ArticleEMBO reports2022
Histidine dephosphorylation of the Gβ protein GPB-1 promotes axon regeneration in C. elegans.
Article in EMBO reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Article
- A phosphohistidine phosphatase promotes starvation survival by dephosphorylating nucleoside diphosphate kinase.Cell reports · 2026Article
- Using phage display for rational engineering of a higher-affinity humanized 3' phosphohistidine-specific antibody.Communications chemistry · 2025Article
- Review
- Mechanistic Insights into Substrate Recognition of Human Nucleoside Diphosphate Kinase C Based on Nucleotide-Induced Structural Changes.International journal of molecular sciences · 2024Article
- Histidine Phosphorylation: Protein Kinases and Phosphatases.International journal of molecular sciences · 2024Review
- PRUNE1 and NME/NDPK family proteins influence energy metabolism and signaling in cancer metastases.Cancer metastasis reviews · 2024Review
- Histidine dephosphorylation of the Gβ protein GPB-1 promotes axon regeneration in C. elegans.EMBO reports · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Histidine phosphorylation is an emerging noncanonical protein phosphorylation in animals, yet its physiological role remains largely unexplored. The protein histidine phosphatase (PHPT1) was recently identified for the first time in mammals. Here, we report that PHIP-1, an ortholog of PHPT1 in Caenorhabditis elegans, promotes axon regeneration by dephosphorylating GPB-1 Gβ at His-266 and inactivating GOA-1 Goα signaling, a negative regulator of axon regeneration. Overexpression of the histidine kinase NDK-1 also inhibits axon regeneration via GPB-1 His-266 phosphorylation. Thus, His-phosphorylation plays an antiregenerative role in C. elegans. Furthermore, we identify a conserved UNC-51/ULK kinase that functions in autophagy as a PHIP-1-binding protein. We demonstrate that UNC-51 phosphorylates PHIP-1 at Ser-112 and activates its catalytic activity and that this phosphorylation is required for PHIP-1-mediated axon regeneration. This study reveals a molecular link from ULK to protein histidine phosphatase, which facilitates axon regeneration by inhibiting trimeric G protein signaling.
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