ACTN4 Mouse Monoclonal Antibody
- Known as:
- ACTN4 Mouse Monoclonal Antibody
- Catalog number:
- APO-000081-M01
- Product Quantity:
- 0.1mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- ACTN4 Mouse Monoclonal Antibody
Related genes to: ACTN4 Mouse Monoclonal Antibody
- Gene:
- ACTN4 NIH gene
- Name:
- actinin alpha 4
- Previous symbol:
- FSGS1
- Synonyms:
- -
- Chromosome:
- 19q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 1992-03-26
- Date modifiied:
- 2016-10-05
Related products to: ACTN4 Mouse Monoclonal Antibody
Related articles to: ACTN4 Mouse Monoclonal Antibody
- Visual dysfunction due to optic neuritis (ON) is an early clinical manifestation of multiple sclerosis (MS). ON is characterized by inflammation of the optic nerve, demyelination, axonal damage, and retinal ganglion cell (RGC) loss. Previously, we showed that spermine oxidase (SMOX), a polyamine catabolizing enzyme, modulates visual function in an experimental model of ON. Using proteomic analysis, the present study aimed to identify SMOX-regulated molecular pathways involved in ON-associated visual dysfunction. - Source: PubMed
Henry Ojo HarryLiu FangAlanazi Abdulaziz HZahedi Kamyar ASoleimani ManoocherZhang DuoSomanath Payaningal RNarayanan S Priya - ObjectiveDisulfidptosis, a newly discovered mechanism of cell death, may play a significant role in cancer initiation, progression, and prognosis. However, studies on the prognostic role of Disulfidptosis-Related Genes (DRGs) across cancers remain limited. This study aims to systematically explore the prognostic value of DRGs in various cancer types by constructing a prognosis model based on DRGs and analyzing their associations with tumor biological characteristics.MethodsThis was a pan-cancer bioinformatics study combined with in vitro qRT-PCR validation. Public transcriptomic and clinical data from cancer patients were obtained from The Cancer Genome Atlas (TCGA). Samples were randomly divided into training and validation cohorts at a 1:1 ratio. In the training cohort, least absolute shrinkage and selection operator (LASSO) regression was used to identify prognosis-related DRGs, followed by multivariate Cox regression to construct a DRG-based risk score. The prognostic value of the risk score was evaluated using Cox regression, Kaplan-Meier survival analysis, and nomogram construction. Gene set activity analysis was performed to assess the associations between the DRG score and tumor-related biological processes, including angiogenesis, epithelial-mesenchymal transition (EMT), and cell cycle activity. To further validate the expression patterns of key DRGs in osteosarcoma, osteosarcoma-related transcriptomic data from TARGET and normal tissue data from GTEx were analyzed. The 16 selected DRGs were intersected with osteosarcoma-related differentially expressed genes, and 10 overlapping genes were further validated by qRT-PCR in osteosarcoma cell lines and normal osteoblasts.ResultsKey DRGs identified via LASSO regression showed significant prognostic value in pan-cancer analysis. The resulting risk model effectively stratified patients by survival outcomes and performed well in both training and validation cohorts, indicating strong clinical potential. SsGSEA revealed associations between DRG risk scores and malignant tumor features such as angiogenesis, EMT, and cell cycle dysregulation. Differential expression and GO enrichment analyses indicated that related genes were involved in metabolism, apoptosis, and immune processes. qRT-PCR validation in normal osteoblasts (hFOB) and seven osteosarcoma cell lines showed that NDUFA11 and NDUFS1 were generally downregulated, whereas ACTB, WASF2, FLNA, PRC1, ACTN4, PGD, RAC1, and FLNB were generally upregulated in most osteosarcoma cell lines compared with hFOB cells. These expression patterns were broadly consistent with the bioinformatics results and support the potential relevance of these genes in osteosarcoma progression.ConclusionBy constructing a prognostic model based on DRGs, this study reveals the significant prognostic value of DRGs across pan-cancers and further validates their association with tumor malignant characteristics. The results suggest that DRG score can serve as an effective prognostic indicator for cancer patient survival and have specific implications in osteosarcoma. In the future, DRG-based scoring systems may serve as novel biomarkers and therapeutic targets. - Source: PubMed
Publication date: 2026/06/29
Wang JinqiuHuang HuiLiu Dehuai - Anaplasma phagocytophilum is an obligatory intracellular bacterium that causes an emerging infectious disease, human granulocytic anaplasmosis. It undergoes a biphasic developmental cycle inside membrane-bound vacuoles within the host human neutrophils, maturing from a proliferating reticulate cell form to an infectious dense core (DC) form that is subsequently spontaneously released from host cells to initiate a new infection cycle. However, how A. phagocytophilum coordinates growth and release is unknown. Here, we found localized cortical F-actin disruption occurs where Anaplasma-containing vacuoles abut on the plasma membrane to release bacteria. Disruption of actin filaments by cytochalasin D and latrunculin B induced unrestrained release of almost all intracellular A. phagocytophilum from host cells, which were significantly less infectious than spontaneously released bacteria. A. phagocytophilum AnkA, a type IV secretion system (T4SS) effector, was found to localize in the cell periphery with cortical F-actin. By immunoprecipitation followed by mass spectrometry, AnkA was found to interact with actin, α-actinin 4 (Actn4) involved in actin cross-linking, and gelsolin for actin filament remodeling. shRNA-knockdown of Actn4 or gelsolin, enhanced release of premature A. phagocytophilum. Glutathione S-transferase (GST)-tagged C-terminus of AnkA (AnkA-C) interacted with actin and gelsolin, whereas the N-terminus (AnkA-N) interacted with Actn4. In vitro pyrene-actin polymerization assay showed that GST-AnkA-C has stronger actin polymerizing activity than GST-AnkA or GST-AnkA-N. Ectopically expressed GFP-AnkA-N localized to the plasma membrane and induced membrane ruffling, whereas GFP-AnkA-C colocalized with and enhanced stress fiber formation. These results demonstrate that AnkA is the first example of bacterial molecules interacting with gelsolin and Actn4. The result suggests that by colocalizing with cortical F-actin and controlling F-actin dynamics and cross-linking, AnkA regulates spatiotemporal release of A. phagocytophilum. The current study unravels a new paradigm of retention/release mechanism of intracellular pathogen regulated by a T4SS effector. - Source: PubMed
Publication date: 2026/06/24
Lin MingqunDuan NanRikihisa Yasuko - Heat stress (HS) is a major environmental threat to swine production that impairs growth performance and health. Because of their limited thermoregulatory capacity, pigs are highly vulnerable to HS, which results in compromised intestinal integrity, systemic inflammation, and metabolic inefficiency. To elucidate the mechanisms underlying HS acclimation in pigs, we conducted a longitudinal multi-omics analysis integrating fecal microbiome, whole-blood transcriptome, and immune cell deconvolution in finishing pigs under thermoneutral (TN) or HS conditions. HS markedly reduced the average daily gain and feed intake. Microbiome profiling revealed condition-specific shifts: TN pigs showed enrichment of short-chain fatty acid (SCFA)-producing genera, such as and , whereas HS pigs exhibited increased 1. Functional predictions indicated preservation of the antioxidant and immunomodulatory pathways (glutathione, retinol, and aminoacyl-tRNA biosynthesis) in TN pigs, whereas HS pigs displayed branched-chain amino acid catabolism, reflecting metabolic acclimation under stress. Transcriptomic analysis revealed acute changes at week 1, with 516 differentially expressed genes enriched in hematopoiesis, focal adhesion, cytoskeletal remodeling, and thyroid hormone signaling. By Week 2, these gene responses had declined, suggesting partial acclimation. Network analysis identified cytoskeletal genes (, , , and ) as the central regulators. Immune deconvolution further showed the HS-driven elevation of cytotoxic T and myeloid subsets, in contrast to B cell populations which were maintained under TN, highlighting divergent immune trajectories. Integration of the microbiome, transcriptome, and immune data revealed two axes: (1) cytotoxic T cells positively associated with 1, but negatively associated with cytoskeletal genes, and (2) B cells positively linked to , , and structural genes. Only the B-cell structural axis formed a coherent cross-layer module, indicatin a recovery-oriented response. These findings demonstrate that resilience to HS requires the coordination of humoral immunity, cytoskeletal reinforcement, and SCFA-producing microbiota. The identified biomarker axis (, B cells, and cytoskeletal genes) provides a mechanistic basis for developing precise strategies to enhance thermal tolerance in swine. - Source: PubMed
Publication date: 2026/05/31
Seok Min-KiLim ChiwoongSeo Young-JunLee Ji-YeongKyoung HyunjinSong MinhoKim Jun-Mo - Podocyte injury and detachment are early cellular events in hypertensive nephropathy, yet their underlying mechanisms are not well clarified. Zyxin, a mechanotransducer located at focal adhesions, regulates actin cytoskeleton remodeling and exhibits diverse biological functions. However, its role in podocytes is poorly understood. In this study, we constructed a hypertensive nephropathy model in podocyte-specific zyxin knockout mice to explore the role of zyxin in hypertensive conditions. In vitro, mechanical stretch and Angiotensin II (AngII) were used to stimulate podocytes. Western blot, real-time PCR, and immunofluorescence were performed to underscore underlying mechanisms. We identified decreased zyxin levels in the glomeruli of a hypertensive nephropathy mouse model. Mechanical stretch and AngII altered zyxin expression and distribution in podocytes. Moreover, podocyte-specific zyxin knockout worsened hypertension-induced renal dysfunction, glomerulosclerosis, glomerular basement membrane thickening, foot process effacement, and podocyte loss. Zyxin knockdown disrupted the actin cytoskeleton, accompanied by reduced α-actinin-4 expression and changes in focal adhesion proteins, including vinculin and paxillin, which may contribute to altered podocyte motility and adhesion. These findings indicate that zyxin is involved in the regulation of podocyte cytoskeletal organization and cell behavior, likely through coordinated effects on multiple cytoskeletal and focal adhesion-related pathways rather than a single downstream mediator. In this context, zyxin may play a protective role in maintaining podocyte stability during hypertensive nephropathy. - Source: PubMed
Publication date: 2026/05/22
He Fang-FangChen Yi-YuanWang Yu-MeiHuang WeiDu Si-JiaSong An-NiHao YuZhang Xiao-LiZhang Chun