CSRP3 antibody - middle region (ARP34181_P050)
- Known as:
- CSRP3 (anti-) - middle region (ARP34181_P050)
- Catalog number:
- arp34181_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- CSRP3 antibody - middle region (ARP34181_P050)
Related genes to: CSRP3 antibody - middle region (ARP34181_P050)
- Gene:
- CSRP3 NIH gene
- Name:
- cysteine and glycine rich protein 3
- Previous symbol:
- -
- Synonyms:
- CLP, MLP, CMD1M
- Chromosome:
- 11p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-07-21
- Date modifiied:
- 2019-04-23
Related products to: CSRP3 antibody - middle region (ARP34181_P050)
Related articles to: CSRP3 antibody - middle region (ARP34181_P050)
- The current photothermal treatments for glioma suffer from inappropriate tumor models, nanoparticle-related long-term intracranial retention, and the absence of real-time electroencephalography monitoring. Herein, we report the development of an integrated photothermal therapy (PTT)-electroencephalogram (EEG) monitoring system based on micropyramid-structured polypyrrole (-PPy) film patches, enabling the accurate and controllable treatment of intracranial gliomas while providing the real-time monitoring of intraoperative complications. The pyramid architecture of the -PPy film endows it with excellent photothermal conversion efficiency and electrochemical behavior, which allow it to simultaneously function as a photothermal agent for tumor ablation and a bioelectrode for electroencephalography signal collection. The flexible and stretchable nature of -PPy allows it to adhere well to tumors for preventing glioma rupture while obtaining stable signal acquisition. More importantly, it can be completely removed after surgery to prevent the long-term toxicity caused by intracranial residues. experiments suggest that it induces C6 glioma cell apoptosis through the upregulation of Anxa5 and Csrp3 coupled with the downregulation of septin-4, effectively activating the apoptotic pathway. In orthotopic tumor models, the integrated system achieves complete tumor ablation while simultaneously monitoring intraoperative neuroelectrophysiological changes in real-time through EEG ( the dynamic analysis of the // wave power spectra), achieving a temperature control accuracy of ±0.8 °C mm. Proteomic analysis revealed that PTT significantly inhibits tumor migration by suppressing mitochondrial complex I (as evidenced by the downregulation of NDUFB2/4) and motor protein pathways. Hence, this platform overcomes critical barriers in glioma therapy by eliminating invasive procedures while ensuring the real-time detection of treatment complications. - Source: PubMed
Publication date: 2026/05/28
Zhang HaoyangShi KeZhang WenxuanChen XueWang XiZhao YanPang HengyuanChen XiWang Jianjiao - Hypertrophic cardiomyopathy (HCM) is a common inherited disease and a leading known cause of sudden cardiac arrest in young adults and athletes. While genetic testing has advanced rapidly in the past decade, the yield of genetic testing remains low. The Clinical Genome Resource (ClinGen) initiative has become a leading resource for defining the clinical relevance of genetic variants with expert groups focusing on evaluating the strength of evidence for each HCM implicated gene. With the rise of large biobanks and population databases, genetic discovery has been significantly advanced. However, whether these databases can be used to validate gene-disease associations curated by ClinGen and provide evidence for novel gene-disease associations remains unclear. Here, we utilized a publicly available database containing 748,879 individuals across three large biobanks (All of Us, UK biobank, Mass General Brigham biobank). We tested the association of rare coding variants in each gene in the HCM ClinGen panel with HCM. In total, 38 genes were tested, and Bonferroni correction was applied accordingly. Of the 12 genes with definitive evidence for HCM (e.g., , , , ), 8 (67%) demonstrated nominally significant association with HCM on a population level, and 5 (42%) remained significant after Bonferroni correction, further supporting the validity of these genes in HCM panels. Several definitive genes which are much less commonly affected in HCM (, , , , , , and ) did not pass our Bonferroni corrected-significance threshold, but all had positively associated effect sizes with HCM. No genes deemed to have moderate or limited evidence had any significant associations with HCM even before Bonferroni correction. Altogether, we show that large biobanks and population databases generally recapitulate established gene-disease associations for HCM and support the ClinGen group's gene curations. The utilization of such publicly accessible databases represents an additional tool for assessing gene validity in monogenic cardiac disorders with an established phenotype, although it may have limited sensitivity and should not be solely relied on. - Source: PubMed
Publication date: 2026/03/21
Dababneh Saif FOng KevinYeung DarwinHawkins Nathaniel MKrahn AndrewLaksman ZacharyTadros RafikRoston Thomas M - Exercise performance and skeletal muscle homeostasis are influenced by myofiber type composition. Cysteine and glycine-rich protein 3 (CSRP3) is highly expressed in the oxidative fiber-rich mammalian soleus muscle. However, the mechanistic basis of CSRP3's involvement in skeletal muscle development and myofiber type specification remains unclear. Here, we used various exercise training (aerobic/anaerobic) bioinformatics datasets and experimental model systems involving live mice and cell lines to determine the role of CSRP3 in driving mitochondrial metabolic reconfiguration, skeletal muscle fiber type remodeling, and improved exercise endurance. CSRP3 promotes the formation of oxidative myofibers while suppressing glycolytic myofiber differentiation. It enhances mitochondrial biogenesis, oxidative phosphorylation capacity, and elevates mitochondrial membrane potential. Conversely, AAV-mediated CSRP3 knockdown perturbs mitochondrial energy metabolism, compromises exercise performance, and reduces the proportion of oxidative myofibers. Mechanistically, CSRP3 binds to D-lactate dehydrogenase (LDHD) via a specific 33-amino acid region, promoting D-lactate metabolism in skeletal muscle. This interaction regulates mitochondrial morphology, biogenesis, oxidative phosphorylation efficiency, and TCA cycle activity, ultimately driving skeletal muscle mitochondrial energy metabolic rewiring and skeletal muscle fiber type remodeling. - Source: PubMed
Publication date: 2026/03/09
Jiang XiuyingWang ZhaoluLi RuiLiu YihaoLiu BopingYang GongsheJin JianjunShi Xin'e - Equine myotonic dystrophy (eMD) is a rare neuromuscular disorder of undetermined origin marked by muscle hypertrophy and stiffness, dystrophic muscle histopathology, and myotonic discharges. In humans, myotonic dystrophy (DM) arises from trinucleotide repeat expansions in dystrophia myotonica protein kinase (DMPK) (DM1) or tetranucleotide expansions in cellular nucleic acid-binding protein (CNBP) (DM2), which disrupt mRNA processing and induce embryonic splicing patterns across multiple genes. In 6 eMD Quarter Horse types, (2-36 months-of-age) and 8 control Quarter Horses we determined: (1) fiber type composition of triceps, gluteal, and semimembranosus muscles; (2) differential gene (DEG) and protein (DEP) expression using transcriptomic and proteomic analyses; (3) presence of repeat expansions in transcripts of DMPK or CNBP and (4) exon 7 retention in CLCN1 or exon 22 splicing in ATP2A1. Predominance and clustering of type 1 fibers, expression of embryonic myosin, and upregulated mitochondrial and sarcomeric DEPs characterized eMD hindlimb musculature. Gene ontology (GO) analysis of 730 upregulated DEGs identified numerous GO terms related to morphogenesis of mesoderm-derived tissues and upregulated genes impacting myoD expression in eMD muscle. Top upregulated DEG involved myogenesis (MYOZ2, SBK2, SBK3, PAMR1), neurons, transcription/translation, cytoskeleton, basement/plasma membranes, and calcium binding/transport. Top upregulated proteins also impacted muscle morphogenesis (MUSTN1, CSRP3, TMSBX4, PDLIM, CALD1) as well as categories of mitochondria, sarcomere, extracellular matrix/ basement membrane, transcription, translation, cell cycle regulation, neurons amongst others. Downregulated DEP primarily impacted mitochondria, the sarcomere and glycogen metabolism. Notably, unlike human myotonic dystrophy, trinucleotide repeat expansions were not found in the DMPK 3'UTR (CTG)n nor tetranucleotide repeat expansions (CCTG)n in intron 1 of CNBP. Isoforms of CLCN1 containing fetal exon 7 were detected in equal frequency in eMD and control muscle and exon 22 was not alternatively spliced in ATP2A1 as has been found in DM1. Thus, distinct from DM1 and DM2, eMD is driven by unique molecular mechanisms impacting skeletal muscle morphogenesis, neurons and regulation of gene transcription/translation that alter fiber type composition, distribution and morphology. The origin of myotonia does not appear to be driven by a mutation in CLCN1 or retention of exon CLCN 7. Expanded splice site analysis and further research is warranted to elucidate the cause of myotonia and the distinct etiology of eMD. - Source: PubMed
Publication date: 2026/01/29
Valberg Stephanie JWilliams Zoë JAmes Elizabeth GMickelson James RNout-Lomas Yvette SLandolt GabrieleSanz MacarenaGardner Keri - Pasture-based feeding is generally associated with superior meat quality, particularly in terms of favorable fatty acid profiles, whereas concentrate-based feeding typically promotes faster growth and higher productivity, albeit often at the expense of certain aspects of meat quality. Therefore, this study provides insights into the molecular mechanisms underlying meat quality variations in lambs raised under different feeding regimes. The findings are expected to contribute to optimized feeding strategies for balancing growth performance and meat quality in lamb production. - Source: PubMed
Publication date: 2026/01/12
Zhang YueGuo YueyingHuang HuanZhang MinSun LinaJin Ye