ANTXR2
- Known as:
- ANTXR2
- Catalog number:
- 001685A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANTXR2
Related genes to: ANTXR2
- Gene:
- ANTXR2 NIH gene
- Name:
- ANTXR cell adhesion molecule 2
- Previous symbol:
- -
- Synonyms:
- CMG2, CMG-2, FLJ31074
- Chromosome:
- 4q21.21
- Locus Type:
- gene with protein product
- Date approved:
- 2003-09-25
- Date modifiied:
- 2018-05-10
Related products to: ANTXR2
Related articles to: ANTXR2
- Physical activity (PA) is a modifiable lifestyle behaviour associated with lower dementia risk; however, molecular pathways bridging PA-related dementia prevention are poorly understood. We leveraged large-scale plasma proteomics to identify biological signatures of objectively monitored PA and cognitive ageing in functionally intact older adults, cross-validated these signatures in independent exercise cohorts and tested associations with both symptomatic and presymptomatic stages of neurodegeneration across multiple Alzheimer's disease and related dementias (ADRD) cohorts. We analysed large-scale plasma proteomics data (SomaScan 7k) across three cohorts including naturalistic, objective PA monitoring (University of California, San Francisco Brain Aging Network for Cognitive Health cohort, = 65), self-reported PA (Atherosclerosis Risk In Communities study, = 10 644) and PA intervention (Health Risk Factors, Exercise Training and Genetics study, = 654). Differential regression models examined individual protein correlates of PA, adjusting for age and sex. Weighted gene co-expression network analysis assembled proteins into unbiased modules of protein co-expression, which were annotated for gene ontology and cell-type enrichment. To test clinical relevance to ADRD, we examined PA-related protein levels across-cohorts of symptomatic Alzheimer's disease and Parkinson's disease (Stanford Alzheimer's Disease Research Center), as well as frontotemporal dementia-spectrum disorders (ARTFL/LEFFTDS Longitudinal Frontotemporal Lobar Degeneration consortium). PA-related plasma proteins were also tested as predictors of antemortem cognitive change and post-mortem brain tissue mass spectrometry proteomic signatures in brain donors from the Religious Orders Study and Rush Memory and Aging Project (ROSMAP) cohort. Differential regression and network analyses identified PA plasma proteomic signatures linked to cell adhesion/extracellular matrix (ECM), immune response and lipid metabolism. Protein co-expression module M12 ECM/neurodevelopment harboured growth factor, cell adhesion and vascular remodelling proteins that (i) were positively associated with PA across exercise cohorts, (ii) positively associated with cognitive function and (iii) negatively associated with Alzheimer's disease, Parkinson's disease and frontotemporal dementia. Furthermore, M12 was enriched for proteins from Alzheimer's disease risk genes and antemortem plasma abundance of anthrax toxin receptor cell adhesion molecule 2 (ANTXR2), an M12 'hub' protein and top PA hit across-cohorts, forecasted longitudinal global cognitive decline and post-mortem brain tissue signatures of synaptic function and proteolysis in ROSMAP. Collectively, our integrated systems biology analysis of six independent plasma proteomic datasets facilitated discovery and validation of blood-detectable molecular signatures of PA and neurodegenerative disease, including PA-related proteins with clinical and biological relevance to early stages of disease. Circulating levels of PA-related proteins reflecting ECM biology (e.g. ANTXR2) may represent key molecular targets for dementia prevention. - Source: PubMed
Publication date: 2026/07/21
Saloner RowanPaolillo Emily WVandeBunte Anna MCadwallader Claire JChen CotySteffen Brian TBennett David ABoeve Bradley FRosen Howard JBoxer Adam LKramer Joel HCasaletto Kaitlin B - Ischemic stroke (IS) currently lacks well-characterized peripheral-blood biomarkers that capture early, pathway-level biology. Programmed cell death (PCD) pathways may shape post-stroke neuroinflammation and could yield clinically informative transcriptional signatures. - Source: PubMed
Publication date: 2026/07/16
Jia QiZhang PengtaoLiu QianqianSang EnzeChen ZhengwenShao JunjieDing YuhaoBai FaguangHuang Qingfeng - We examined extracellular vesicle (EV) protein alterations after burn injury to elucidate molecular pathways linking immune-neural communication and the pathophysiology of burns. - Source: PubMed
Publication date: 2026/07/29
Grimsrud Kristin NGreen TajiaTang YiruiClayton Shannon MWard Briana MWang DavidDurbin-Johnson BlytheWang AijunPalmieri Tina L - Duchenne muscular dystrophy (DMD) is a progressive neuromuscular disorder for which monitoring biomarkers are urgently needed. We aimed to evaluate whether proteins in serum can accurately monitor patients' function within the duration of a clinical trial. - Source: PubMed
Publication date: 2026/07/13
Degan ChiaraTobin Rebecca Ade Vries Sharon IJiménez-Requena AlbertPeco AmelaGuglieri MichelaDiaz-Manera Jordivan der Burgt Yuri E Mvan Vlijmen Bart J M Hathout YetribSzigyarto Cristina Al-KhaliliDang Utkarsh JTsonaka RoulaSpitali Pietro - CMG2/ANTXR2 functions as a Collagen VI receptor required for extracellular matrix homeostasis and as the primary portal for anthrax toxin entry. Mutations in CMG2 cause Hyaline Fibromatosis Syndrome (HFS), a rare and often fatal genetic disorder characterized by excessive extracellular matrix accumulation, yet the molecular mechanisms regulating CMG2 function remain poorly understood. We show that CMG2 is controlled by ordered cycles of S-acylation and deacylation that regulate its folding, trafficking, and signalling competence. S-acylation by ZDHHC7 on two juxtamembrane cysteines protects CMG2 from ER-associated degradation by stabilizing folding intermediates, leading to a ~ 5-fold increase in folded receptors competent for ER exit. In the Golgi, ZDHHC3-dependent acylation of a third cysteine promotes Arf6-mediated CMG2 transport to the plasma membrane, where it exerts its functions. Ligand binding triggers recruitment of the thioesterase APT2, which enables release of CMG2 from the actin cytoskeleton and endocytosis, linking extracellular recognition to intracellular signalling and uptake. Inhibition of APT2 reduces Collagen VI turnover and strongly attenuates anthrax toxin toxicity in a zebrafish model, showing lipidation cycles as regulators of receptor function and potential therapeutic targets. - Source: PubMed
Publication date: 2026/07/06
Abrami LaurenceJoliot OctaveBlaskovic SanjaValentin GuillaumeHevia Covadonga FMercier VincentKunz BéatriceMesquita Francisco Svan der Goot F Gisou