GFRA3 _ GFR_alpha_3 Protein
- Known as:
- GFRA3 _ GFR_alpha_3 Protein
- Catalog number:
- 10213-H03H
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Smart Serology
- Gene target:
- GFRA3 _ GFR_alpha_3 Protein
Related genes to: GFRA3 _ GFR_alpha_3 Protein
- Gene:
- GFRA3 NIH gene
- Name:
- GDNF family receptor alpha 3
- Previous symbol:
- -
- Synonyms:
- GFRa-3
- Chromosome:
- 5q31.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-02-27
- Date modifiied:
- 2016-10-05
Related products to: GFRA3 _ GFR_alpha_3 Protein
Related articles to: GFRA3 _ GFR_alpha_3 Protein
- Degenerative Joint Disease (DJD) is a form of highly prevalent osteoarthritis in humans and animals, including cats, which causes significant pain and hypersensitivity. Despite its prevalence, the mechanisms underlying the DJD-associated pain in cats are poorly understood. While transient receptor potential (TRP) ion channels are expressed in the dorsal root ganglia (DRG) and are implicated in osteoarthritis pain (e.g., through Artemin/GFRA3-mediated changes to TRPV1 and TRPA1 electrical properties), there is currently only indirect evidence of TRP ion channel expression in the feline DRG. This study aims to address this knowledge gap. - Source: PubMed
Publication date: 2026/03/17
Wheeler Joshua JTamamoto-Mochizuki ChieGruen Margaret ELascelles B Duncan XMishra Santosh K - Although inflammatory processes in rheumatoid arthritis have been described, mechanisms driving pain are poorly defined. Here, we used a multitude of approaches to uncover the neural basis and causes of inflammatory pain. We show in mice with cartilage autoantibody-induced arthritis that early immune activation and a cytokine storm were mainly driven by vascular cells and monocytes/macrophages in the dorsal root ganglion. However, persistently elevated interferons and receptor activation of the MNK1/MNK2-eIF4E signaling pathway at all disease phases caused sensory-motor dysfunction and pain by inducing hyperexcitability and sensitization of a GFRA3 C-fiber subtype of joint-innervating sensory neurons. Signaling pathway inhibition in vivo reversed pain and restored limb function. Like mice, human sensory neurons expressed interferon receptors, and type 1 interferons and signaling were increased only in individuals with painful rheumatoid arthritis. The finding that joint pain before and during arthritis is caused by a defined cytokine and signaling pathway holds promise for targeted therapies for pain relief in arthritis. - Source: PubMed
Publication date: 2026/03/10
Su JieZhang Ming-DongKupari JussiKwak DongohPicton LaurenceXu Bingzedo Nascimento Leandro FloresHu YizhouGonzalez AlejandroUsoskin DmitryXu ZhongweiSzczot MarcinEl Manira AbdeljabbarHolmdahl RikardErnfors Patrik - This study aimed to elucidate IL-17 inhibitors' mechanisms in psoriasis, offering a theoretical basis for tackling clinical issues like treatment resistance and relapse. - Source: PubMed
Publication date: 2025/12/25
Wei YanLiu MengMou Kuan-HouWang Li-JuanZheng Yan - Glioblastoma is the most frequent and aggressive primary brain cancer in adults, and the prognosis is poor. The neurotrophic factor glial cell-derived neurotrophic factor (GDNF) and its receptors, which are involved in neuronal development, have in experimental studies been suggested to drive tumorigenic processes in glioblastoma, but the role and expression in glioblastoma in patients is under-investigated. The aim of this study was to investigate the expression of GDNF, GDNF family receptor 1-4 (GFRA1-4), and the downstream REarranged during Transfection (RET) receptor in human glioblastoma tissue by RNA in situ hybridization, immunohistochemistry, and immunofluorescence. Expression was quantified by software-based classifiers. The results showed that GDNF was expressed in approximately 10% of tumor cells. The GFRA1 receptor was widely expressed in tumor cells, often colocalizing with the astrocytic tumor cell marker glial fibrillary acidic protein (GFAP), and in a smaller fraction of tumor cells expressing the stem cell markers oligodendrocyte transcription factor 2 (OLIG2) and SRY-Box Transcription Factor 2 (SOX2). The GFRA2 receptor expression was very limited, whereas expression of GFRA3, GFRA4, and RET, respectively, was almost absent. In conclusion, GDNF and its primary receptor GFRA1 were expressed in patient glioblastoma tissue. Potential clinical value needs further investigation. - Source: PubMed
Publication date: 2025/09/28
Ewald Jesper DupontKnudsen Arnon MøldrupWohlleben HelleChristiansen LoneMichaelsen Signe RegnerAnand AtulKristensen Bjarne Winther - Human-induced pluripotent stem cell (hiPSC) technology enables generation of various cell types, offering significant potential for regenerative medicine and personalized disease modeling. However, optimizing the functional maturity of differentiated cells is crucial for improving their reliability in research. Here, we introduce a deep-proteomics-based "receptor-ligand matching" (RLM) strategy to inventory surface receptors on differentiated cells and adjust the culture conditions accordingly. Focusing on an NGN2-induced neuron (iN) model, which rapidly produces glutamatergic neurons but exhibits modest synaptic activity, we identified 3,934 iN membrane proteins, including dozens of growth factor receptors and, notably, the complete GDNF receptor family (GFRA1, GFRA2, and GFRA3) previously undetected. Supplementing culture media with selected ligands enhanced neuronal health, neurite density, and synaptogenesis. Electrophysiology measurements confirmed greater functional synaptic maturity and responsiveness in optimized iNs compared to conventionally generated iNs. The RLM strategy offers a versatile approach to enhance the health and functionality of potentially any hiPSC-derived cell type. - Source: PubMed
Publication date: 2025/08/21
Dimitrov DimitarLien YiHori TetsuyaGoda YukikoRosenmund ChristianTaoufiq Zacharie