EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #78058_C
胶质细胞源性神经营养因子
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总览
胶质细胞源性神经营养因子 (GDNF) 是一种神经营养因子，属于肿瘤生长因子 (TGF)-β 超家族。GDNF 生长因子家族还包括神经营养因子 (Neurturin)、Persephin 和 Artemin，它们具有七个保守的半胱氨酸残基，称为半胱氨酸结 (Treanor et al.)。GDNF 家族配体通过与特定的 GDNF 家族受体 α (GFRα) 共受体结合发出信号，并激活 RET 受体酪氨酸激酶 (Durbec et al.)。目前已鉴定出四种不同形式的 GFRα 共受体（GFRα 1-4）；GDNF 在与 RET 形成复合物之前会与 GFRα1 特异性结合 (Airaksinen & Saarma)。体内和体外研究表明，GDNF 能够促进中脑多巴胺能神经元的存活和形态分化，并增加其对高亲和力多巴胺的摄取（Granholm et al.; Lin et al.）。此外，GDNF 还被证实对因退化毒素而死亡的多巴胺能神经元具有修复作用（Aoi et al.）。GDNF 可与人重组 BDNF（脑源性神经营养因子；产品号#78005）、BrainPhys™ 神经元培养基（产品号#05790）以及其他添加剂一起使用，将人多能干细胞 (hPSC) 衍生的神经祖细胞分化为神经元（Bardy et al.）。
分类
细胞因子
细胞类型
神经细胞，PSC衍生，神经干/祖细胞，神经元
种属
人
研究领域
神经科学，干细胞生物学
纯度
≥ 95 %
实验数据
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
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相关材料与文献
技术资料 (5)
文献 (2)
Supramolecular nanostructure mimics GDNF trophic effects in vitro on human dopaminergic neurons
NPJ Regenerative Medicine 2025 Aug
Abstract
Peptide-based supramolecular nanostructures offer a versatile platform with substantial promise for clinical translation in regenerative medicine. These systems allow for the incorporation of biologically active sequences and can be engineered to modulate tissue-specific parameters such as stiffness,diffusivity,and biodegradability. We developed here a bioactive supramolecular nanostructure containing a peptide designed based on glial cell-derived neurotrophic factor. These nanostructures form scaffolds that mimic important trophic effects provided by this growth factor on iPSC-derived human dopaminergic neurons. Our in vitro data show that the nanostructures promote cell viability,confer neuroprotection against 6-hydroxydopamine toxicity,enhance neuronal morphology,facilitate electrophysiological maturation,and induce genes involved in neuronal survival. We also found that the scaffold promoted axonal extension in midbrain human organoids. These findings suggest that the supramolecular system could be useful to improve outcomes in cell-based therapies for Parkinson’s disease,where progressive dopaminergic degeneration is a hallmark.
Dysregulation of sphingolipid-metabolizing enzymes in Friedreich's ataxia: In vitro and in vivo insights into therapeutic targeting.
iScience 2026 Jul
Abstract
Friedreich's ataxia (FRDA) is an inherited neurodegenerative disorder caused by a GAA repeat expansion within the FXN gene,leading to reduced frataxin levels. This deficiency results in mitochondrial dysregulation,oxidative stress,and progressive cell death. Currently,only one approved treatment exists for FRDA in the United States,Canada,and the European Union,which improves neurological outcomes but has not been fully evaluated for broader disease symptoms. Therefore,identifying new therapeutic targets remains essential. Sphingolipids are increasingly recognized for their roles in neurodegeneration with emerging evidence indicating their dysregulation in FRDA. Here,we investigate whether sphingolipid-metabolizing enzymes are similarly affected and assess the therapeutic potential of targeting them. Our findings demonstrate that these enzymes are dysregulated across multiple FRDA models. Importantly,their modulation in vitro and in vivo significantly reduces mitochondrial dysfunction,enhances frataxin expression,and improves key pathological features of the disease,highlighting sphingolipid metabolism as a promising therapeutic target for FRDA.
更多信息
| 物种 | 人 |
|---|---|
| 纯度 | ≥ 95 % |
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产品仅供研究使用，不用于针对人或动物的诊断或治疗。
产品仅供研究使用，不用于针对人或动物的诊断或治疗。
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