by the occurrence of a massive enrichment of genes with 3’UTR T repeats longer than 11 base pairs in the most differentially expressed genes. This enrichment was confirmed by analysis of two published consensus sets of RER differentially expressed probe sets for a large number of primary colorectal cancers. Sequence analysis of the 3’UTRs of a selection of the most differentially expressed genes shows that they all contain deletions in these repeats in all RER+ cell lines studied. These data strongly imply that deregulation of mRNA stability through accumulation of mutations in repetitive regulatory 3’UTR sequences underlies the striking difference in expression profiles between RER+ and RER- colorectal cancers.

2010-10-19 | GSE24795 | GEO

Ribonucleotide excision repair is essential to prevent skin cancer [CD45+ CD49f- epidermal cells]

Project description:Large numbers of ribonucleotides are incorporated into the eukaryotic nuclear genome during S-phase due to imperfect discrimination against ribonucleoside triphosphates by the replicative DNA polymerases. Ribonucleotides, by far the most common DNA lesion in replicating cells, destabilize the DNA, and an evolutionarily conserved DNA repair machinery, ribonucleotide excision repair (RER), ensures ribonucleotide removal. Complete lack of RER is embryonically lethal. Partial loss-of-function mutations in the genes encoding subunits of RNase H2, the enzyme essential for initiation of RER, cause the SLE-related type I interferonopathy Aicardi-Goutières syndrome. Here we establish that selective inactivation of RER in mouse epidermis results in spontaneous DNA damage, epidermal hyperproliferation associated with loss of hair follicle stem cells and hair follicle function. The animals develop keratinocyte intraepithelial neoplasia and invasive squamous cell carcinoma with complete penetrance, despite potent type I interferon production and skin inflammation. Compromised RER-mediated genome maintenance might represent an important tumor-promoting principle in human cancer.

2019-05-29 | GSE115004 | GEO

Ribonucleotide excision repair is essential to prevent skin cancer [CD49f+ epidermal cells]

2019-05-29 | GSE115003 | GEO

Transcriptional profiling of equine endometrium before, during and after capsule disintegration during normal pregnancy and after oxytocin-induced luteostasis in non-pregnant mares

Project description:mRNA profiles of (1) equine endometrium collected 14, 22, and 28 days after ovulation from pregnant mares and (2) equine endometrium collected 20 days after ovulation from pregnant mares, and from non-pregnant mares which displayed and failed to display extended luteal function following the administration of oxytocin.

2021-09-01 | GSE180022 | GEO

Transcriptomic analysis reveals the key regulators and molecular mechanisms underlying myometrial activation during equine placentitis

Project description:Placentitis was induced in five mares at approximately 290d of gestation (placentitis group), four mares with gestationally age-matched (290 d) pregnancies did not receive any treatment (control group), and the remaining three mares were maintained until approximately 330 d of gestation (prepartum group). For induction of placentitis in the former group, Streptococcus equi subsp. zooepidemicus was introduced intracervically.

2020-04-09 | GSE139986 | GEO

Equine Cervical Remodelling during Prepartum Period and Placentitis: A Transcriptomic Approach (Stroma)

2021-05-08 | GSE162466 | GEO

Equine Cervical Remodelling during Prepartum Period and Placentitis: A Transcriptomic Approach (Mucosa)

2021-05-08 | GSE162465 | GEO

Plasma proteins in persistent endometritis and healthy mares

Project description:The study collected eight mares with chronic endometritis and eight healthy mares, respectively. In LC-MS analysis, the DDA method was employed to identify quantitatively differential proteins.

2024-03-14 | PXD047408 | 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