ArticleScientific reports2018
On-target action of anti-tropomyosin drugs regulates glucose metabolism.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 27 citations in OpenAlex.
- HIF-1-regulated TPM3 links hypoxia to motility and invasion beyond the hypoxic fraction in triple-negative breast cancer.NPJ breast cancer · 2026Article
- A truncation mutant of adenomatous polyposis coli impairs apical cell extrusion through elevated epithelial tissue tension.Cytoskeleton (Hoboken, N.J.) · 2025Article
- The tropomyosin 3.1/3.2 inhibitor ATM-3507 alters B-cell actin dynamics and impairs the growth and motility of diffuse large B-cell lymphoma cell lines.Frontiers in immunology · 2025Article
- Preexisting tissue mechanical hypertension at adherens junctions disrupts apoptotic extrusion in epithelia.Molecular biology of the cell · 2024Article
- Motor properties of Myosin 5c are modulated by tropomyosin isoforms and inhibited by pentabromopseudilin.Frontiers in physiology · 2024Article
- Research Advances in the Role of the Tropomyosin Family in Cancer.International journal of molecular sciences · 2023Review
- TPM2 attenuates progression of prostate cancer by blocking PDLIM7-mediated nuclear translocation of YAP1.Cell & bioscience · 2023Article
- Stress deprivation of tendon explants or Tpm3.1 inhibition in tendon cells reduces F-actin to promote a tendinosis-like phenotype.Molecular biology of the cell · 2022Article
- Integration of single-cell datasets reveals novel transcriptomic signatures of β-cells in human type 2 diabetes.NAR genomics and bioinformatics · 2020Article
- Tropomyosin Tpm3.1 Is Required to Maintain the Structure and Function of the Axon Initial Segment.iScience · 2020Article
- Targeting and extending the eukaryotic druggable genome with natural products: cytoskeletal targets of natural products.Natural product reports · 2020Review
- Tropomodulins Control the Balance between Protrusive and Contractile Structures by Stabilizing Actin-Tropomyosin Filaments.Current biology : CB · 2020Article
- A new twist on tropomyosin binding to actin filaments: perspectives on thin filament function, assembly and biomechanics.Journal of muscle research and cell motility · 2020Review
- Actin-tropomyosin distribution in non-muscle cells.Journal of muscle research and cell motility · 2020Review
- Molecular integration of the anti-tropomyosin compound ATM-3507 into the coiled coil overlap region of the cancer-associated Tpm3.1.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of novel small molecule inhibitors of the cancer-associated tropomyosin 3.1 (Tpm3.1) provides the ability to examine the metabolic function of specific actin filament populations. We have determined the ability of these anti-Tpm (ATM) compounds to regulate glucose metabolism in mice. Acute treatment (1 h) of wild-type (WT) mice with the compounds (TR100 and ATM1001) led to a decrease in glucose clearance due mainly to suppression of glucose-stimulated insulin secretion (GSIS) from the pancreatic islets. The impact of the drugs on GSIS was significantly less in Tpm3.1 knock out (KO) mice indicating that the drug action is on-target. Experiments in MIN6 β-cells indicated that the inhibition of GSIS by the drugs was due to disruption to the cortical actin cytoskeleton. The impact of the drugs on insulin-stimulated glucose uptake (ISGU) was also examined in skeletal muscle ex vivo. In the absence of drug, ISGU was decreased in KO compared to WT muscle, confirming a role of Tpm3.1 in glucose uptake. Both compounds suppressed ISGU in WT muscle, but in the KO muscle there was little impact of the drugs. Collectively, this data indicates that the ATM drugs affect glucose metabolism in vivo by inhibiting Tpm3.1's function with few off-target effects.
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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.