SRRM2 Antibody - C-terminal region (ARP33112_P050)
- Known as:
- SRRM2 Antibody - C-terminal region (ARP33112_P050)
- Catalog number:
- arp33112_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- SRRM2 Antibody - C-terminal region (ARP33112_P050)
Related genes to: SRRM2 Antibody - C-terminal region (ARP33112_P050)
- Gene:
- SRRM2 NIH gene
- Name:
- serine/arginine repetitive matrix 2
- Previous symbol:
- -
- Synonyms:
- SRm300, SRL300, KIAA0324, Cwc21
- Chromosome:
- 16p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2001-09-24
- Date modifiied:
- 2015-08-26
Related products to: SRRM2 Antibody - C-terminal region (ARP33112_P050)
Related articles to: SRRM2 Antibody - C-terminal region (ARP33112_P050)
- Nuclear speckles (NS) are membraneless nuclear organelles that act as critical hubs for pre-messenger RNA splicing. Defects in splicing are linked to several human diseases, including cancer, Alzheimer's disease, and dystrophies. While CLK kinases regulate the mobilization of splicing factors from NS, the molecular mechanisms underlying NS assembly and dissolution remain unclear. Using an adaptation of the Biotinylation by Antibody Recognition technique, we identified polyphosphate (polyP) as a novel and essential regulator of NS dynamics. Polyphosphate, a highly conserved polyanion composed of a chain of phosphate molecules, is involved in several functions in mammalian cells. Here, we show that polyP interacts with the NS core component SRRM2, and its depletion disrupts NS organization releasing splicing factors into the nucleoplasm. RNA-seq analysis reveals that polyP depletion increases exon exclusion, particularly in transcripts with multiple isoforms, highlighting its role in splicing regulation. Mechanistically, we demonstrate that polyP acts as a physiological inhibitor of CLK3 kinase, preventing the phosphorylation of SR proteins and thereby maintaining NS stability. Our findings not only expand our understanding of NS biology but also provide new insights into the polyP involvement in splicing-related diseases. - Source: PubMed
Lázaro BlancaTadeo Francisco JRodríguez AndreaAyuso-Molina LucíaMartínez-Láinez Joan MarcQuandt EvaBernard MaribelBorghi FilipySaiardi AdolfoJuan-Mateu JonàsJiménez JavierClotet JosepBru Samuel - Nuclear speckles are conserved, membrane-less organelles linked to various post-transcriptional processes. Here, we examined their roles in human cells by engineered, acute removal of SON and SRRM2, two conserved speckle core components characterized by intrinsically disordered regions (IDRs). Their removal results in a significant downregulation of GC-rich genes with short introns clustered within GC-rich isochores, caused by inefficient and chaotic splicing; in contrast, the expression or splicing of genes outside these isochores remains unaffected. Comparative analysis across eukaryotes, from fungi to mammals, reveals that both GC-rich isochores and speckles are found exclusively in amniotes; moreover, the IDRs of SON have undergone notable expansion in the latter. Together, these findings suggest that the expansion of IDRs in vertebrates facilitated an increase in GC content by creating a condensate essential for splicing the by-products of this process: GC-rich, leveled exon-intron architectures. - Source: PubMed
Publication date: 2026/02/25
Małszycki MichałMartina LisaIlık İbrahim AvşarSalgado Figueroa DanielaDasgupta NirmalyaÇoşar Menşura FerayKim Keun-TaeCarraco GilFauler BeatrixMeierhofer DavidMielke ThorstenImai HirooAlev CantaşAy FerhatAktaş Tuğçe - Kawasaki disease (KD) is the leading cause of acquired heart disease in children, though its etiology and underlying mechanisms remain elusive. Emerging evidence indicates that long noncoding RNAs (lncRNAs) regulate endothelial-to-mesenchymal transition (EndMT), a cellular process implicated in vascular pathology. However, the specific involvement of lncRNAs in KD-associated coronary artery damage via EndMT remains undefined. Here, we show that the lncRNA SRRM2-AS1 is markedly elevated in the serum of children with KD and is internalized by coronary artery endothelial cells. Overexpression of SRRM2-AS1 in human coronary artery endothelial cells (HCAECs) increased cell migration and induced EndMT, as confirmed by elevated mesenchymal marker expression and morphological changes. Mechanistically, bioinformatics analysis, dual-luciferase reporter assays, and gene expression profiling revealed SRRM2 as a direct target of SRRM2-AS1. Our findings suggest that SRRM2 promotes EndMT through ubiquitin C (UBC) and the PI3K/Akt/GSK-3β/β-catenin signaling pathway. In a mouse model of KD, recombinant AAV9-mediated SRRM2-AS1 overexpression intensified coronary artery inflammation and increased vimentin expression, further supporting its role in EndMT. Collectively, these results demonstrate that SRRM2-AS1 drives EndMT in KD via the SRRM2/UBC/PI3K/Akt/GSK-3β/β-catenin axis, thereby contributing to coronary artery damage. Consequently, SRRM2-AS1 emerges as a promising therapeutic target for KD-associated vasculopathy, offering potential avenues to mitigate cardiovascular complications in affected children. - Source: PubMed
Publication date: 2026/02/24
Song ShiyangZhang HuiLin RenchaoZhang JingyiZhang QianqianLi ChanghaoXia YushanZeng JingjingLu KongchangGe DonghuiQiu HuixianNiu ChaoJia ChangZhang ChunxiangHe YueeChu MaopingRong Xing - - Source: PubMed
Publication date: 2026/02/05
Cuinat Silvestre - - Source: PubMed
Publication date: 2026/02/05
Rapp Christina KRodler JuliaMauss-Schwarzer KatharinaGothe FlorianReu-Hoefer SimoneAschmann-Mühlhans DoritEgger MarkusEber ErnstPrenzel FreerkGriese Matthias