ACTR2 Antibody
- Known as:
- ACTR2 Antibody
- Catalog number:
- csb-pa001248esr1hu
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- CusAb
- Gene target:
- ACTR2 Antibody
Related genes to: ACTR2 Antibody
- Gene:
- ACTR2 NIH gene
- Name:
- actin related protein 2
- Previous symbol:
- -
- Synonyms:
- ARP2
- Chromosome:
- 2p14
- Locus Type:
- gene with protein product
- Date approved:
- 1999-05-17
- Date modifiied:
- 2019-01-10
Related products to: ACTR2 Antibody
Related articles to: ACTR2 Antibody
- : Gliomas are among the most common and heterogeneous primary brain tumors, exhibiting substantial molecular and transcriptomic diversity that complicates diagnosis, grading, and treatment planning. Advances in artificial intelligence (AI), particularly machine learning (ML), offer powerful opportunities to analyze high-dimensional gene expression data and support precision oncology. This study proposes an interpretable ML framework to classify brain tumor subtypes-glioblastoma, astrocytoma, and oligodendroglioma-and to predict tumor grades (2, 3, and 4) using microarray-based gene expression data. The analysis was conducted on the REMBRANDT dataset, comprising 464 labeled samples (221 glioblastoma, 148 astrocytoma, 67 oligodendroglioma, and 28 controls) and 314 tumor samples for grade classification. The ML models achieved high performance for disease classification, with accuracies of 99.6% (AUC 99.89%) for glioblastoma, 98.3% (AUC 99.83%) for astrocytoma, and 98.95% (AUC 100%) for oligodendroglioma. Tumor grade predictions also performed strongly, achieving 83.7% accuracy (AUC 88.2%) for grade II vs. III, 91.3% (AUC 94.8%) for grade II vs. IV, and 84.2% (AUC 90.8%) for grade III vs. IV. SHAP analysis identified key genes contributing to the model predictions (e.g., , and ), and KEGG enrichment identified the candidate pathways involved in vesicular transport, metabolism, and immune signaling. Overall, our findings demonstrate that interpretable ML models can accurately differentiate glioma subtypes and grades, and SHAP analysis can help identify the strongest predictors of our models. These findings provide additional insights into the heterogeneous genetic and molecular landscape of brain gliomas and are intended to complement, not replace, conventional histopathological diagnosis. - Source: PubMed
Publication date: 2026/04/25
Al-Rumaihi GhayaSumon Md Shaheenur IslamHassanein AhmedMalluhi MarwanHossain Sakib AbrarRaad Tahmid ZamanChowdhury Muhammad E HRazali RozaimiPedersen Shona - Macroautophagy/autophagy is a critical cellular process that maintains the cellular homeostasis by degrading and recycling cytotoxic material. Despite its importance, the intricate mechanisms governing this process remain partially elusive. Here, we designed and performed a genome-wide loss-of-function screen on a mouse haploid ESC mutant library and identified the actin-binding protein CORO1C (coronin 1C) as a previously unrecognized regulator of mammalian autophagy. Interactions between CORO1C and the ACTR2/ARP2 (actin related protein 2)-ACTR3/ARP3 complex are essential for branched actin network assembly, SQSTM1/p62 body formation, and maintaining autophagosome structural integrity. Unlike CORO1A and CORO1B, CORO1C possesses a unique second actin-binding site involved in regulating the branched actin network and autophagic process. Notably, newborn mice died earlier in starvation than wild-type littermates and multiple tissues showed autophagy-deficient phenotypes. Moreover, the adult -deficient mice exhibit severe spatial learning memory impairment. Collectively, our research uncovered the surprising role of CORO1C in promoting the formation of branched actin network and its central role in the assembly of structures vital to autophagy.: ACTR2/ARP2: actin related protein 2; ACTR3/ARP3: actin related protein 3; ARPC2: actin related protein 2/3 complex, subunit 2; ATG: autophagy related; ATG5: autophagy related 5; BafA1: bafilomycin A; CQ: chloroquine; FACS: fluorescence-activated cell sorting; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; haESC: haploid embryonic stem cell; HML: haploid-mutant library; IF: immunofluorescence; KO: knockout; MAP1LC3B/LC3: microtubule-associated protein 1 light chain 3B; RB1CC1/FIP200: RB1-inducible coiled-coil 1; SQSTM1/p62: sequestosome 1; STX17: syntaxin 17; TEM: transmission electron microscopy; WB: western blotting; WT: wild type. - Source: PubMed
Publication date: 2026/04/20
Zhang GuozhongYu NingqingSun YiLi XiaowenSun LihongLiu GuangHuang Yue - Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease characterized by the pathological accumulation of collagen-rich extracellular matrix, resulting in irreversible lung remodeling and respiratory failure. The incomplete understanding of IPF pathogenesis has hindered the development of effective therapeutics. Here, we investigate the mechanism by which the actin-related protein 2/3 complex subunit 2 (ARPC2) contributes to the fibrotic response in lung fibroblasts. Modulating of ARPC2 expression levels altered the expression of profibrotic genes, including α-smooth muscle actin (), in TGF-β1-treated MRC-5 cells at the transcriptional level. We further show that ARPC2 regulates the TGF-β1-mediated nuclear translocation of myocardin-related transcription factor-A (MRTFA), a central driver of fibrotic gene induction. Our data indicate that ARPC2 plays a distinct role in profibrotic gene expression and MRTFA nuclear localization, distinguishing its function from other components of the actin-related protein 2/3 (ARP2/3) complex. Furthermore, ARPC2 appears to modulate the TGF-β1-dependent formation of MRTFA/G-actin complexes. Finally, transcriptomic analysis of cells depleted of ARPC2, ACTR2, or MRTFA revealed that ARPC2 and MRTFA co-regulate a specific repertoire of fibrotic genes. These observations support a profibrotic function for ARPC2 during fibroblast-to-myofibroblast transition (FMT), highlighting it as a potential therapeutic target for IPF. - Source: PubMed
Publication date: 2026/03/17
Du Eun JoKim HyunseongBae Seo-GyeongAn SihyeonRyoo Kanghyun - Phosphatase and tensin homolog (PTEN) is a critical regulator of cell proliferation, differentiation, and inflammatory balance. However, its downstream proteomic effects in periodontal ligament stem cells (PDLSCs) remain poorly understood. This study aimed to elucidate the proteomic alterations induced by PTEN inhibition and identify potential molecular pathways underlying periodontal regeneration. - Source: PubMed
Publication date: 2026/03/20
Phothichailert SuphalakNowwarote NunthawanKornsuthisopon ChatvadeeMurakami ShinyaSrithanyarat Supreda SuphanantachatOsathanon Thanaphum - Minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) are two key nephrotic syndrome types with significant clinical implications. MCD predominantly affects children, while FSGS is more common in adults, often leading to irreversible kidney dysfunction. Despite shared features like podocyte injury and immune dysregulation, their pathological and clinical presentations differ. Understanding gene expression changes in these diseases could reveal new therapeutic targets. Single-cell transcriptomic datasets (GSE213030 and GSE176465) were analyzed to investigate cellular interactions in MCD and FSGS. Machine learning algorithms developed diagnostic models, and immune subtypes were identified for detailed subtype analysis. Key genes were validated using qRT-PCR and immunohistochemical staining in a mouse model, focusing on their association with M1 macrophage activation. Integrated single-cell analysis identified six key genes (, , , , , and ) central to macrophage activation. These genes were closely linked to M1 macrophage activation, as confirmed through transcriptomic profiling and spatial co-expression patterns in Sprague-Dawley (SD) rat models. Machine learning models validated their predictive value in disease progression from MCD to FSGS. This study highlights six hub genes as potential biomarkers for predicting MCD-to-FSGS progression. Their roles in macrophage activation suggest these genes may serve as novel therapeutic targets for personalized treatment strategies, particularly for patients at high risk of disease transition. - Source: PubMed
Publication date: 2026/02/01
Wang Ting-TingLu HongShen TongChen Shi-LiangHe Yi-BoSong Ding-MingCui Xiang-FeiTong Ming