ArticleJournal of molecular modeling2012
A selectivity study on mTOR/PI3Kα inhibitors by homology modeling and 3D-QSAR.
Article in Journal of molecular modeling, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
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.
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Who cites it
6 citing papers in PubMed.
- An Updated Review on Developing Small Molecule Kinase Inhibitors Using Computer-Aided Drug Design Approaches.International journal of molecular sciences · 2023Review
- Design, Synthesis, Biological Evaluation, and Molecular Modeling of 2-Difluoromethylbenzimidazole Derivatives as Potential PI3Kα Inhibitors.Molecules (Basel, Switzerland) · 2022Article
- Development of Multi-Target Chemometric Models for the Inhibition of Class I PI3K Enzyme Isoforms: A Case Study Using QSAR-Co Tool.International journal of molecular sciences · 2019Article
- Design and Validation of FRESH, a Drug Discovery Paradigm Resting on Robust Chemical Synthesis.ACS medicinal chemistry letters · 2015Article
- Determination and validation of mTOR kinase-domain 3D structure by homology modeling.OncoTargets and therapy · 2015Article
- Targeting the Cellular Signaling: BRAF Inhibition and Beyond for the Treatment of Metastatic Malignant Melanoma.Dermatology research and practice · 2012Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The phosphatidylinositol-3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway plays a critical role in the regulation of cellular growth, survival and proliferation. mTOR and PI3K have attracted particular attention as cancer targets. These kinases belong to the phosphatidylinositol-3-kinase-related kinase (PIKK) family and therefore have considerable homology in their active sites. To accelerate the discovery of inhibitors with selective activity against mTOR and PI3K as cancer targets, in this work, a homology model of mTOR was developed to identify the structural divergence in the active sites between mTOR and PI3Kα. Furthermore, two highly predictive comparative molecular similarity index analyses (CoMSIA) models were built based on 304 selective inhibitors docked into mTOR and PI3Kα, respectively (mTOR: q(2) = 0.658, r(pre)(2) = 0.839; PI3Kα: q(2) = 0.540, r(pre)(2) = 0.719). The results showed that steric and electrostatic fields have an important influence on selectivity towards mTOR and PI3Kα-a finding consistent with the structural divergence between the active sites. The findings may be helpful in investigating selective mTOR/PI3Kα inhibitors.
Indexed as
Identifiers
21523553What OpenQuestion holds
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.