Recombinant Human GFRA1 /GDNFRA Protein
- Known as:
- Recombinant Human GFRA1 /GDNFRA Protein
- Catalog number:
- gf-876
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Proxinobio
- Gene target:
- Recombinant Human GFRA1 /GDNFRA Protein
Related genes to: Recombinant Human GFRA1 /GDNFRA Protein
- Gene:
- GFRA1 NIH gene
- Name:
- GDNF family receptor alpha 1
- Previous symbol:
- GDNFRA
- Synonyms:
- RETL1, GDNFR, GFR-ALPHA-1, RET1L, TRNR1
- Chromosome:
- 10q25.3
- Locus Type:
- gene with protein product
- Date approved:
- 1997-01-17
- Date modifiied:
- 2016-10-05
Related products to: Recombinant Human GFRA1 /GDNFRA Protein
Related articles to: Recombinant Human GFRA1 /GDNFRA Protein
- Although circadian disruption has been implicated in gynecologic malignancies, genetic evidence for a causal relationship between insomnia and ovarian cysts remains lacking. The biological pathways linking sleep disturbance to ovarian pathology are therefore poorly understood, limiting mechanistic insights and therapeutic development. - Source: PubMed
Publication date: 2026/03/11
Geng HaiyanWu HaoLiu MingZhu JianjunSong Lili - Studies have shown that substance use liability is associated with novelty seeking, anxiety-like behavior, and pain sensitivity. We examined whether common genetic variation in outbred Sprague-Dawley rats explained variation in behavioral measures from three assays with established links to substance use: locomotor response to a novel environment, elevated plus maze, and tail flick. We estimated single-nucleotide polymorphism heritability and performed genome-wide association analyses using permutation-derived significance thresholds (N=534-654 rats across traits). Heritability estimates ranged from 0.14-0.38 across eleven traits. Three independent loci were identified: chromosome 1 for elevated plus maze open-arm behavior (α=0.05), chromosome 14 for elevated plus maze immobility (α=0.10), and chromosome 17 for tail flick latency (α=0.05). Candidate genes included , , and (chromosome 1); and (chromosome 14); and and (chromosome 17). We compared these loci with our genome wide association study of a F intercross of selectively bred high- and low-responder rats, originally derived from Sprague-Dawleys, that model individual differences in externalizing and internalizing behavior. The current loci are distinct from the ones identified in the bred lines. This difference likely reflects selection history in the high- and low-responder Fs, which focused on facets of exploratory locomotion, while loci for anxiety and pain sensitivity traits were identified in the outbreds. This highlights the benefit of using both outbred and selectively bred rats to probe causal variants contributing to individual differences in substance use liability. The current outbred findings implicate monoaminergic signaling, transcriptional control, and lipid metabolism as testable mechanisms for addiction-relevant behaviors. - Source: PubMed
Publication date: 2026/02/19
Chitre Apurva SHebda-Bauer Elaine KEmery Michael ALi FeiNguyen Khai-MinhWang YizhiCheng RiyanPolesskaya OksanaWatson Stanley JLi JunAkil HudaPalmer Abraham A - To characterize the prenatal phenotypic spectrum, genetic findings, and pregnancy outcomes of fetal renal agenesis (RA), and to clarify the complementary roles of chromosomal microarray analysis (CMA) and whole exome sequencing (WES) in phenotype-stratified prenatal evaluation. - Source: PubMed
Publication date: 2026/01/31
Zhang NaHuang RuibinFu FangZhou HangLi RuLiao Can - The rotator cuff is a group of four muscles in the shoulder, which aid in movement and rotation of the upper arm. Rotator cuff tears (RCTs) within tendons of these muscles are common musculoskeletal injuries, often resulting in intramuscular fat, fibrosis, and muscle atrophy. Fatty infiltration specifically correlates with high rates of retear following repair. The cellular sources and molecular cues that cause these pathologies are unknown and therefore non-surgical cell/drug therapies for RCTs do not exist. Thus, we first sought to determine the cellular source(s) and molecular underpinnings of fatty atrophy and fibrosis associated with massive RCTs. Using a murine model of massive RCTs combined with lineage tracing, we demonstrate that muscle resident non-myogenic mesenchymal cells (NMMCs) are responsible for the fatty and fibrotic RCT pathologies. Utilizing sorted cells from rotator cuff muscles and "deep" single cell RNA-sequencing, we identified a specific cell population associated with RCT-induced fibrosis, while nerve-associated NMMCs are drivers of the RCT-induced intramuscular fat pathology. Finally, we demonstrate that RCT-induced fatty infiltration occurs at least partially via the loss of GDNF-GFRA1-RET signaling, since local treatment of murine RCTs with a small molecule RET agonist reduces development of the RCT-induced intramuscular fat. - Source: PubMed
Publication date: 2026/02/13
Rueckert HelenMirando Anthony JLeinroth Abigail PIbarra JulianaChakkalakal Joe VHilton Matthew J - Multiple symptoms have been observed in COVID-19 patients, including migraine and facial pain which may result from the sensitization of the trigeminal ganglion (TG) and brainstem. Recent studies suggest that SARS-CoV-2 may invade trigeminal nerve endings in the nasal cavity. However, despite these insights, the precise underlying mechanisms remain poorly understood. Here, we investigated the cellular and molecular changes in the TG and brainstem with a special attention for the spinal trigeminal nucleus in the K18-hACE2 mouse model infected with SARS-CoV-2. We first confirmed the expression of the cellular proteins playing a role in SARS-CoV-2 cell entry (ACE2, TMPRSS2, and NRP1) in both structures. We reported the expression of the viral nucleocapsid (N) and spike (S) proteins in TG and brainstem at 6 days post infection by multimodal approaches (RNAseq, RNAscope, and immunofluorescence). In the TG, S and N proteins were detected in nerve fibers as well as in TRPV1 and CGRP nociceptive neurons. Transcriptomic analyses of the TG from infected K18-hACE2 revealed significant changes in gene expression, including , , , , and genes. Additionally, increased immunoreactivity for ATF3 and Iba1 was detected in the TG of infected mice. In the brainstem, SARS-CoV-2 protein was exclusively found in neurons, with no detection in astrocytes or microglial cells, the latter exhibiting an activated form in SARS-CoV-2 mice. Bulk RNA-Seq analysis revealed a robust inflammatory response characterized by cytokine and chemokine storm, inflammasome activation (, ,, and ), markers of neuronal activation (, , ), neuronal injury (), and pain-associated genes (, , , , ). As found in the TG, we observed that infected neurons were found within a dense network of CGRP nociceptive nerve fibers in the trigeminal brainstem. Finally, we provided gene interaction networks and identified specific SARS-CoV-2 biomarkers , , ,, and in TG and brainstem, which could serve as potential indicators of disease severity. In conclusion, this study reports a robust set of transcriptomic and cellular changes triggered by SARS-CoV-2 in the TG and brainstem, offering a potential mechanistic explanation for sensory abnormalities, such as migraine and pain, observed in COVID-19 patients. - Source: PubMed
Publication date: 2026/02/16
Huang JianReboussin ElodieBianchi LolaEnond ChristelleMorosan SerbanMalet IsabelleFouquet StéphaneGenestant EugénieBlond FrédéricRostène WilliamBaudouin ChristopheMelik Parsadaniantz StéphaneMarot StéphaneMarcelin Anne-GenevieveCayetanot FlorenceGuillonneau XavierBodineau LaurenceBourgeais-Rambur LaurenceRéaux-Le Goazigo Annabelle