Ask about this productRelated genes to: FGF4 protein
- Gene:
- FGF4 NIH gene
- Name:
- fibroblast growth factor 4
- Previous symbol:
- HSTF1
- Synonyms:
- K-FGF, HBGF-4, HST, HST-1, KFGF
- Chromosome:
- 11q13.3
- Locus Type:
- gene with protein product
- Date approved:
- 1988-04-20
- Date modifiied:
- 2014-11-19
Related products to: FGF4 protein
Related articles to: FGF4 protein
- Environmental toxicants (ENVOTOX) have emerged as critical risk factors for congenital malformations (CMFs) in the modern industrial era. Although epidemiological evidence underscores their adverse impact on pregnancy outcomes, the underlying molecular mechanisms remain insufficiently defined. This review consolidates current insights into exposome toxicity profiling, developmental pathway disruptions, and molecular mapping to identify potential biomarkers and mechanistic links between ENVOTOX and CMFs. Protein-protein interaction (PPI) network analysis identified 35 CMF-associated proteins, with ten fibroblast growth factors (FGFs: FGF4, FGF5, FGF8, FGF9, FGF10, FGF16, FGF17, FGF18, FGF20, and FGF22) prioritized as hub nodes. Molecular docking analysis showed high binding affinity of FGF9 and FGF4 toward dioxin-associated toxicants, with dibenzo-p-dioxin (DBPDO) exhibiting the strongest interaction (binding energy: -7.2 kcal/mol), followed by polychlorinated dibenzofurans (PCDBFs) (-6.7 kcal/mol) with FGF9. Notably, FGF9 exhibited mutagenic binding potential at ASN146, mediated through π-donor hydrogen bonding with DBPDO. Comparative toxicity data further highlighted the acute risks, as DBPDO demonstrated a lower LD (2.26 mol/kg) relative to PCDBFs (4.134 mol/kg). Collectively, this review emphasizes the central role of FGFs in mediating ENVOTOX-induced teratogenicity and offers molecular-level perspectives to guide biomarker discovery and intervention strategies for mitigating CMF risk. - Source: PubMed
Shukla Adarsh KumarMahajan RashmiTyagi Anuj KumarSwaroop Kamendra - Bone marrow aspirate concentrate (BMAC) is a promising orthobiologic therapy, yet the impact of patient demographics on its proteomic profile remains poorly understood. This study investigates how smoking status, age, sex, and BMI modulate BMAC's protein composition, focusing on 109 analytes across inflammation, immune response, and tissue regeneration pathways. BMAC samples from 120 patients (iliac crest: n = 77; humeral head: n = 43) were stratified by smoking status (current, former, never-smokers) and analyzed via antibody microarrays. Nonparametric statistical analyses (Kruskal-Wallis, Dunn's post hoc) with false discovery rate (FDR) corrections revealed significant proteomic alterations in iliac crest-derived BMAC from smokers, including upregulated pro-inflammatory cytokines (IL-17, TNF-α; p < 0.05, FDR-adjusted) and downregulated anabolic factors (TGF-β1, BMP-9). Former smokers exhibited intermediate profiles, suggesting partial recovery postcessation. Sex-based differences (e.g., BMP-5, FGF-4) were noted but did not survive FDR correction. Humeral head samples showed minimal smoking-related changes, highlighting site-specific effects. These findings underscore smoking's catabolic influence on BMAC's therapeutic potential and advocate for pretreatment cessation protocols. - Source: PubMed
Herna ColinCipriani MadisonSachdev RanjanJedlicka Sabrina - 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 - Sarcomatoid carcinoma of the upper urinary tract (SCUT) is a rare and aggressive malignancy. Due to its rarity, the molecular landscape and the prevalence of potentially targetable alterations are poorly characterized. We aimed to compare the clinical, pathological, and genomic profiles of SCUT and upper tract urothelial carcinoma (UTUC). - Source: PubMed
Publication date: 2026/07/21
Jaime-Casas SalvadorSalgia Nicholas JZugman MiguelGoes VitorMoradi AliShah KoralWinayak RahulBarragan-Carrillo ReginaFann JadonZhang GeorgeMercier BenjaminCastro Daniela VDizman NazliHsu JoAnnChehrazi-Raffle AlexanderDorff TanyaYip WesleyPal Sumanta KTripathi Abhishek - Unlike in hematologic malignancies like acute promyelocytic leukemia (APL), the tumorigenic role of RARA fusions in solid tumors, including melanomas, remains largely unknown. Here, we present a comprehensive clinicopathologic and molecular analysis of two cutaneous melanomas harboring RARA fusions. Both melanomas were of the acral subtype, affecting the feet of adults (median age: 60.5 years) without sex predilection. At diagnosis, Breslow thickness ranged from 1.2 to 5.5 mm, ulceration was present in one case, and the median mitotic rate was 4/mm. Tumor cells exhibited variable cytomorphology, including spindled and epithelioid features, with occasional rhabdoid morphology. Molecular analysis revealed a consistently low tumor mutational burden (median: 4.5 mutations/Mb). One acral melanoma was triple wild-type (lacking mutations in BRAF, NRAS, and NF1) and showed no gene amplifications, but harbored a LOC107984974::RARA fusion. The other acral melanoma carried an NF1 loss-of-function mutation and multiple gene amplifications involving 11q13.3 (CCND1, FGF3, FGF4, FGF19), 11q13.5-q14.1 (PAK1), 12q15 (MDM2), and 6q24.3 (SHPRH), along with two RARA fusions: RARA::LRP5 and RARA::RNF169. Over a median follow-up of 23 months, one patient developed a distant metastasis involving the brain approximately 20 months after the initial diagnosis. At last follow-up, one patient was alive with disease, while the other remained alive without clinical or radiological evidence of recurrence. These findings expand the current understanding of the molecular landscape of acral melanomas and may provide insights into the potential utility of targeted therapies against RARA fusions in a subset of melanomas, analogous to their therapeutic role in APL. - Source: PubMed
Publication date: 2026/07/03
Abdelhammed Mokhtar HYang Richard KLenskaya VolhaTorres-Cabala Carlos ACho Woo Cheal