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
- FGF/FGFR alterations are recurrent but heterogeneous in head and neck cancer, and which types predict benefit from selective fibroblast growth factor receptor (FGFR) inhibition is unknown. - Source: PubMed
Publication date: 2026/08/02
Xue LiqiongZhu GuopeiWang PeiguoYang KunyuSun YanLi WeidongLi ZhendongJiang CuihongCai QingqingFang MeiyuHu ManGe MinghuaZhou WeiLi SichenGuo Ye - Cranial neural crest (CNC) cells are essential developmental contributors to the remarkable diversity of vertebrate skull shapes, yet how underlying gene regulatory networks (GRNs) evolve to produce highly derived morphologies remains a challenging question. Syngnathid fishes (seahorses, pipefishes, pipehorses, and seadragons) are an opportune family of species in which to address this problem because of their unusual and extensive cranial diversity and their loss of craniofacial patterning genes, and . Here we investigated whether syngnathid craniofacial evolution experienced only a few localized network changes or required global rewiring of CNC GRNs. Using comparative single-cell RNA sequencing, ATAC-seq and whole genome alignments across Gulf pipefish, threespine stickleback, and zebrafish, we found that the core pharyngeal arch CNC gene network is notably conserved in syngnathids despite their derived morphology. However, we identified key local changes including expression of in percomorph CNC-derived pharyngeal arch cells that is not shared with more basally diverging zebrafish, as well as syngnathid-specific changes in conserved regulatory elements associated with the genes and . We propose that, while loss of expression causes severe craniofacial defects in zebrafish, pharyngeal CNC expression of in the percomorph fish lineage provided functional redundancy and relaxed constraint on , and that altered regulation of Fgf pathway modulators could contribute to craniofacial elaboration. Our findings support a model in which local GRN modifications, rather than widespread network rewiring, underlie the evolution of derived syngnathid craniofacial structures. - Source: PubMed
Publication date: 2026/07/21
Healey HopeRehmann ClaraBassham SusanCresko William A - Supernumerary teeth are common congenital dental anomalies resulting from disrupted epithelial-mesenchymal interactions during tooth development. Although Hedgehog signaling is known to regulate tooth development, its temporal requirement for tooth number determination remains elusive. To investigate the role of early epithelial Hedgehog signaling, we conditionally deleted Smo in the dental epithelium using Pitx2-Cre, which initiates recombination at E10.5, prior to the onset of K14-Cre activity. Smo mutant mice developed two supernumerary mandibular incisors together with defective ameloblast differentiation and disrupted enamel formation. BrdU labeling revealed significantly increased cell proliferation in the lingual cervical loop, with no changes in apoptosis. In situ hybridization showed reduced expression of Wnt inhibitors Dkk1 and Sostdc1, accompanied by upregulation of the Wnt target gene Lef1, indicating aberrant activation of the Wnt/β-catenin pathway in Smo incisors. Treatment with SHH in vitro upregulated Dkk1 and Sostdc1 expression, confirming that Hedgehog signaling positively regulates these Wnt inhibitors. Moreover, the Smo mutant mice exhibited decreased expression of Fgf3, Sp6, Dlx2, and Msx2, genes implicated in ameloblast differentiation and dental patterning. Together, these findings demonstrate that epithelial Hedgehog signaling is required during early odontogenesis to establish normal tooth patterning through coordinated regulation of Wnt signaling and epithelial-mesenchymal communication, while simultaneously promoting ameloblast differentiation. - Source: PubMed
Publication date: 2026/07/28
Gao ShanhuiZhao YugeWang YanLi JianyingQiu MengshengHuang HuarongLi Feixue - Primary breast squamous cell carcinoma (PBSCC) with HER2-positive status is exceptionally rare, with fewer than 100 cases reported globally, and HER2 positivity occurring in only 5.8-7.1% of these cases. No established treatment standards exist for this entity. We present the case of a 43-year-old woman with HER2-positive PBSCC who exhibited a poor response to neoadjuvant TCHP therapy (Miller-Payne grade 2). Local recurrence occurred just 3 months after mastectomy. Second-line therapy with pyrotinib plus capecitabine provided 9 months of disease control before lung metastasis emerged. Subsequent molecular profiling revealed a E545K mutation (VAF 40.3%), co-amplified with and . Although third-line treatment with trastuzumab deruxtecan (T-DXd) achieved a partial response, the progression-free survival (PFS) was limited to only 5 months. A repeat biopsy confirmed HER2 downregulation (from 3+ to 2+), identifying antigen loss as a key mechanism of acquired resistance. A review of the literature indicates that the pathological complete response rate of HER2-positive PBSCC to standard HER2-targeted therapy is remarkably low, far inferior to the 50-60% pCR rates achieved with dual HER2 blockade in HER2-positive invasive ductal carcinoma. This case underscores that upon failure of HER2-targeted therapy accompanied by HER2 antigen loss, the treatment strategy should pivot towards molecularly-guided precision therapy. Based on evidence such as that from the TRIUMPH trial, priority should be given to agents targeting the detected alterations, such as or inhibitors, rather than persisting with HER2-targeted approaches. - Source: PubMed
Publication date: 2026/07/09
Yang FangGuo SiyuLi PingYang MengqiWu Xuan - Opioid use disorder (OUD) remains a critical global health challenge. The nucleus accumbens (NAc), a key region of the brain reward system, plays an essential role in opioid-induced neuroadaptations. Characterizing gene expression alterations in reward-system regions, such as the NAc, is essential for elucidating the molecular mechanisms underlying addiction. In recent years, bioinformatics has emerged as a rapidly advancing field and has played a pivotal role in elucidating molecular mechanisms and in advancing computational biology. - Source: PubMed
Publication date: 2026/06/02
Pourmand Seyed MahmoudNazari ShahrzadNazari ElhamArezoomandan RezaHassanzadeh GholamrezaEshrati SaharKarami-Zarandi MortezaSaberi-Zafarghandi Mohammad Bagher