Ask about this productRelated genes to: FGF10 antibody
- Gene:
- FGF10 NIH gene
- Name:
- fibroblast growth factor 10
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 5p12
- Locus Type:
- gene with protein product
- Date approved:
- 1996-12-16
- Date modifiied:
- 2016-10-05
Related products to: FGF10 antibody
Related articles to: FGF10 antibody
- This study characterizes the expression of fibroblast growth factors (FGFs) and their receptors in the porcine corpus luteum (CL) across distinct stages of the oestrous cycle, and evaluates the regulatory role of FGF2 on angiogenesis, steroidogenesis, and cell survival in vitro. The CL was classified morphologically into four phases: Phase I (days 1-8; corpus haemorrhagicum; ELP), Phase II (days 9-14; highly vascularized CL; MLP), Phase III (day 15 onward; ischemic regression; LLP), and Phase IV (corpus albicans; avascular and regressed; RR). Each phase included 10 biological replicates (n = 10). Quantitative RT-PCR revealed significant upregulation (p < 0.001) of FGF1, FGF2, FGF7, FGFR1, FGFR2, and FGFR4 during early and mid-luteal stages. FGFR3 and FGFR2IIIC showed no significant variation, while FGFR2IIIB was downregulated (p < 0.001) during early/mid-luteal stages and upregulated during luteal regression. FGF10 expression declined significantly (p < 0.001) during regression. Western blotting Densitometry confirmed trends mRNA expression. In-vitro supplementation of FGF2 (1, 10, and 100 ng/ml) during the mid-luteal stage enhanced mRNA expression of angiogenic (vWF), steroidogenic (StAR, CYP11A1, 3β-HSD), and cell survival (PCNA, BAX) markers. StAR, CYP11A1, and 3β-HSD were significantly upregulated (p < 0.001) from 24 to 72 h in a dose-dependent manner. vWF and PCNA showed significant increases at 48 and 72 h, while BAX expression progressively declined (p > 0.001). The 100 ng/ml dose elicited the most pronounced effects. These findings suggest that FGF family members exert autocrine/paracrine effects that support luteal cell proliferation, differentiation, angiogenesis, steroidogenesis, and survival, underscoring their critical role in porcine ovarian physiology. - Source: PubMed
Publication date: 2026/04/09
Nanda RishiChouhan V SYadav PoonamSamad H ABorah SanjibSoren SimsonDutta DevojyotiMaurya V PSingh Gyanendra - Uterine glands are endometrial exocrine epithelia that support early embryo development. Their secretions are particularly essential for conceptus elongation in cattle. Uterine glands develop from the luminal epithelium and elongate into the stromal layer toward the myometrium. This process is regulated by growth factors, WNT proteins, and the surrounding extracellular matrix (ECM); however, the precise mechanisms that govern bovine uterine gland morphogenesis remain unclear. In this study, we determined how these signaling factors and ECM components affect the tubular formation of bovine uterine gland fragments in 3D culture systems. Uterine gland fragments were enzymatically isolated from bovine endometria and 3D-cultured in Matrigel with or without growth factors (EGF, FGF1, FGF2, FGF7, FGF10, and IGF-1) and WNT (WNT3A, WNT5A, and WNT7A) proteins. Of these, only EGF stimulated the elongation of uterine gland fragments and eventually induced the formation of uterine gland-like structures. EGF-induced tubulogenesis was accompanied by a rapid increase in cell proliferation and alterations in cell-ECM interactions. The supplementation of collagen Ⅰ with Matrigel further promoted the elongation of the tubular structures. Although the addition of collagen Ⅰ did not alter the gene expression profiles of the uterine gland-like structures, the integrin-ROCK pathway contributed to the collagen-induced enhancement of elongation. Our findings clarified that EGF and collagen Ⅰ, but not FGFs, IGF-1, or WNTs, are key regulators for the tubular formation of 3D-cultured bovine uterine gland fragments. This 3D culture system provides a new platform to examine the cellular and molecular mechanisms underlying bovine uterine gland morphogenesis. - Source: PubMed
Publication date: 2026/04/09
Sugino YosukeIchikawa ReiMatsuyama ShuichiYamamoto YukiKawano KoheiKimura Koji - Mammalian palates are composed of the anterior hard palate and the posterior soft palate. However, the correlation of the genesis, pattern formation, and morphogenesis between the hard and soft palates remains elusive. - Source: PubMed
Publication date: 2026/03/20
Wang BiyingXue JunyuanBian YufanDeng JiaminLiu BoLi NanZhu LeiXiao JingLiu ChaoLiu Han - Orofacial clefts (OFCs) are common craniofacial malformations broadly classified as syndromic or non-syndromic. While syndromic OFCs are often caused by rare, high-impact variants, non-syndromic OFCs are typically associated with multiple low-impact common variants. However, growing evidence suggests that rare variants may also contribute to non-syndromic OFCs. To explore this, we performed exome sequencing in 45 individuals from 20 Colombian families, predominantly from the Caribbean region, a genetically distinct and underrepresented population. Our goal was to identify rare variants potentially contributing to both syndromic and non-syndromic OFCs. We identified 15 rare protein-altering variants in 11 families that showed strong phenotype-genotype concordance. Four probands carried a previously reported common ACSS2 variant (c.1487 T > C), with two probands also harbouring variants in Pleckstrin Homology Domain Containing (PLEKH) genes. Five variants were previously reported in ClinVar (two with conflicting interpretations, one pathogenic, and two of uncertain significance), while ten were novel. Variants were found in known OFC-associated genes (MID1, FLNA, FGF10) and emerging candidates (ZFHX4, PLEKHA5, PLEKHA7). These findings provide further evidence that rare variants in developmental and signalling pathways contribute to both syndromic and non-syndromic OFCs, reinforcing previous studies and expanding the catalogue of candidate genes in underrepresented populations. - Source: PubMed
Publication date: 2026/03/30
Silva AlejandroJaramillo Oquendo CarolinaBernal Jaime EMartinez Julio CesarCollins AndrewBriceño IgnacioBenavides EscildaLópez Arrieta ZuliethEnnis Sarah - Hepatic stellate cells (HSCs) are activated during cholestasis. However, beyond liver fibrosis, whether HSCs influence bile acid (BA) synthesis and homeostasis remain largely unknown. This study investigates the role of activated HSCs (aHSCs) in the regulation of hepatic BA metabolism. - Source: PubMed
Publication date: 2026/03/26
Li SantieTong GaozanXue MeiShen LeyiZhu KunxuanFeng JianjunFan JunfuLu JunjieYi XiaojingWang LuhaiLiang JiaqiCong WeitaoLi Xiaokun