Ask about this productRelated genes to: GRK1 antibody
- Gene:
- GRK1 NIH gene
- Name:
- G protein-coupled receptor kinase 1
- Previous symbol:
- RHOK
- Synonyms:
- GPRK1, RK
- Chromosome:
- 13q34
- Locus Type:
- gene with protein product
- Date approved:
- 1994-07-21
- Date modifiied:
- 2014-11-18
Related products to: GRK1 antibody
Related articles to: GRK1 antibody
- To describe novel variants in the G protein-coupled receptor kinase 1 () gene associated with Oguchi disease and to analyze the different multimodal imaging results. - Source: PubMed
Publication date: 2026/05/18
Molina Martín Julio CesarGarcía Gerardo P GarcíaCampos Mollo EzequielGarcía Navarro María MagdalenaMolina Martín Luis AlbertoDesco Esteban CarmenPiñero David P - - Source: PubMed
Publication date: 2026/03/02
Rana VipinRoy RupakTripathi Amit Nandan - This study aimed to report the clinical, electrophysiological, and genetic findings in two siblings of an Egyptian family with type 2 Oguchi disease, with multimodal imaging performed for proper evaluation. - Source: PubMed
Publication date: 2026/01/11
Fathy NadaElbagoury Nagham MAbdel-Hamid Mohamed SElKitkat Rania SShehab Azza A - Anthracnose is a highly contagious and destructive plant disease caused by Colletotrichum gloeosporioides. The objective of this study was to investigate the antifungal activity and mechanism of ginsenoside Rk1 (GRk1) against C. gloeosporioides. In vitro experiments demonstrated that GRk1 exhibited substantial antifungal activity, with EC values of 64.58 mg L, surpassing the plant-derived pesticide d-limonene. Additionally, GRk1 could effectively suppress the dissemination of anthracnose spots in postharvest fruit. By observing the microstructure of C. gloeosporioides, it was observed that the mycelium structure underwent notable changes, and autophagosomes engulfed the organelles in the experimental groups. Fluorescent staining revealed specific signals in mycelial autophagosomes, and Western Blot analysis confirmed the upregulation of the autophagy-related protein Atg8. These findings indicate that GRk1 may activate the autophagy process by promoting Atg8 expression. Proteomic analysis revealed that the expression of Sec20 and Mpv17 proteins was significantly downregulated, whose dysregulated expression is associated with the crosstalk between SNAREs and peroxisomes during vesicle trafficking and metabolic processes. Assessment of catalase (CAT) activity, hydrogen peroxide (H₂O₂) content, and superoxide anion (O₂) levels further demonstrated that GRk1 could disrupt intracellular reactive oxygen species (ROS) homeostasis in mycelia. Moreover, the introduction of the ROS scavenger N-acetylcysteine (NAC) markedly inhibited autophagy, indicating that GRk1 promotes autophagy by inducing oxidative stress. Collectively, GRk1 inhibits pathogens via the ROS-autophagy axis. These findings suggested that GRk1 holds potential as a promising alternative to fungicides for the biological control of anthracnose. - Source: PubMed
Publication date: 2025/09/30
Li Xin-YvLiu Yu-JieMeng Xian-HuaGong ChuYang Jun-LiQiang YinWang JunHou Xiu-Dan - Autosomal dominant retinitis pigmentosa (adRP) is an inherited retinal dystrophy characterized by progressive vision loss and eventual blindness. The P23H mutation (proline to histidine substitution at codon 23) in the rhodopsin (RHO) gene represents the most common form of adRP in North Americans. Currently, there is no cure for P23H adRP. Genome editing targeting the mutant RHO allele, leaving a functional wildtype (WT) allele, is an attractive approach for P23H adRP, as only one copy of RHO is needed for normal retinal function. We re-engineered an I-Cre meganuclease, called RHO1-2, to target a 22bp recognition sequence encompassing the mutation responsible for the p.P23H RHO mutation. , RHO1-2, cuts human P23H RHO but not WT RHO. we delivered scAAV5:GRK1:RHO1-2 via subretinal injection in early-stage degeneration using the only large animal model of human p.P23H RHO adRP (TgP23H pigs). We tested RHO1-2 efficacy and durability, on retinal function using full-field electroretinograms and on retinal structure using spectral domain optical coherence tomography and immunohistochemistry. We observe that RHO1-2 treatment: arrests rod photoreceptor degeneration, resurrects rod-driven retinal function that does not exist in untreated TgP23H pigs, restores mislocalized rhodopsin expression and rebuilds rod inner and outer segments (IS/OS). Rod rescue maintains cones. A year after RHO1-2 treatment, we show that TgP23H pigs use rod-driven vision to navigate a maze. Our results demonstrate that genome editing via RHO1-2 meganuclease is a viable treatment to cure human p.P23H RHO adRP. They also suggest that meganuclease-based editors can be effective for other IRDs. - Source: PubMed
Publication date: 2025/09/25
Jalligampala ArchanaYoung Jacob MFeist JackWang WeiBarone FrancescaAlston David CFransen James WJaikumar GitaKamboj KautukMooreman CaitlinNash StephenNoel Jennifer MPangeni GobindaPrestigiacomo Joseph CSahu BhubananandaTurner CaitlinKaplan Henry JGreen Jonathan AWells Kevin DBartsevich Victor VChatterton Jon EDavis MaraEvans Kathryn SLape JanelLewis Whitney Cvan de Beek RebeccaViles Kristi DJantz DerekGregg Ronald GSmith JeffMcCall Maureen A