ArticleInvestigational new drugs2013
A novel proteasome inhibitor acting in mitochondrial dysfunction, ER stress and ROS production.
Article in Investigational new drugs, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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
18 citing papers in PubMed.
- Proteasomal degradation of intracellularly expressed Amblyomin-X limits suicide gene therapy potential in melanoma cells.FEBS open bio · 2026Article
- Biochemical Characterization of a Kunitz-Type Protease Inhibitor From Mimosa regnellii and Its Effects on Melanoma Cell Viability and Angiogenesis.Chemistry & biodiversity · 2026Article
- Tick Salivary Kunitz-Type Inhibitors: Targeting Host Hemostasis and Immunity to Mediate Successful Blood Feeding.International journal of molecular sciences · 2023Review
- Structural and functional properties of the Kunitz-type and C-terminal domains of Amblyomin-X supporting its antitumor activity.Frontiers in molecular biosciences · 2023Article
- A novel 8-hydroxyquinoline derivative induces breast cancer cell death through paraptosis and apoptosis.Apoptosis : an international journal on programmed cell death · 2022Article
- A Kunitz-type inhibitor from tick salivary glands: A promising novel antitumor drug candidate.Frontiers in molecular biosciences · 2022Review
- Insights into the Role of Tick Salivary Protease Inhibitors during Ectoparasite-Host Crosstalk.International journal of molecular sciences · 2021Review
- Amblyomin-X, a recombinant Kunitz-type inhibitor, regulates cell adhesion and migration of human tumor cells.Cell adhesion & migration · 2020Article
- Modulation of stress and immune response by Amblyomin-X results in tumor cell death in a horse melanoma model.Scientific reports · 2020Article
- New therapeutic target for pediatric anaplastic ependymoma control: study of anti-tumor activity by a Kunitz-type molecule, Amblyomin-X.Scientific reports · 2019Article
- Deciphering Biological Processes at the Tick-Host Interface Opens New Strategies for Treatment of Human Diseases.Frontiers in physiology · 2019Review
- Preclinical evaluation of Amblyomin-X, a Kunitz-type protease inhibitor with antitumor activity.Toxicology reports · 2019Article
- Honokiol induces apoptosis and autophagy via the ROS/ERK1/2 signaling pathway in human osteosarcoma cells in vitro and in vivo.Cell death & disease · 2018Article
- Inhibition of PTEN Attenuates Endoplasmic Reticulum Stress and Apoptosis via Activation of PI3K/AKT Pathway in Alzheimer's Disease.Neurochemical research · 2017Article
- Promising pharmacological profile of a Kunitz-type inhibitor in murine renal cell carcinoma model.Oncotarget · 2016Article
- Amblyomin-X induces ER stress, mitochondrial dysfunction, and caspase activation in human melanoma and pancreatic tumor cell.Molecular and cellular biochemistry · 2016Article
- Inhibition of metabotropic glutamate receptor 5 induces cellular stress through pertussis toxin-sensitive Gi-proteins in murine BV-2 microglia cells.Journal of neuroinflammation · 2014Article
- Exendin-4 attenuates endoplasmic reticulum stress through a SIRT1-dependent mechanism.Cell stress & chaperones · 2014Article
Corrections and comments
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Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In cancer-treatment, potentially therapeutic drugs trigger their effects through apoptotic mechanisms. Generally, cell response is manifested by Bcl-2 family protein regulation, the impairment of mitochondrial functions, and ROS production. Notwithstanding, several drugs operate through proteasome inhibition, which, by inducing the accumulation and aggregation of misfolded or unfolded proteins, can lead to endoplasmic reticulum (ER) stress. Accordingly, it was shown that Amblyomin-X, a Kunitz-type inhibitor identified in the transcriptome of the Amblyomma cajennense tick by ESTs sequence analysis of a cDNA library, obtained in recombinant protein form, induces apoptosis in murine renal adenocarcinoma (RENCA) cells by: inducing imbalance between pro- and anti-apoptotic Bcl-2 family proteins, dysfunction/mitochondrial damage, production of reactive oxygen species (ROS), caspase cascade activation, and proteasome inhibition, all ER-stress inductive. Moreover, there was no manifest action on normal mouse-fibroblast cells (NHI3T3), suggesting an Amblyomin-X tumor-cell selectivity. Taken together, these evidences indicate that Amblyomin-X could be a promising candidate for cancer therapy.
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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.