ArticleCell biochemistry and biophysics2026
Comparative Phosphoproteomic Profiling and Network-based Interactome Analysis of GRK5 and GRK6.
Article in Cell biochemistry and biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Integrative analysis of YTHDC1 phosphoproteome unveils its phosphomodulatory network linked to splicing and tumorigenesis.Frontiers in bioinformatics · 2026Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
G protein-coupled receptor kinases GRK5 and GRK6 are pivotal regulators of cellular signaling, extending beyond GPCR desensitization to modulate non-receptor pathways critical for neuronal development, immune responses, and oncogenic processes. Leveraging a comprehensive analysis of 3825 human phosphoproteomic datasets, this study identifies predominant phosphorylation sites (pS484 and pT485 in GRK5, pS484 in GRK6) and elucidates their co-phosphoregulated proteins, substrates, and interaction networks. Shared co-phosphoregulated proteins, including BRD9 and RBBP6, underscore conserved roles in mRNA processing and cellular proliferation, essential for maintaining tissue homeostasis and implicated in cancer progression. Divergent functions potentially emerge from sequence distinctions like nuclear localization signal in GRK5 driving neuronal-specific regulation via substrates like MAP1B (cytoskeletal remodeling) and ATRX (chromatin dynamics), while GRK6 palmitoylation anchors immune modulation through targets such as GIT1 (cell migration) and HSP90AA1 (inflammation). Proteogenomic profiling reveals upregulation of both kinases, particularly at pS484, in breast cancer, positioning them as oncogenic drivers in tumor growth and metastasis. These findings illuminate how GRK5 and GRK6 orchestrate balanced yet specialized signaling networks, offering biologically grounded insights for targeted therapies in neurological disorders, autoimmune conditions, and aggressive cancers like triple-negative breast cancer.
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Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.