ReviewDrug metabolism reviews2011
Regulatory functions of glutathione S-transferase P1-1 unrelated to detoxification.
Review in Drug metabolism reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.
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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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
56 citing papers in PubMed, 1 synthesis or guideline pooled it, 117 citations in OpenAlex.
- Evaluation of common protein biomarkers involved in the pathogenesis of respiratory diseases with proteomic methods: A systematic review.Immunity, inflammation and disease · 2023Pooled it
- DLST-driven metabolic alterations link skin to blood glucose: A translational study from mouse to human.Molecular metabolism · 2026Article
- Innovative strategies to overcome cancer drug resistance: from nanodelivery systems to targeted therapeutics.Discover oncology · 2026Review
- Exosomal Cargo-Derived Mediators of Ovarian Cancer Chemoresistance.Molecular diagnosis & therapy · 2026Review
- Hydrophobic tagging: A promising paradigm for targeted protein degradation.Cell insight · 2026Review
- Impact of proteostasis workload on sensitivity to proteasome inhibitors in multiple myeloma.Clinical and experimental medicine · 2025Review
- Article
- Significance ofClinical Medicine Insights. Oncology · 2025Article
- GSTP1 knockdown induces metabolic changes affecting energy production and lipid balance in pancreatic cancer cells.Molecular & cellular oncology · 2025Article
- Upregulation of GSTP1 mediated by chimeric TFE3 promotes TFE3-tRCC progression by targeting JNK signaling pathway.World journal of surgical oncology · 2024Article
- Adaptations in glutathione-based redox protein signaling pathways and alcohol drinking across species.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Article
- Protein Oxidative Modifications in Neurodegenerative Diseases: From Advances in Detection and Modelling to Their Use as Disease Biomarkers.Antioxidants (Basel, Switzerland) · 2024Review
- Article
- Adaptive changes in tumor cells in response to reductive stress.Biochemical pharmacology · 2024Article
- Glutathione transferase P1 is modified by palmitate.PloS one · 2024Article
- Review
- The Multifaceted Role of Glutathione S-Transferases in Health and Disease.Biomolecules · 2023Review
- Global distribution of treatment resistance gene markers for leishmaniasis.Journal of clinical laboratory analysis · 2022Review
- Computational repurposing of therapeutic small molecules from cancer to pulmonary hypertension.Science advances · 2021Article
- Nrf2 activation does not affect adenoma development in a mouse model of colorectal cancer.Communications biology · 2021Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Glutathione S-transferase P1-1 (GSTP) is one member of the family of GSTs and is ubiquitously expressed in human tissues. The literature is replete with reports of high levels of GSTP linked either with cancer incidence or drug resistance, and yet no entirely cogent explanation for these correlations exists. The catalytic detoxification properties of the GST isozyme family have been a primary research focus for the last four decades. However, it has become apparent that they have undergone structural and functional convergence where evolutionary selective pressures have favored the emergence of noncatalytic properties of GSTP that has imbued this isozyme with expanded biological importance. For example, GSTP has now been linked with two cell-signaling functions that are critical to survival. Through protein:protein interactions, GSTP can sequester c-jun N-terminal kinase (JNK) and act as a negative regulator of this stress kinase. Pharmacologically, this activity has been linked with the activity of GSTP inhibitors in stimulating myeloproliferation. In addition, GSTP is linked with the forward S-glutathionylation reaction, a post-translational modification that impacts the function/activity of a number of proteins. Catalytic reversal of S-glutathionylation is well characterized, but the role of GSTP in catalyzing the forward reaction contributes to the "glutathionylation cycle." Moreover, GSTP is itself susceptible to S-glutathionylation, providing an autoregulatory loop for the cycle. Because oxidative stress regulates both S-glutathionylation and JNK-signaling pathways, such links may help to explain the aberrant patterns of GSTP expression in the cancer phenotype. As such, there is an ongoing preclinical and clinical platform of drug discovery and development around GSTP.
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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.