FGF3 Antibody (C_term) Blocking Peptide
- Known as:
- FGF3 Antibody (C_term) Blocking Peptide
- Catalog number:
- BP9879b
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Abgen
- Gene target:
- FGF3 Antibody (C_term) Blocking Peptide
Related genes to: FGF3 Antibody (C_term) Blocking Peptide
- Gene:
- FGF3 NIH gene
- Name:
- fibroblast growth factor 3
- Previous symbol:
- INT2
- Synonyms:
- HBGF-3
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2019-04-23
Related products to: FGF3 Antibody (C_term) Blocking Peptide
Related articles to: FGF3 Antibody (C_term) Blocking Peptide
- Esophagogastric junction adenocarcinomas (EGJA) pose a serious threat to health and are increasing in incidence. The Siewert classification is the recognized anatomical classification system for guiding the surgical approaches in EGJA. However, the definition of EGJA and its optimal resection strategy remain controversial. This study aims to investigate the distinct molecular relationship between EGJA subtypes and other upper gastrointestinal cancers at the molecular level. - Source: PubMed
Publication date: 2026/03/24
Qin XiaoXu LinWang XiaozhenQi YouchaoZhong WeiShang BinWang ZhouChen Gang - Anaplastic lymphoma kinase () rearrangement has been identified in approximately 1% of lung squamous cell carcinomas (LUSCCs). Due to its rarity, the efficacy of anaplastic lymphoma kinase-tyrosine kinase inhibitors in the treatment of -positive LUSCCs is poorly characterized. - Source: PubMed
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Li ShengshuDu XiaosongZhang XinxinMa HaixiaYang YanliLi YuanWei QinChen YanLi HongweiBu PengLiu DujuanHan SongyanChen Deyi - Hemifacial microsomia (HFM) is a genetically complex craniofacial disorder. While GWAS and family studies have identified multiple candidate genes, functional validation rates remain low (<10%). - Source: PubMed
Publication date: 2026/04/07
Li ZhifengZhang Zhiyong - Mutations in the fibroblast growth factor 10 () gene in humans cause aplasia of the lacrimal and salivary glands (ALSG). In patients with ALSG, heterozygous loss-of-function mutations are found, and haploinsufficiency results in the absence of these secretory organs. Lacrimal glands (LGs) are formed through epithelial thickening, budding, and branching morphogenesis. To compare the variable phenotypes of the Harderian glands (HGs) previously reported, we examined the development of LGs in wild-type (WT), , and null mice. Pax6 immunostaining was performed to visualize the LG primordia from embryonic day 15.5 (E15.5) onwards. In situ hybridization of the genes encoding the epithelial receptor of FGF10, FGFR2b, and its other ligands was performed to determine their potential involvement in LG development. LG primordia were not observed in mice bilaterally at E16.5 or later stages. At E15.5, budding from the developing conjunctival epithelium (CE) was observed in a small fraction of the LG primordia. In contrast, the -null CE failed to promote budding. Among , , , , and , was expressed in the mesenchyme surrounding developing LG epithelial cells, whereas was expressed in the LG epithelium of WT mice. was initially expressed in the mesenchyme surrounding the nascent LG epithelium, but its expression subsequently became diffused. Thus, we conclude that among the FGFR2b ligands, initial LG formation is dependent on the mesenchymal factors FGF10 and FGF7, and FGF1 is likely to function as an epithelial factor in the LG primordia. A single allele of was found to be insufficient to support the budding process during LG morphogenesis. - Source: PubMed
Publication date: 2026/02/24
Ikeda ShioriSato KeitaTajika YukiFujita HirofumiBando TetsuyaNohno TsutomuMiyaishi SatoruOhuchi Hideyo - ESR1 alterations present a common mechanism of resistance to endocrine therapy (ET) in hormonally driven tumors. The clinical significance of these alterations continues to evolve with newly approved targeted therapies and a range of ongoing investigational trials. - Source: PubMed
Publication date: 2026/01/19
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