FGF17 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- FGF17 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb100092
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- FGF17 antibody Polyclonal Antibodies Primary antibodies
Related genes to: FGF17 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- FGF17 NIH gene
- Name:
- fibroblast growth factor 17
- Previous symbol:
- -
- Synonyms:
- FGF-13
- Chromosome:
- 8p21.3
- Locus Type:
- gene with protein product
- Date approved:
- 1998-12-22
- Date modifiied:
- 2014-11-19
Related products to: FGF17 antibody Polyclonal Antibodies Primary antibodies
Related articles to: FGF17 antibody Polyclonal Antibodies Primary antibodies
- Fibroblast growth factor 17 (FGF17) is implicated in neurodevelopment and synaptic function, yet its role in motivation remains unclear. This study compared serum FGF17 levels (measured using ELISA) between 74 patients with major depressive disorder (MDD) and 72 healthy controls (HCs), and examined its relationship with negative symptoms measured by the Motivation and Pleasure (MAP) and Expression (EXP) subscales of the Clinical Assessment Interview for Negative Symptoms (CAINS). Compared to HCs, patients with MDD exhibited lower FGF17 levels. Within the MDD group, serum FGF17 showed small to modest negative correlations with the ratings of the MAP and EXP scores. Moreover, multiple linear regression showed that FGF17 was a potential predictor of these scores after FDR correction. These preliminary findings suggest that reduced peripheral FGF17 levels are associated with motivational deficits in patients with MDD, warranting further investigation into its role in the neurobiology of "negative-like" symptoms in this clinical group. - Source: PubMed
Publication date: 2026/04/07
Zhu ZhenhuaYin XuyuanHuang JiaWang YiQi QiWang PeijieLui Simon S YHui LiChan Raymond C K - The reprogramming of glutamine metabolism holds a pivotal position in the energy provision and biosynthesis of tumors. However, the regulatory mechanism of this phenomenon in non-small cell lung cancer (NSCLC) is still not well-understood. NSCLC is a type of malignancy that has a high incidence and mortality rate globally. There is an urgent need to elucidate the role of glutamine metabolism in its pathological mechanism. This clarification may provide theoretical guidance for developing new therapeutic approaches. - Source: PubMed
Publication date: 2026/01/02
Kong QinghuaWang XiaoyanDing Wei - The role of FGF is the least understood of the morphogens driving mammalian gastrulation. Here, we have investigated FGF function in a 2D gastruloid model for human gastrulation. We observed a ring of FGF-dependent ERK activity that closely follows the emergence of primitive streak (PS)-like cells but expands further inward. This ERK activity pattern depends on localized activation of basolateral FGF receptor 1 (FGFR1) by endogenous FGF gradients and is required for PS-like differentiation, with loss of PS-like cells upon FGF receptor inhibition rescued by direct ERK activation. Single cell transcriptome analysis confirmed that, among the ligands, FGF2 is broadly expressed, FGF8 is transiently expressed during PS-like differentiation and FGF4/17 are specifically expressed in PS-like cells - similar to the human and monkey embryo but different from the mouse. FGF4 knockdown greatly reduced PS-like differentiation, while FGF17 knockdown primarily affected subsequent mesoderm differentiation. FGF8 expression was spatially and temporally displaced from PS markers and FGF4 expression, while knockdown expanded PS-like cells, suggesting FGF8 may limit PS-like differentiation. Thus, we have identified a previously unreported role for FGF-dependent ERK signaling in 2D gastruloids and possibly the human embryo, where FGF4 and FGF17 signal through basolateral FGFR1 to induce PS-like cells and derivatives, potentially restricted by FGF8. - Source: PubMed
Publication date: 2026/02/09
Jo KyoungLiu Zong-YuanPatel GauriYu ZhiyuanYao LiAngTeague SethJohnson CraigSpence JasonHeemskerk Idse - As targeted therapy assumes an increasingly pivotal role in comprehensive cancer treatment, there is a growing imperative to develop natural drugs that exhibit low toxicity and minimal side effects. Polysaccharides derived from the traditional Chinese herbal medicine Arisaema erubescens have been reported to show antitumor potential, however the key structural features and specific molecular targets responsible for their pharmacological effects are still vague. To address this question, a homogeneous polysaccharide TNX05 (Mw ≈ 9 kDa) was obtained and characterized from Arisaema erubescens. Structural analysis suggested that TNX05 was a galactoglucan with a backbone of 1, 4-α--Glcp, 1, 4-β--Glcp, and 1, 3-β--Galp residues, with side chains-→1-α/β--Glcp-(6 → 1)-α--Glcp and →1)-α--Glcp-substituted at the C-4 and C-6 of the 1, 4-α--Glcp units, respectively. Combining enzymatic hydrolysis, molecular docking, and protein-binding assays we showed a key core domain (TNX05II), which exhibited micromolar-range binding affinity for ten tumor-associated targets: Glypican-6 (GPC-6), glucuronic acid epimerase (Glce), S100 calcium-binding protein A4 (S100A4), S100A6, nucleoside diphosphate kinase 1 (NME1), fibroblast growth factor 17 (FGF17), proto-oncogene tyrosine-protein kinase Src (SRC), kelch-like ECH-associated protein 1 (KEAP1), Galectin-3 (Gal-3), and protein phosphatase 3 catalytic subunit alpha (PPP3CA). Additionally, TNX05II was significantly resistant to α-glucosidase degradation. This study suggests a possible key structure-target relationship underlying TNX05's antitumor activity, providing a molecular basis for the antitumor mechanism of Arisaema polysaccharides. - Source: PubMed
Publication date: 2025/11/29
Zhu YueJin CanDing Kan - Schizophrenia (SCZ) is a severe and hereditary neurodevelopmental disorder with unknown etiology. Here, we found that the SCZ risk gene BRD2, as an epigenetic reader, is consistently expressed in developing mouse and human cortical astrocytes. Astrocyte-specific Brd2 knockout in mice leads to dysregulation of immune responses and reduces Fgf17 expression, resulting in SCZ-like behaviors, including impaired sensorimotor gating, memory, and cognitive deficits. Moreover, BRD2 inhibition using JQ1 in forebrain organoids leads to FGF17 reduction, inducing developmental deficits involved in neural patterning and gliogenesis. The decrease of FGF17 expression was also found in SCZ patient-derived forebrain organoids, similar to BRD2-inhibited forebrain organoids. FGF17 treatment partially rescued the disrupted gene expression in BRD2-inhibited human forebrain organoids. Taken together, these findings suggest that disrupting the BRD2-FGF17 signaling pathway in early brain development may contribute to the pathogenesis of schizophrenia and may represent a potential therapeutic target for SCZ. - Source: PubMed
Publication date: 2025/09/14
Yu XiaoDu JiachengZhou ChengerHuang YonghengLi HuijuanCohen Bruce MChung SangmiShao Zhicheng