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285 results for “Rapamycin”
Data from: Chronic Rapamycin administration via drinking water mitigates the pathological phenotype in a Krabbe disease mouse model through autophagy activation.
<p>ABSTRACT </p><p>Krabbe disease (KD) is a rare disorder caused by a deficiency of the lysosomal enzyme galactosylceramidase (GALC), resulting in the accumulation of the cytotoxic metabolite psychosine (PSY) in the nervous system. This accumulation triggers demyelination and neurodegeneration. Despite ongoing research, the underlying pathogenic mechanisms remain incompletely understood, and there is currently no cure available.</p><p>Previous studies from our lab revealed the presence of autophagy dysfunctions in KD pathogenesis, as evidenced by the presence of p62-tagged protein aggregates in the brains of KD mice and increased p62 levels in the KD sciatic nerve. We also demonstrated that the autophagy inducer Rapamycin (RAPA) can partially restore the wild-type (WT) phenotype in KD primary cells by reducing the number of p62 aggregates.</p><p>In this study, we tested RAPA in the Twitcher (TWI) mouse, a spontaneous KD mouse model. We administered the drug ad libitum via drinking water (15 mg/L) starting from post-natal day (PND) 21-23. We longitudinally monitored the motor performance of the mice through grip strength and rotarod tests, along with various biochemical parameters related to KD pathogenesis (i.e. autophagy markers expression, myelination, astrogliosis, and PSY accumulation).</p><p>Our findings demonstrate that RAPA significantly enhances motor functions at specific treatment time points and reduces astrogliosis in TWI brain, spinal cord, and sciatic nerves. Using western blot and immunohistochemistry, we observed a decrease in p62 aggregates in TWI nervous tissues, which corroborates our earlier in-vitro results. Furthermore, RAPA treatment partially reduces PSY levels in the spinal cord.</p><p>In conclusion, our results support the consideration of RAPA as a supportive therapy for KD. Importantly, as RAPA is already available in pharmaceutical formulations for clinical use, its potential for KD treatment can be promptly evaluated in clinical trials.</p>
Rapamycin rejuvenates oral health in aging mice
<p>Periodontal disease is an age-associated disorder clinically defined by periodontal bone loss, inflammation of the specialized tissues that surround and support the tooth, and microbiome dysbiosis. Currently, there is no therapy for reversing periodontal disease, and treatment is generally restricted to preventive measures or tooth extraction. The FDA-approved drug rapamycin slows aging and extends lifespan in multiple organisms, including mice. Here we demonstrate that short-term treatment with rapamycin rejuvenates the aged oral cavity of elderly mice, including regeneration of periodontal bone, attenuation of gingival and periodontal bone inflammation, and revertive shift of the oral microbiome toward a more youthful composition. This provides a geroscience strategy to potentially rejuvenate oral health and reverse periodontal disease in the elderly.</p>
Epigenetic aging signatures in mice livers are slowed by dwarfism, calorie restriction and rapamycin treatment
<p>Processed dataset and source data for iPython notebooks hosted by: https://doi.org/10.5281/zenodo.291961</p>
The social network of target of rapamycin complex 1 in plants
<p>The target of rapamycin complex 1 (TORC1) is a highly conserved serine–threonine protein kinase crucial for coordinating growth according to nutrient availability in eukaryotes. It works as a central integrator of multiple nutrient inputs such as sugar, nitrogen, and phosphate and promotes growth and biomass accumulation in response to nutrient sufficiency. Studies, especially in the past decade, have identified the central role of TORC1 in regulating growth through interaction with hormones, photoreceptors, and stress-signaling machinery in plants. In this review, we comprehensively analyse the interactome and phosphoproteome of the Arabidopsis TORC1 signaling network. Our analysis highlights the role of TORC1 as a central hub kinase communicating with the transcriptional and translational apparatus, ribosomes, chaperones, protein kinases, metabolic enzymes, and autophagy and stress response machinery to orchestrate growth in response to nutrient signals. This analysis also suggests that along with the conserved downstream components shared with other eukaryotic lineages, plant TORC1 signaling underwent several evolutionary innovations and co-opted many lineage-specific components. Based on the protein–protein interaction and phosphoproteome data, we also discuss several uncharacterized and unexplored components of the TORC1 signaling network, highlighting potential links for future studies.</p>
Data from: Pooled genome-wide CRISPR activation screening for rapamycin resistance genes in Drosophila cells
<p>Loss-of-function and gain-of-function genetic perturbations provide valuable insights into gene function. In <em>Drosophila</em> cells, while genome-wide loss-of-function screens have been extensively used to reveal mechanisms of a variety of biological processes, approaches for performing genome-wide gain-of-function screens are still lacking. Here, we describe a pooled CRISPR activation (CRISPRa) screening platform in <em>Drosophila</em> cells and apply this method to both focused and genome-wide screens to identify rapamycin resistance genes. The screens identified three genes as novel rapamycin resistance genes: a member of SLC16 family of monocarboxylate transporters (<em>CG8468)</em>, a member of the lipocalin protein family (<em>CG5399</em>), and a zinc finger C2H2 transcription factor (<em>CG9932</em>). Mechanistically, we demonstrate that <em>CG5399</em> overexpression activates the RTK-Akt-mTOR signaling pathway and that activation of insulin receptor (InR) by <em>CG5399</em> requires cholesterol and clathrin-coated pits at the cell membrane. This study establishes a novel platform for functional genetic studies in <em>Drosophila</em> cells.</p>
Rapamycin Therapy in Head and Neck Squamous Cell Carcinoma
ClinicalTrials.gov study NCT01195922. IPD Sharing: NO. Countries: 1. Publications: 3.
Prospective Study of Rapamycin for the Treatment of SLE
ClinicalTrials.gov study NCT00779194. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Rapamycin Versus Mycophenolate Mofetil in Kidney-Pancreas Recipients
ClinicalTrials.gov study NCT00533442. IPD Sharing: Not stated. Countries: 1. Publications: 4.
Nanoparticle Albumin-Bound Rapamycin, Temozolomide, and Irinotecan Hydrochloride in Treating Pediatric Patients With Recurrent or Refractory Solid Tumors
ClinicalTrials.gov study NCT02975882. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Study of Oral Rapamycin Plus Bare Metal Stents vs Drug Eltuting Stents
ClinicalTrials.gov study NCT00552669. IPD Sharing: Not stated. Countries: 1. Publications: 39.
RAPAMYCIN FOR KIDNEY ANGIOMYOLIPOMAS
ClinicalTrials.gov study NCT00126672. IPD Sharing: NO. Countries: 1. Publications: 2.
Topical Rapamycin to Erase Angiofibromas in TSC
ClinicalTrials.gov study NCT01526356. IPD Sharing: Not stated. Countries: 2. Publications: 1.
Pilot Study of Rapamycin as Treatment for Autosomal Dominant Polycystic Kidney Disease (ADPKD)
ClinicalTrials.gov study NCT00286156. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Cognition, Age, and RaPamycin Effectiveness - DownregulatIon of thE mTor Pathway
ClinicalTrials.gov study NCT04200911. IPD Sharing: YES. Countries: 1. Publications: 1.
Dose-Ranging Efficacy and Safety Study of Topical Rapamycin Cream for Facial Angiofibroma Associated With Tuberous Sclerosis Complex
ClinicalTrials.gov study NCT03826628. IPD Sharing: NO. Countries: 9. Publications: 1.
Nivolumab (Opdivo®) Plus ABI-009 (Nab-rapamycin) for Advanced Sarcoma and Certain Cancers
ClinicalTrials.gov study NCT03190174. IPD Sharing: NO. Countries: 1. Publications: 2.
Study of Decitabine in Combination With Sequential Rapamycin or Ribavirin in High Risk AML Patients
ClinicalTrials.gov study NCT02109744. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Rapamycin as a Means of Interference With Reconsolidation of Posttraumatic Stress Disorder-related Traumatic Memory
ClinicalTrials.gov study NCT01449955. IPD Sharing: Not stated. Countries: 1. Publications: 2.
Multi-omic, histopathologic, and clinicopathologic effects of once-weekly oral rapamycin in a naturally occurring feline model of hypertrophic cardiomyopathy: A pilot study
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Data from: Pooled genome-wide CRISPR activation screening for rapamycin resistance genes in Drosophila cells
Open the record for dataset details and reuse information.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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