CDNF Recombinant Protein
- Known as:
- CDNF Recombinant Protein
- Catalog number:
- ZR-40-550
- Product Quantity:
- 0.005 mg
- Category:
- -
- Supplier:
- Zyagen
- Gene target:
- CDNF Recombinant Protein
Related genes to: CDNF Recombinant Protein
- Gene:
- CDNF NIH gene
- Name:
- cerebral dopamine neurotrophic factor
- Previous symbol:
- ARMETL1
- Synonyms:
- -
- Chromosome:
- 10p13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-05-27
- Date modifiied:
- 2015-09-11
Related products to: CDNF Recombinant Protein
Related articles to: CDNF Recombinant Protein
- Parkinson's disease (PD) is a neurodegenerative disorder characterised by the death of dopaminergic neurons in the substantia nigra (SN). Cerebral dopamine neurotrophic factor (CDNF) is a neurotrophic factor that is selective for stressed neurons and acts on the endoplasmic reticulum (ER), which is stressed in the pathophysiology of PD, namely in dopaminergic neurons. Additionally, ER stress is intimately associated with dysregulation of N-glycosylation; therefore, the improvement of ER homeostasis is likely to regulate N-glycosylation, recovering the healthy brain N-glycome. Furthermore, encapsulation of CDNF in a hydrogel system for sustained delivery of CDNF at the target site is of interest to prevent its rapid elimination. In this study, a collagen-based hydrogel was optimised to deliver CDNF into the brain of a PD model, and its effects on modulating the animals' functional behaviour and the intrinsic N-glycome of the brain were assessed. Modulation of the brain N-glycoprofile was observed in a dose-dependent manner, mainly in the core-fucosylated glycans. The alterations observed were amplified using a collagen hydrogel as the mode of delivery. Consequently, this research demonstrated the capacity to administer CDNF to the brain via a biomaterial system and its influence on transforming the N-glycomic signature from a diseased state to a healthier one. - Source: PubMed
Publication date: 2026/03/30
Rebelo Ana LúciaAbbah Sunny AMartin-Saldaña SergioAljaabary AmalTrotier AlexandreDowd EilisDrake Richard RMarchetti-Deschmann MartinaPandit Abhay - Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized primarily by the irreversible loss of dopaminergic neurons in the substantia nigra pars compacta (SNpc) of the midbrain. Although its etiology is complex, mitochondrial dysfunction has been widely recognized as a central hub in the pathogenesis of PD. Concurrently, neurotrophic factors (NTFs), particularly glial cell line-derived neurotrophic factor (GDNF) family ligands (GFLs) and cerebral dopamine neurotrophic factor (CDNF), which exhibit specific trophic effects on dopaminergic neurons, play a crucial role in the endogenous neuroprotective system. This review aims to move beyond simple mechanistic descriptions and critically analyze the interaction of the “NTFs-mitochondria axis” in PD. We will systematically examine experimental evidence supporting the role of this axis (from in vitro to in vivo models) and clarify its strengths and limitations. Emphasis is placed on the fundamental translational challenges revealed by GFLs-based clinical trials (such as GDNF and neurturin [NRTN]), including delivery bottlenecks, treatment timing, and limitations of disease models. Finally, we evaluate the potential and obstacles of novel strategies targeting this axis (such as new viral vectors, small molecule agonists, mitochondria-targeted drugs, and combination therapies). A deep understanding and addressing the dysregulation of the NTFs-mitochondrial network holds promise for opening new avenues in the development of disease-modifying therapies, but it is essential to remain keenly aware of existing challenges. - Source: PubMed
Publication date: 2026/03/11
Chang JunkaiLi ZisenLiu TingtingCheng XiangshuWei Jianshe - Cerebral Dopamine Neurotrophic Factor (CDNF) is known to protect neurons in various pathologies. HER-096 is a CDNF-derived brain-penetrating peptidomimetic which also possesses neuroprotective properties. However, the mechanism underlying the cytoprotective effects is not fully understood. Using primary cortical co-culture of neurons and astrocytes we have found that both CDNF and HER-096 can induce intracellular calcium signals predominantly in astrocytes by release of Ca from endoplasmic reticulum to cytosol. This decrease in the ER Ca pool activates store-operated calcium entrance (SOCE). Initial Ca signal in these cells could be inhibited by the sigma-1 receptor antagonist BD-1047. CDNF and HER-096 reduced the glutamate-induced delayed Ca deregulation and mitochondrial depolarisation which leads to significant protection against glutamate-induced excitotoxicity. Thus, the CDNF and HER-096 sigma-1 receptor mediated Ca signal in astrocytes and neurons, from the ER, could modify the effects of high concentrations of glutamate that lead to neuroprotection. - Source: PubMed
Publication date: 2026/01/27
Komilova NafisaEsteras NoemiPreziuso AlessandraMillichap LaurenDomanska AusraLudwig AnastasiaKulesskaya NataliaHuttunen Henri JHolmström Kira MAbramov Andrey YAngelova Plamena R - Cerebral dopamine neurotrophic factor (CDNF) has emerged as a key cytoprotective molecule, with well-documented neuroprotective effects in Parkinson's disease models and, more recently, demonstrated cardioprotective properties. In this study, we investigated the protective role of CDNF and its isolated domains (CDNF-N and CDNF-C) in isolated hearts subjected to ischemia/reperfusion (I/R) injury. Our data showed that the infarct area at risk decreased from approximately 40% in untreated hearts to about 20% in the presence of CDNF or CDNF-C, but not CDNF-N, indicating that CDNF-C is the principal mediator of CDNF's cardioprotective activity. This effect is mediated by activation of the PI3K/AKT signaling pathway, as the cardioprotective action of CDNF-C was abolished by wortmannin, a PI3K/AKT inhibitor. The study also examined the interaction between CDNF and the KDEL receptor (KDEL-R) at the plasma membrane using cardiomyocytes (H9c2 cells, neonatal primary cardiomyocytes, and human induced pluripotent stem cell-derived cardiomyocytes - hiPSC-dCM) exposed to endoplasmic reticulum (ER) stress induced by thapsigargin. Confocal microscopy revealed that KDEL-R translocates to the plasma membrane under ER stress, where it binds to both full-length CDNF and CDNF-C. However, only the full-length protein undergoes internalization by cardiomyocytes, suggesting that the N-domain is critical for CDNF endocytosis. Following internalization, CDNF traffics primarily to lysosomes, with a minor fraction localizing to mitochondria and the ER. Collectively, these findings identify exogenous CDNF - through its C-domain - as a novel cardiomyokine and highlight its therapeutic potential in cardiac injury and ER stress-related disorders via KDEL-R-mediated PI3K/AKT activation. - Source: PubMed
Publication date: 2026/01/24
de Oliveira Dahienne FerreiraMaciel LeonardoDos Santos Silva AntonioDa Coutinho Keyla CristinyPalhano Fernando LucasSantiago Marcelo FFoguel Debora - - Source: PubMed
Publication date: 2026/01/08
Song JieSun JiaYuYalikun AinizierZhou HongYuChen HuiLi Li