Human Recombinant GDNF

Glial cell line-derived neurotrophic factor

Human Recombinant GDNF

Glial cell line-derived neurotrophic factor

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Glial cell line-derived neurotrophic factor
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Overview

Glial cell line-derived neurotrophic factor (GDNF) is a neurotrophic factor and a member of the tumor growth factor (TGF)-beta superfamily. The GDNF family of growth factors also includes neurturin, persephin, and artemin, which have seven conserved cysteine residues called cysteine-knots (Treanor et al.). GDNF family ligands signal through binding to specific GDNF-family receptor-α (GFRα) co-receptors and activate the RET receptor tyrosine kinase (Durbec et al.). Four different forms of GFRα co-receptors have been characterized (GFRα 1-4); GDNF binds specifically to GFRα1 prior to forming a complex with RET (Airaksinen & Saarma). GDNF is known to promote survival and morphological differentiation of midbrain dopaminergic neurons in both in vivo and in vitro studies and increases their high-affinity dopamine uptake (Granholm et al.; Lin et al.). GDNF has also been shown to have restorative effects on dying dopaminergic neurons in response to degenerative toxins (Aoi et al.). GDNF, together with Human Recombinant BDNF (brain-derived neurotrophic factor; Catalog #78005), BrainPhys™ Neuronal Medium (Catalog #05790), and other supplements, can be used to differentiate human pluripotent stem cell (hPSC)-derived neural progenitor cells into neurons (Bardy et al.).
Subtype
Cytokines
Cell Type
Neural Cells, PSC-Derived, Neural Stem and Progenitor Cells, Neurons
Species
Human
Area of Interest
Neuroscience, Stem Cell Biology
Purity
≥ 95%

Data Figures

(A) The biological activity of Human Recombinant GDNF was tested by its ability to promote the proliferation of C6 cells. Cell proliferation was measured after 7 days of culture using a fluorometric assay method. The EC50 is defined as the effective concentration of the growth factor at which cell proliferation is at 50% of maximum. The EC50 in the example above is 2.17 μg/mL. (B) 1 μg of Human Recombinant GDNF was resolved with SDS-PAGE under reducing (+) and non-reducing (-) conditions and visualized by Coomassie Blue staining. Human Recombinant GDNF is a homodimer of 15.2 kDa subunits with a predicted total molecular mass of 30.4 kDa.

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
78058, 78058.1, 78058.2, 78058.3
Lot #
All
Language
English
Document Type
Safety Data Sheet
Catalog #
78058, 78058.1, 78058.2, 78058.3
Lot #
All
Language
English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Resources and Publications

Publications (2)

Dysregulation of sphingolipid-metabolizing enzymes in Friedreich's ataxia: In vitro and in vivo insights into therapeutic targeting. Z. Ramchunder et al. 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.
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.