DIVAA FGF_2 Positive Control
- Known as:
- DIVAA FGF_2 Positive Control
- Catalog number:
- 3450-048-04
- Product Quantity:
- 100 ng/10 uL
- Category:
- -
- Supplier:
- Trevigen
- Gene target:
- DIVAA FGF_2 Positive Control
Related genes to: DIVAA FGF_2 Positive Control
- Gene:
- FGF2 NIH gene
- Name:
- fibroblast growth factor 2
- Previous symbol:
- FGFB
- Synonyms:
- -
- Chromosome:
- 4q28.1
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
- Gene:
- FGF13 NIH gene
- Name:
- fibroblast growth factor 13
- Previous symbol:
- -
- Synonyms:
- FHF2, FGF2
- Chromosome:
- Xq26.3-q27.1
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-16
- Date modifiied:
- 2018-02-13
- Gene:
- NUDT6 NIH gene
- Name:
- nudix hydrolase 6
- Previous symbol:
- -
- Synonyms:
- gfg-1, gfg, FGF2AS, FGF-AS
- Chromosome:
- 4q28.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-09-03
- Date modifiied:
- 2016-10-05
Related products to: DIVAA FGF_2 Positive Control
(+) Control probe (DNA), biotinylated(+) Control probe (RNA), biotinylated(-) Control probe (DNA), biotinylated(-) Control probe (RNA), biotinylated(DRAAGQPAG)3 (repeat-sequence peptide of the P. vivax circumsporozoite protein, CSP) control blocking peptide(Draxin) C1ORf187 WB control: PC-Drax Host: Rabbit Affinity purifed(Draxin) C1ORf187, WB control(I) LightCycler 1. 0; (Internal Control can't be used for this system) ; (II) LightCycler2. 0; (III) PE5700, MJ_Opticon etc. single color systems; (IV) ABI7000, ABI7300, ABI7500, ABI7900, ABI StepO(NANP)5 peptide (repeat-sequence peptide of the P. falciparum circumsporozoite protein, CSP) control blocking peptide(NVDP)4 peptide (minor repeat-sequence peptide of the P. falciparum circumsporozoite protein, CSP) control blocking peptide(PPPPNAND)3 peptide (repeat-sequence peptide of the P. berghei circumsporozoite protein, CSP) control blocking peptide(WB control) Fel D1 Immunogen: peptide Host: Rabbit(WB control) FelD1 Immunogen: peptide Host: Rabbit, Clone MOPC-21, Isotype IgG1Application FC, IP, WB, IHC(P), IHC(F), negative control Concentration 0.1 mg/ml, Clone MOPC-21, Isotype IgG1Application FC, IP, WB, IHC(P), IHC(F), negative control Concentration 0.1 mg/ml Related articles to: DIVAA FGF_2 Positive Control
- Desmoplasia, a dense fibrotic reaction, is a hallmark of pancreatic ductal adenocarcinoma (PDAC) and fuels chemoresistance through multiple mechanisms. Here, we evaluated heparanase (HPSE), an endoglycosidase that remodels extracellular matrix (ECM) and drives fibrogenesis, as a potential target in PDAC. Immunohistochemical analysis of human PDAC tissues showed elevated HPSE expression, along with increased levels of fibroblast growth factors 1 and 2 (FGF1/2), reflecting their liberation by HPSE-catalyzed heparan sulfate cleavage. High expression of all three proteins was associated with worse overall and disease-free survival. In vitro coculture assays showed that the HPSE inhibitor PI-88 suppressed PDAC cell-induced activation of pancreatic stellate cells (PSCs) and prevented ECM stiffening without inducing cytotoxicity. Mechanistically, tumor-derived HPSE activated ERK signaling and promoted FGF1/2 production in PSCs, both of which were effectively suppressed by PI-88. In orthotopic mouse models, gemcitabine treatment upregulated HPSE and FGF1/2, whereas gemcitabine-resistant tumors exhibited further increases in these factors, accompanied by enhanced PSC activation and collagen deposition. Importantly, triple therapy with PI-88, gemcitabine, and Abraxane significantly suppressed tumor growth and prolonged survival relative to all mono- and doublet regimens. Immune profiling revealed that this combination reduced PSC activation, contracted M2 macrophage and regulatory T cell populations, and expanded M1 macrophages, CD8⁺ T cells, and NK cells. In conclusion, these data underscore HPSE as a key driver of fibrosis and chemoresistance in PDAC and support HPSE inhibition as a promising strategy to enhance therapeutic efficacy. - Source: PubMed
Publication date: 2026/05/08
Chen Chang-JungWang Hao-ChenHuang Wen-YenChang Stanley Shi-ChungChang AlarngLin Chieh-LiangYang Chih-YaShan Yan-Shen - Developmental and epileptic encephalopathies (DEEs) comprise a clinically and genetically heterogeneous group of severe neurodevelopmental disorders, frequently caused by pathogenic variants in genes encoding neuronal ion channels or synaptic proteins. The fibroblast growth-factor 12 (FGF12) encodes a binding protein for voltage-gated sodium channels. Variants in FGF12 have recently been associated with autosomal dominant DEEs characterized by early-onset epilepsy and neurodevelopmental impairment. We report three patients with a duplication involving exons 1-4 of FGF12 on chromosome 3q28-q29 and systematically review 24 previously published cases of FGF12-related DEE. Clinical features, electroencephalographic findings, neuroimaging data, and responses to anti-seizure medications (ASMs) were analyzed across a total cohort of 27 patients. Eighteen patients carried FGF12 missense variants, including the recurrent pathogenic p.Arg114His variant (n = 14), p.Gly112Ser (n = 2), p.Glu87Lys (n = 1), and one exon 4 missense variant (chr3:g.192335434C>T). Nine patients had copy number duplications involving FGF12. Seizure onset ranged from 1 day to 4 years of age, with 54.1% presenting in the neonatal period. Tonic seizures were the most common seizure type, and 79.1% of patients exhibited moderate to severe intellectual disability. Brain MRI showed mild cerebral and/or cerebellar atrophy in 41.6% of cases. Across reported cases, variable responsiveness to ASMs was observed, with sodium channel blockers including carbamazepine and phenytoin frequently associated with seizure reduction. This study expands the clinical and genetic spectrum of FGF12-related DEE and highlights considerable phenotypic variability across variant types. While treatment responses were heterogeneous, sodium channel blockers were commonly associated with clinical improvement. These findings support cautious consideration of sodium channel targeting therapies in FGF12-DEE and underscore the need for systematic studies to better define genotype treatment relationships. - Source: PubMed
Publication date: 2026/04/29
Aldurayhim FatimahBasit SulmanBashir ShahidHousawi Yousef HussainMir Ali - Gastric cancer (GC) is the fifth most prevalent cancer and the fifth leading cause of cancer-related mortality worldwide. The current gold standard for clinical diagnosis is gastroscopy, which, despite its high sensitivity and specificity, is limited by its invasive nature and high cost, making it unsuitable for large-scale screening. Furthermore, the diagnostic process lacks biomarkers that offer both high sensitivity and specificity. A screening model incorporating five methylation-based biomarkers (ELMO1, FGF12, NPY, SEPTIN9, ZNF671) was developed. Using these methylation profiles, GC risk prediction models were constructed employing Random Forest. - Source: PubMed
Publication date: 2026/04/25
Long FengyingXu YiWu KangFu XiaoyuGao TangjieLuo ShiyaDai LizhongChen Xiao-Ping - Myxofibrosarcoma (MFS) is a rare soft-tissue sarcoma with limited systemic therapy options, necessitating preclinical platforms that better simulate clinical drug responses. We investigated how 2D monolayers versus 3D spheroids shape the baseline transcriptome and doxorubicin (DOX)-responsive programs across six patient-derived MFS cell lines. RNA sequencing revealed that 3D culture induces a distinct transcriptomic state characterized by the enrichment of microenvironment-associated stress programs, such as hypoxia, inflammatory/NF-κB signaling, and glycolysis, alongside the suppression of proliferation-related pathways. Although the global DOX-induced transcriptional response was highly environment-dependent, we identified a robust core of six regulators-MCRIP1, FGF12, HGF, EMSY, FZD2, and SECISBP2-whose transcriptional changes consistently correlated with cell survival rates across both 2D and 3D geometries. These genes are involved in transcriptional plasticity, redox homeostasis, and bypass survival signaling, providing a mechanistic basis for DOX resistance that transcends culture conditions. Our findings demonstrate that while culture geometry is a critical determinant of the MFS transcriptome, a robust set of environment-agnostic regulators dictates DOX efficacy. Integrating 3D systems with these specific transcriptomic readouts enhances the interpretability of drug screenings and supports the prioritization of rational therapeutic combinations for this rare sarcoma. - Source: PubMed
Publication date: 2026/04/21
Yoshimatsu YukiShiota YomogiKondo Tadashi - The poor prognosis of lung adenocarcinoma (LUAD) remains unimproved. This study aimed to identify lymph node metastasis (LNM)-related and cellular immunity-related prognostic genes in LUAD and propose novel strategies to improve its prognosis. LUAD-related datasets were obtained from public databases. Prognostic genes and a prognostic model were obtained through various bioinformatics analyzes, and the immunotherapy response in risk groups was assessed. Subsequently, the expression levels of prognostic genes and the intercellular communication relationships were explored at the single-cell level. Moreover, malignant cells were identified, and their differentiation mechanisms were explored via inferCNV analysis. Additionally, FURIN was silenced and overexpressed to investigate its effects on the invasion, metastasis, and lymphangiogenesis of LUAD cells in vitro. RGS20, KYNU, RAET1E, FGF12, GJB2, CACNA2D2, FURIN, and GDF10 were identified as prognostic genes with LNM. In 4 datasets, LUAD patients with the high LNM and immune cell-related risk scores exhibited higher mortality rates compared to those in the low-risk group. Furthermore, individuals in the low-risk group demonstrated a greater propensity to derive advantages from immunotherapeutic interventions. Epithelial cells were identified as key cells, with CACNA2D2 being significantly up-regulated during their late-stage differentiation. Basal cells, the malignant subset within epithelial cells, showed elevated FURIN expression in the pre-differentiation phase, which declined in the middle and late phases. Functionally, FURIN was found to enhance the migratory and proliferative capacities of LUAD cells. Moreover, we demonstrated that FURIN accelerated lymphatic metastasis and lymphangiogenesis in vitro. In this paper, we identified LUAD prognostic genes with LNM and immune cell signatures, emphasized treating LUAD patients according to LNM- and immune cell-related risk scores, and provided novel ideas on how to improve poor prognosis and develop targeted therapy for LUAD. - Source: PubMed
Lin ChuanChen XuanSun YongTang XiaomeiJiang Yi