FLNA Antibody (Phospho-Ser2152) (OAAF00047)
- Known as:
- FLNA Antibody (Phospho-Ser2152) (OAAF00047)
- Catalog number:
- oaaf00047
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- FLNA Antibody (Phospho-Ser2152) (OAAF00047)
Related genes to: FLNA Antibody (Phospho-Ser2152) (OAAF00047)
- Gene:
- FLNA NIH gene
- Name:
- filamin A
- Previous symbol:
- FLN1, FLN, OPD2, OPD1
- Synonyms:
- ABP-280
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1993-03-18
- Date modifiied:
- 2019-04-23
Related products to: FLNA Antibody (Phospho-Ser2152) (OAAF00047)
Related articles to: FLNA Antibody (Phospho-Ser2152) (OAAF00047)
- Congenital short bowel syndrome (CSBS) is a rare intestinal disorder characterized by inborn shortening of the bowel with mainly mutations in Coxsackie and Adenovirus receptor-like membrane protein (CLMP) and Filamin A (FLNA) genes. Clinical features are not well described; therefore, we aim to improve patient care by evaluating diagnostic approaches and identifying prognostic factors through the analysis of published cases. - Source: PubMed
Publication date: 2026/08/13
Remund BarblinSchibli SusanneSokollik Christiane - PurposeTo elucidate the dynamic molecular evolution and immune heterogeneity in diabetic retinopathy (DR) and identify diagnostic biomarkers.MethodsMulti-omics integrative analysis was performed on peripheral blood transcriptomic data from diabetic patients with and without DR. Techniques included differential expression analysis, immune infiltration profiling, unsupervised clustering, and LASSO regression for biomarker selection. Findings were validated in an independent high-glucose-treated endothelial cell model.ResultsDR progression exhibits staged molecular evolution from diabetes (immune suppression) to early DR (cell cycle inhibition, immune burst) and advanced DR (metabolic stress, persistent immune dysregulation). Six co-downregulated immune modules indicated systemic immune suppression. Patients were classified into three immune subtypes: vascular-inflammatory, metabolic disorder, and oxidative stress-tissue remodeling. A diagnostic model based on IK, PLBD2, FLNA, H6PD, and ZMAT2 achieved an AUC of 0.876 for distinguishing DR from diabetes alone.ConclusionThis study delineates the dynamic molecular landscape and immune heterogeneity of DR, providing a potential multi-gene diagnostic signature and a framework for patient stratification, which may facilitate early detection and personalized management. - Source: PubMed
Publication date: 2026/08/04
Zhang JiweiZhang LinglinYu ZhihongYang GaojieYu Liling - FLNA encodes filamin A, a cytoskeletal actin-binding protein with critical roles in neuronal migration, mechano-transduction, and organ morphogenesis. Pathogenic FLNA variants are classically associated with periventricular nodular heterotopia (PVNH), epilepsy, and multisystem manifestations, although interpretation of missense variants remains challenging because of marked variable expressivity and limited functional evidence. - Source: PubMed
Publication date: 2026/08/03
Bombaci AlessandroMicaglio EmanueleBenedetti SaraStufano GianlucaCutillo GianniDoddato GabriellaRossi Sergio SoerenMazzeo SalvatorePappone CarloFilippi MassimoSalsone Maria - Diabetic retinopathy (DR) reflects retinal microvascular injury and systemic immune-metabolic stress, and most public DR transcriptomic datasets lack paired microbiome/metabolomic profiles. We used gutMGene v2.0 as a curated microbe/metabolite-host gene prior and integrated it with peripheral blood transcriptomics from GSE221521. Candidate genes were refined by weighted gene co-expression network analysis (WGCNA), repeated resampling, cross-dataset assessment, mechanism scoring, peripheral blood mononuclear cell (PBMC) single-cell localization and filamin A ()-centered single-cell gene regulatory network (GRN) virtual knockout. The gutMGene prior contained 238 host genes; 15 DR-associated genes overlapped this prior, and WGCNA retained ten candidate gut microbe and microbial metabolite-related genes (GMMRGs): , , , , , , , , and . Resampling prioritized as the most consistent candidate. Cross-dataset assessment localized the strongest signal to type 2 diabetes (T2D) PBMCs, retinal endothelial cells and advanced proliferative diabetic retinopathy with diabetic macular edema (PDR + DME) retinal tissue, with weaker separation in whole blood, broad retinal tissue and six-donor type 1 diabetes (T1D) PBMCs. virtual knockout predicted cell-context-dependent perturbation of immune-related transcriptional programs, including in DR B cells and in DR monocytes/NK cells. This prior-guided study identifies within a ten-gene GMMRG set as a circulating host-response signal that links curated microbe/metabolite-host records to immune-vascular and cytoskeletal remodeling in DR. - Source: PubMed
Publication date: 2026/07/10
Ma ChuanxueWang YujunLiu Yi - Neural stem cells (NSCs) are the basis of neurogenesis and neural regeneration and are widely used as models for drug test and disease therapy. However, how NSCs self-renewal is modulated is not fully understood. In this study, we show that cytoskeletal Filamin A (FLNA) acts as a negative regulator in NSCs proliferation or self-renew. FLNA can be localized to the nucleoli of both NE-4C and C17.2 cell lines. FLNA silencing activated the expression of Pol Ⅰ products. In contrast, FLNA overexpression dampened rDNA transcription, suggesting that FLNA suppresses NSCs proliferation by downregulating Pol Ⅰ-directed transcription. Mechanistically, FLNA downregulates Pol I-directed transcription by inhibiting RRN3 expression and the occupancies of the Pol I transcription machinery factors at the rDNA promoter. In addition, FLNA suppresses NSCs proliferation by maintaining high levels of P53 and PTEN expression. Finally, we show that FLNA silencing does not affect the identity of neural stem cells, but inhibits neuronal differentiation from neural stem cells. These findings provide a novel insight into the mechanisms by which FLNA negatively regulates NSCs self-renew. - Source: PubMed
Publication date: 2026/07/21
Wu ZihuiZhou XiangyuSong XiaoyeWang YeYu DeenZhao ShashaDeng Wensheng