ArticleCell reports2014
Botch is a γ-glutamyl cyclotransferase that deglycinates and antagonizes Notch.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 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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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Hepatic glutathione depletion ameliorates MASLD through selective protein oxidation and inhibition of lipogenesis.The Journal of clinical investigation · 2026Article
- The Paulinella chromatophore transit peptide part2 adopts a structural fold similar to the γ-glutamyl-cyclotransferase fold.Plant physiology · 2025Article
- The strategic breakdown: CHAC enzymes as regulators of glutathione homeostasis and disease implications.Frontiers in molecular biosciences · 2025Review
- CHAC1: a master regulator of oxidative stress and ferroptosis in human diseases and cancers.Frontiers in cell and developmental biology · 2024Review
- Inhibition of the NOTCH and mTOR pathways by nelfinavir as a novel treatment for T cell acute lymphoblastic leukemia.International journal of oncology · 2023Article
- Fucosyltransferase 9 promotes neuronal differentiation and functional recovery after spinal cord injury by suppressing the activation of Notch signaling.Acta biochimica et biophysica Sinica · 2023Article
- Characterization of the 5'-flanking region of the human and mouse CHAC1 genes.Biochemistry and biophysics reports · 2020Article
- YTHDF2 destabilizes mRNA (New York, N.Y.) · 2020Article
- Structural and Functional Analyses of Human ChaC2 in Glutathione Metabolism.Biomolecules · 2019Article
- Ras Downstream Effector GGCT Alleviates Oncogenic Stress.iScience · 2019Article
- Mesenchymal stem cells alleviate the early brain injury of subarachnoid hemorrhage partly by suppression of Notch1-dependent neuroinflammation: involvement of Botch.Journal of neuroinflammation · 2019Article
- Genetic Control of Rod Bipolar Cell Number in the Mouse Retina.Frontiers in neuroscience · 2018Article
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- ChaC2, an Enzyme for Slow Turnover of Cytosolic Glutathione.The Journal of biological chemistry · 2017Article
- Importance of rare gene copy number alterations for personalized tumor characterization and survival analysis.Genome biology · 2016Article
- Lens ER-stress response during cataract development in Mip-mutant mice.Biochimica et biophysica acta · 2016Article
- Translational and post-translational regulation of mouse cation transport regulator homolog 1.Scientific reports · 2016Article
- RipAY, a Plant Pathogen Effector Protein, Exhibits Robust γ-Glutamyl Cyclotransferase Activity When Stimulated by Eukaryotic Thioredoxins.The Journal of biological chemistry · 2016Article
- Human CHAC1 Protein Degrades Glutathione, and mRNA Induction Is Regulated by the Transcription Factors ATF4 and ATF3 and a Bipartite ATF/CRE Regulatory Element.The Journal of biological chemistry · 2015Article
Corrections and comments
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Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
Botch promotes embryonic neurogenesis by inhibiting the initial S1 furin-like cleavage step of Notch maturation. The biochemical process by which Botch inhibits Notch maturation is not known. Here, we show that Botch has γ-glutamyl cyclotransferase (GGCT) activity that deglycinates Notch, which prevents the S1 furin-like cleavage. Moreover, Notch is monoglycinated on the γ-glutamyl carbon of glutamate 1,669. The deglycinase activity of Botch is required for inhibition of Notch signaling both in vitro and in vivo. When the γ-glutamyl-glycine at position 1,669 of Notch is degylcinated, it is replaced by 5-oxy-proline. These results reveal that Botch regulates Notch signaling through deglycination and identify a posttranslational modification of Notch that plays an important role in neurogenesis.
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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.