FLNB
- Known as:
- FLNB
- Catalog number:
- Y213600
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- FLNB
Related genes to: FLNB
- Gene:
- FLNB NIH gene
- Name:
- filamin B
- Previous symbol:
- FLN1L, LRS1
- Synonyms:
- TAP, TABP, ABP-278, FH1
- Chromosome:
- 3p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-06-20
- Date modifiied:
- 2015-12-16
Related products to: FLNB
Anserine Filamin B, Beta Elisa Kit (FLNb)Anserine anti - Filamin B, Beta Elisa Kit (FLNb)anti-FLNBanti-FLNBanti-FLNB type: Primary antibodies host: MouseAntibody to Filamin B Beta (FLNb) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitAntibody to Filamin B Beta (FLNb) Organism: Homo sapiens (Human) Type: Polyclonal Source: RabbitBiotin-linked Antibody to Filamin B Beta (FLNb); Reactivity: Homo sapiens (Human) Clonality: Polyclonal Source: RabbitBovine Filamin B, Beta ELISA , FLNBBovine Filamin B, Beta ELISA , FLNBBovine Filamin B, Beta Elisa Kit (FLNb)Canine Filamin B, Beta ELISA , FLNBCanine Filamin B, Beta ELISA , FLNBCanine Filamin B, Beta Elisa Kit (FLNb)Chicken Filamin B, Beta ELISA , FLNB Related articles to: FLNB
- Pancreatic ductal adenocarcinoma (PDAC) is a highly lethal malignancy marked by substantial molecular heterogeneity and variable response to gemcitabine-based therapy. While KRAS mutations are nearly universal, the broader RTK-RAS and MAPK signaling architecture and its relationship to treatment response remain incompletely defined. We conducted an integrative clinical-genomic analysis of 184 PDAC tumors stratified by age at diagnosis and gemcitabine exposure, interrogating somatic alterations across curated RTK-RAS/MAPK gene sets. Conversational artificial intelligence agents (AI-HOPE-RTK-RAS and AI-HOPE-MAPK) enabled dynamic cohort construction and pathway-level analyses, with findings validated using standard statistical methods. In late-onset PDAC, ERBB2 and RET mutations were significantly enriched in gemcitabine-treated tumors. Early-onset cases demonstrated differential enrichment of CACNA2D family alterations in non-treated tumors and higher frequencies of FLNB and TP53 mutations in treated disease. Importantly, late-onset patients not treated with gemcitabine who lacked RTK-RAS or MAPK alterations exhibited significantly improved overall survival. These findings reveal age- and treatment-dependent pathway dependencies beyond canonical KRAS status and support a precision oncology framework in PDAC. Conversational AI facilitated rapid, multidimensional clinical-genomic integration to uncover clinically relevant signaling substructures. - Source: PubMed
Publication date: 2026/03/26
Diaz Fernando CWaldrup BrigetteCarranza Francisco GManjarrez SophiaVelazquez-Villarreal Enrique - Congenital tooth agenesis impairs masticatory function and aesthetics and adversely affects craniofacial development. Although largely considered genetic in origin, its exact etiology remains unclear. This study reports three familial cases of nonsyndromic congenital tooth agenesis (NSTA). Whole genome sequencing (WGS) revealed five pathogenic variants: filamins-B (FLNB) (c.5186C>A, p.Ser1729Ter), methylcrotonyl coenzyme a carboxylase 2 (MCCC2) (c.91C>T, p.Gln31Ter; c.484C>T, p.Gln162Ter; c.340C>T, p.Gln114Ter), laminin subunit alpha 2 (LAMA2) (c.1084A>T, p.Arg362Ter), cathepsin C (CTSC) (c.748C>T, p.Arg250Ter), and chromatin remodeling protein microrchidia family CW-type zinc finger 4 (MORC4) (c.1726C>T, p.Arg576Ter). Among these variants, LAMA2 was associated with a severe tooth agenesis phenotype. The findings offer novel clues toward understanding the etiopathogenesis of this condition. - Source: PubMed
Zheng YuemeiWang DanJiang TongyangYang DanquLu Hong - The etiology of Idiopathic Congenital Talipes Equinovarus (ICTEV) remains poorly understood. Several theories have been proposed, including genetic factors. Unlike genes, which are essentially static in composition and size, transcriptome or microRNA (miRNA) varies greatly and might be influenced by multiple variables. This research aims to determine the expression of MiRNA that influences the occurrence of ICTEV in the Indonesian population. - Source: PubMed
Publication date: 2026/03/27
Muhammad HilmiHaryana Sofia MMagetsari RahadyanSetiasari Dicka WYurnalis Fadhilla AHuwaidi A FaizTrimahendra Alfin IWijayatno Qonita J - Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by profound molecular heterogeneity and inconsistent responses to gemcitabine-based therapy. Although KRAS mutations are nearly ubiquitous, the broader RTK-RAS and MAPK signaling networks, and their association with therapeutic response, remain insufficiently characterized. We performed an integrative clinical-genomic study of 184 PDAC tumors, stratified by age at diagnosis and gemcitabine exposure, systematically evaluating somatic alterations within curated RTK-RAS/MAPK gene panels. Conversational artificial intelligence agents (AI-HOPE-RTK-RAS and AI-HOPE-MAPK) were deployed to dynamically construct cohorts and conduct pathway-level analyses, with results subsequently confirmed using conventional statistical approaches. Among late-onset PDAC cases, ERBB2 and RET mutations were significantly enriched in gemcitabine-treated tumors. In early-onset disease, CACNA2D family alterations were more common in untreated tumors, whereas FLNB and TP53 mutations were observed at higher frequencies in treated cases. Notably, late-onset patients who did not receive gemcitabine and lacked RTK-RAS or MAPK pathway alterations demonstrated significantly improved overall survival. These findings identify age- and treatment-specific signaling dependencies extending beyond canonical KRAS alterations and reinforce a precision oncology framework in PDAC. Conversational AI enabled rapid, multidimensional integration of clinical and genomic data, facilitating the identification of clinically meaningful pathway architectures. - Source: PubMed
Publication date: 2026/03/05
Diaz Fernando CWaldrup BrigetteCarranza Francisco GManjarrez SophiaVelazquez-Villarreal Enrique - PIEZOs are mechanically gated ion channels that transduce force into electrochemical signals. PIEZO1 responds to diverse stimuli including membrane stretch and shear stress, whereas PIEZO2 is generally tuned to detect cellular indentation. The functional specialization of PIEZO2 is proposed to underlie its distinct physiological roles, including mediating the sense of touch. How PIEZO2 achieves this selectivity despite its close structural similarity to PIEZO1 is unclear. Here we combine single-molecule MINFLUX fluorescence nanoscopy with electrophysiology to link the conformational states of PIEZO2 to channel gating in intact cells. We find that PIEZO2 is intrinsically more rigid than PIEZO1, and that disparate mechanical stimuli paradoxically evoke opposite conformational and gating responses in each channel. These unique gating properties arise in part from a connection to the actin cytoskeleton, and we identify filamin-B (FLNB) as a molecular tether that is required for this interaction. This complex alters how force is transmitted to PIEZO2 and confers heightened sensitivity to and selectivity for cellular indentation. PIEZO2 and FLNB are co-expressed in somatosensory neurons and colocalize within tens of nanometres at the end organs of cutaneous mechanosensory afferents. These findings help to explain why PIEZO2 is a specialized mechanosensor and provide a molecular blueprint for understanding how cells decode diverse mechanical stimuli across tissues and organ systems. - Source: PubMed
Publication date: 2026/03/04
Mulhall Eric MYarishkin OlegHill Rose ZKoster Anna KPatapoutian Ardem