Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Annexin A2 causes motor incoordination via muscle-cerebellum axis in sarcopenia

ABSTRACT: Annexin A2 causes motor incoordination via muscle-cerebellum axis in sarcopenia

ORGANISM(S): Mus Musculus

SUBMITTER: Dongyun Gu

PROVIDER: PXD068704 | iProX | Mon Sep 22 00:00:00 BST 2025

REPOSITORIES: iProX

ACCESS DATA

Json Xml

Publications

Annexin A2 Causes Motor Incoordination via Muscle-Cerebellum Axis in Sarcopenia.

Jiao Xin X Wang Zengguang Z Chang Hanwen H Li Yongjin Y Wang Binbin B Shao Xinfa X Zhang Yuxin Y Lin Yixuan Y Jia Xinlin X Zhou Xianhao X Li Wentao W Luo Dinghao D Deng Tanjun T Lin Xingzuan X Xu Chen C Gan Yaokai Y Gu Dongyun D

Journal of cachexia, sarcopenia and muscle 20260201 1

<h4>Background</h4>Sarcopenia is a prevalent age-related disorder characterized by progressive muscle atrophy. Impaired balance is one of its most critical clinical consequences, often leading to falling and even bone fractures. As the cerebellum plays a central role in regulating motor coordination, elucidating the molecular mechanisms underlying imbalance in sarcopenia, particularly those mediated by the muscle-cerebellum axis, remains an important yet unresolved question.<h4>Methods</h4>4D la ...[more]

PMID: 41588637

Similar Datasets

Role of annexin A2 in muscle repair

Project description:Repair of injured muscle involves repair of injured myofibers through the involvement of dysferlin and its interacting partners, including annexin. Studies with mice and patients have established that dysferlin deficit leads to chronic inflammation and adipogenic replacement of the diseased muscle. However, longitudinal analysis of annexin deficit on muscle pathology and function is lacking. Here we show that unlike annexin A1, but similar to dysferlin, lack of annexin A2 (AnxA2) causes poor myofiber repair and progressive weakening with age. However, unlike dysferlin-deficient muscle, AnxA2-deficient muscles do not exhibit chronic inflammation or adipogenic replacement. Deletion of AnxA2 in dysferlin deficient mice reduces inflammation, adipogenic replacement, and loss in muscle function caused by dysferlin deficit. These results show that: a) AnxA2 facilitates myofiber repair, b) chronic inflammation and adipogenic replacement of dysferlinopathic muscle requires AnxA2, and c) inhibiting AnxA2-mediated inflammation is a novel therapeutic avenue for dysferlinopathy.

2016-10-04 | GSE87557 | GEO

Mus musculus

Project description:Role of annexin A2 in muscle repair

| PRJNA345192 | ENA

Expression data of J3T-1, J3T-2, J3T-1shA, J3T-2A glioma

Project description:We have previously established two sibling glioma subclones, J3T-1 and J3T-2, showing distinct invasive and angiogenic phenotypes. J3T-1, expressing high annexin A2, demonstrates robust angiogenesis and tumor invasion around neovasculature. J3T-2, expressing low annexin A2, demonstrates diffuse invasion along white matter tracts. Knockdown of annexin A2 in J3T-1 (J3T-1shA) resulted in diffuse invasion pattern, and overexpression of annexin A2 in J3T-2 (J3T-2A) showed prominent angiogenesis. We used microarrays to identify genes which promote the phenotypic transition regulated by annexin A2.

2020-04-20 | GSE138374 | GEO

Sugt1 loss skeletal muscle stem cells impairs muscle regeneration and causes premature muscle aging

Project description:Sugt1 loss skeletal muscle stem cells impairs muscle regeneration and causes premature muscle aging

| PRJNA972697 | ENA

Role of the Muscle-Brain-Gut axis in the regulation of skeletal muscle mass

Project description:We propose that the Muscle-Brain-Gut axis regulates skeletal muscle mass through the defined mechanism.

2023-12-11 | GSE249324 | GEO

Role of the Muscle-Brain-Gut axis in the regulation of skeletal muscle mass II

Project description:We propose that the Muscle-Brain-Gut axis regulates skeletal muscle mass through the defined mechanism.

2023-12-13 | GSE249515 | GEO

Binding partners of Annexin A2 in MDA-MB-231 cells

Project description:A mass-spec of proteins found bound to Annexin A2 following a immunoprecipitation of Annexin A2 from cell lysate of MDAMB231 cells plated 1) on plastic or 2) on collagen-1

2023-10-11 | MSV000093084 | MassIVE

The Bap1-SMN axis in Dpp4+ skeletal muscle mesenchymal cells regulates survival of motor neurons

Project description:The Bap1-SMN axis in Dpp4+ skeletal muscle mesenchymal cells regulates survival of motor neurons

| PRJNA787105 | ENA

Project description:Integrin beta6/Annexin A2 axis triggers autophagy to orchestrate hepatocellular carcinoma radioresistance

| PRJNA1170233 | ENA

Aberrant calcium influx causes fiber type shift and mitochondrial loss in skeletal muscle

Project description:Skeletal muscle excitation-contraction (EC) coupling is independent of calcium influx. In fact alternative splicing of the voltage-gated calcium channel CaV1.1 actively suppresses calcium currents in mature muscle. Why this might be necessary is not known. However, splicing defects causing aberrant expression of the calcium-conducting embryonic CaV1.1e splice variant correlate with muscle weakness in myotonic dystrophy. Here we deleted CaV1.1 exon 29 in mice. The continued expression of CaV1.1e resulted in increased calcium influx during EC coupling and spontaneous calcium sparks. While overall motor performance was normal, muscle force was reduced, endurance enhanced, and the fiber type composition shifted toward slower fibers. In contrast, oxidative enzyme activity and the mitochondrial content declined. Together with the dysregulation of key regulators of the slow program these findings indicate that limiting calcium influx during skeletal muscle EC coupling is important for the calcium signalâs secondary function in the activity-dependent regulation of fiber type composition. Differential gene expression between soleus and EDL muscle fibres from wildtype and Cav1.1 delta E29 mice.

2016-04-01 | E-GEOD-67803 | 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