Strong reversal of the lung fibrosis disease signature by autotaxin inhibitor...Maté Ongenaert
Strong reversal of the lung fibrosis disease signature by autotaxin inhibitor GLPG1690 in a mouse model for IPF
Maté Ongenaert (Mechelen, Belgium), Maté Ongenaert, Sonia Dupont, Roland Blanqué, Reginald Brys, Ellen van der Aar, Bertrand Heckmann
ERS - European Respiratory Society International Congress 2016. Session: Therapeutic horizons: novel targets and pharmacological models
Background and objectives
GLPG1690 is a novel potent autotaxin (ATX) inhibitor shown to be efficacious in the mouse bleomycin (BLM) lung fibrosis model. Here, we analyze the impact of GLPG1690 on the gene expression signature in mouse fibrotic lung tissue.
Methods
Lung fibrosis was induced by intranasal administration of BLM. Animals were treated with GLPG1690 or vehicle.Whole superior right lung was used for RNA extraction. Full transcriptome analysis was performed using the Agilent SurePrint G3 mouse chip. Analysis was performed using empirical Bayes methods and linear models. Public human IPF expression data were re-analyzed.
Results
GLPG1690 strongly reduced lung fibrosis as shown by reduction of Ashcroft scores and collagen content. Microarray analysis of the lungs revealed that GLPG1690 strongly reversed the impact of gene expression caused by BLM (367 out of the 2375 probes). As GLPG1690 treatment affects 395 probes, this treatment effect is highly relevant in the model. Gene clusters affected by BLM treatment and reverted by GLPG1690 are related to extracellular matrix (such as Tnc and Spp1), collagen (Col3a1) and cytokines/chemokines (Cxcl12). Several of the affected genes are known to be involved in the development or progression of lung fibrosis in IPF patients.
Conclusions
These data provide further mechanistic understanding of the efficacy of ATX inhibition in a pre-clinical lung fibrosis model, highlighting a role for extracellular matrix and inflammation biology. These data strongly suggest that GLPG1690 may be beneficial in treating IPF patients and support its evaluation in a clinical study
The target of rapamycin (TOR) is a key modulator of ageing in different organisms, ranging from yeast to rodents, and it is likely that this function has been conserved also in humans (mTOR, mammalian target of rapamycin). The signaling pathway of mTOR senses and integrates a variety of environmental inputs to regulate not only the organismal growth but also its homeostasis. This pathway regulates many important cellular processes that are implicated in the appearance of age-related diseases including cancer, obesity, type 2 diabetes, and neurodegeneration in late life. Here, are been reviewed the recent knowledge in the understanding of the mTOR pathway and its role in ageing and disease. Special emphasis in mTORC1 will be done due to this particular complex can be modulated by some compounds such as rapamycin. Moreover, are going to be discussed pharmacological approaches to treat human pathologies related with mTORC1 deregulation.
Strong reversal of the lung fibrosis disease signature by autotaxin inhibitor...Maté Ongenaert
Strong reversal of the lung fibrosis disease signature by autotaxin inhibitor GLPG1690 in a mouse model for IPF
Maté Ongenaert (Mechelen, Belgium), Maté Ongenaert, Sonia Dupont, Roland Blanqué, Reginald Brys, Ellen van der Aar, Bertrand Heckmann
ERS - European Respiratory Society International Congress 2016. Session: Therapeutic horizons: novel targets and pharmacological models
Background and objectives
GLPG1690 is a novel potent autotaxin (ATX) inhibitor shown to be efficacious in the mouse bleomycin (BLM) lung fibrosis model. Here, we analyze the impact of GLPG1690 on the gene expression signature in mouse fibrotic lung tissue.
Methods
Lung fibrosis was induced by intranasal administration of BLM. Animals were treated with GLPG1690 or vehicle.Whole superior right lung was used for RNA extraction. Full transcriptome analysis was performed using the Agilent SurePrint G3 mouse chip. Analysis was performed using empirical Bayes methods and linear models. Public human IPF expression data were re-analyzed.
Results
GLPG1690 strongly reduced lung fibrosis as shown by reduction of Ashcroft scores and collagen content. Microarray analysis of the lungs revealed that GLPG1690 strongly reversed the impact of gene expression caused by BLM (367 out of the 2375 probes). As GLPG1690 treatment affects 395 probes, this treatment effect is highly relevant in the model. Gene clusters affected by BLM treatment and reverted by GLPG1690 are related to extracellular matrix (such as Tnc and Spp1), collagen (Col3a1) and cytokines/chemokines (Cxcl12). Several of the affected genes are known to be involved in the development or progression of lung fibrosis in IPF patients.
Conclusions
These data provide further mechanistic understanding of the efficacy of ATX inhibition in a pre-clinical lung fibrosis model, highlighting a role for extracellular matrix and inflammation biology. These data strongly suggest that GLPG1690 may be beneficial in treating IPF patients and support its evaluation in a clinical study
The target of rapamycin (TOR) is a key modulator of ageing in different organisms, ranging from yeast to rodents, and it is likely that this function has been conserved also in humans (mTOR, mammalian target of rapamycin). The signaling pathway of mTOR senses and integrates a variety of environmental inputs to regulate not only the organismal growth but also its homeostasis. This pathway regulates many important cellular processes that are implicated in the appearance of age-related diseases including cancer, obesity, type 2 diabetes, and neurodegeneration in late life. Here, are been reviewed the recent knowledge in the understanding of the mTOR pathway and its role in ageing and disease. Special emphasis in mTORC1 will be done due to this particular complex can be modulated by some compounds such as rapamycin. Moreover, are going to be discussed pharmacological approaches to treat human pathologies related with mTORC1 deregulation.
Metabolic investigation of segmental overgrowth: new insights in pathogenic m...BiologInc
[Biolog Webinar] Dr. Luigi Boccuto's presentation of his investigation of the pathogenic mechanisms of segmental overgrowth caused by mosaic mutations in the genes of the PI3K-AKT pathway. He will describe how Biolog Phenotype MicroArray™ Technology is used to identify new treatment targets and test compounds with potential therapeutic effects.
Alterations of the genes involved in the PI3K and estrogen-receptor pathways ...Enrique Moreno Gonzalez
Chemotherapy with trastuzumab is widely used for patients with human epidermal growth
factor receptor 2-positive (HER2+) breast cancer, but a significant number of patients with
the tumor fail to respond, or relapse. The mechanisms of recurrence and biomarkers that indicate the response to the chemotherapy and outcome are not fully investigated.
Metabolic investigation of segmental overgrowth: new insights in pathogenic m...BiologInc
[Biolog Webinar] Dr. Luigi Boccuto's presentation of his investigation of the pathogenic mechanisms of segmental overgrowth caused by mosaic mutations in the genes of the PI3K-AKT pathway. He will describe how Biolog Phenotype MicroArray™ Technology is used to identify new treatment targets and test compounds with potential therapeutic effects.
Alterations of the genes involved in the PI3K and estrogen-receptor pathways ...Enrique Moreno Gonzalez
Chemotherapy with trastuzumab is widely used for patients with human epidermal growth
factor receptor 2-positive (HER2+) breast cancer, but a significant number of patients with
the tumor fail to respond, or relapse. The mechanisms of recurrence and biomarkers that indicate the response to the chemotherapy and outcome are not fully investigated.
Basic Mutagenic signal Transduction or the cancer signal transduction that control cell cycle are important pathways to understand cancer in molecular level and to invent targeted treatment.
Tumor suppression and inflammation: controlling the senescence associated se...adamfreund
This is the powerpoint presentation from a talk I gave at a conference in October, 2009. It will be hard to follow without the spoken part, but it will hopefully give anyone who is interested a brief introduction to my thesis research.
George D. Demetri, MD, Prof. Jean-Yves Blay, MD, and Steven DuBois, MD, MS, prepared useful practice aids pertaining to advanced sarcoma for this CME activity titled "The Promise of New Concepts and Innovative Therapy in Advanced Sarcoma: From Established Targets to TRK Inhibition and Beyond." For the full presentation, monograph, complete CME information, and to apply for credit, please visit us at http://bit.ly/2L3jwcf. CME credit will be available until December 26, 2019.
Similar to Signaling events triggered by inactivation of the TSC1-2 Complex: Implications for TSC/LAM pathology and treatment (20)
JMeter webinar - integration with InfluxDB and GrafanaRTTS
Watch this recorded webinar about real-time monitoring of application performance. See how to integrate Apache JMeter, the open-source leader in performance testing, with InfluxDB, the open-source time-series database, and Grafana, the open-source analytics and visualization application.
In this webinar, we will review the benefits of leveraging InfluxDB and Grafana when executing load tests and demonstrate how these tools are used to visualize performance metrics.
Length: 30 minutes
Session Overview
-------------------------------------------
During this webinar, we will cover the following topics while demonstrating the integrations of JMeter, InfluxDB and Grafana:
- What out-of-the-box solutions are available for real-time monitoring JMeter tests?
- What are the benefits of integrating InfluxDB and Grafana into the load testing stack?
- Which features are provided by Grafana?
- Demonstration of InfluxDB and Grafana using a practice web application
To view the webinar recording, go to:
https://www.rttsweb.com/jmeter-integration-webinar
DevOps and Testing slides at DASA ConnectKari Kakkonen
My and Rik Marselis slides at 30.5.2024 DASA Connect conference. We discuss about what is testing, then what is agile testing and finally what is Testing in DevOps. Finally we had lovely workshop with the participants trying to find out different ways to think about quality and testing in different parts of the DevOps infinity loop.
Let's dive deeper into the world of ODC! Ricardo Alves (OutSystems) will join us to tell all about the new Data Fabric. After that, Sezen de Bruijn (OutSystems) will get into the details on how to best design a sturdy architecture within ODC.
LF Energy Webinar: Electrical Grid Modelling and Simulation Through PowSyBl -...DanBrown980551
Do you want to learn how to model and simulate an electrical network from scratch in under an hour?
Then welcome to this PowSyBl workshop, hosted by Rte, the French Transmission System Operator (TSO)!
During the webinar, you will discover the PowSyBl ecosystem as well as handle and study an electrical network through an interactive Python notebook.
PowSyBl is an open source project hosted by LF Energy, which offers a comprehensive set of features for electrical grid modelling and simulation. Among other advanced features, PowSyBl provides:
- A fully editable and extendable library for grid component modelling;
- Visualization tools to display your network;
- Grid simulation tools, such as power flows, security analyses (with or without remedial actions) and sensitivity analyses;
The framework is mostly written in Java, with a Python binding so that Python developers can access PowSyBl functionalities as well.
What you will learn during the webinar:
- For beginners: discover PowSyBl's functionalities through a quick general presentation and the notebook, without needing any expert coding skills;
- For advanced developers: master the skills to efficiently apply PowSyBl functionalities to your real-world scenarios.
Essentials of Automations: Optimizing FME Workflows with ParametersSafe Software
Are you looking to streamline your workflows and boost your projects’ efficiency? Do you find yourself searching for ways to add flexibility and control over your FME workflows? If so, you’re in the right place.
Join us for an insightful dive into the world of FME parameters, a critical element in optimizing workflow efficiency. This webinar marks the beginning of our three-part “Essentials of Automation” series. This first webinar is designed to equip you with the knowledge and skills to utilize parameters effectively: enhancing the flexibility, maintainability, and user control of your FME projects.
Here’s what you’ll gain:
- Essentials of FME Parameters: Understand the pivotal role of parameters, including Reader/Writer, Transformer, User, and FME Flow categories. Discover how they are the key to unlocking automation and optimization within your workflows.
- Practical Applications in FME Form: Delve into key user parameter types including choice, connections, and file URLs. Allow users to control how a workflow runs, making your workflows more reusable. Learn to import values and deliver the best user experience for your workflows while enhancing accuracy.
- Optimization Strategies in FME Flow: Explore the creation and strategic deployment of parameters in FME Flow, including the use of deployment and geometry parameters, to maximize workflow efficiency.
- Pro Tips for Success: Gain insights on parameterizing connections and leveraging new features like Conditional Visibility for clarity and simplicity.
We’ll wrap up with a glimpse into future webinars, followed by a Q&A session to address your specific questions surrounding this topic.
Don’t miss this opportunity to elevate your FME expertise and drive your projects to new heights of efficiency.
Epistemic Interaction - tuning interfaces to provide information for AI supportAlan Dix
Paper presented at SYNERGY workshop at AVI 2024, Genoa, Italy. 3rd June 2024
https://alandix.com/academic/papers/synergy2024-epistemic/
As machine learning integrates deeper into human-computer interactions, the concept of epistemic interaction emerges, aiming to refine these interactions to enhance system adaptability. This approach encourages minor, intentional adjustments in user behaviour to enrich the data available for system learning. This paper introduces epistemic interaction within the context of human-system communication, illustrating how deliberate interaction design can improve system understanding and adaptation. Through concrete examples, we demonstrate the potential of epistemic interaction to significantly advance human-computer interaction by leveraging intuitive human communication strategies to inform system design and functionality, offering a novel pathway for enriching user-system engagements.
"Impact of front-end architecture on development cost", Viktor TurskyiFwdays
I have heard many times that architecture is not important for the front-end. Also, many times I have seen how developers implement features on the front-end just following the standard rules for a framework and think that this is enough to successfully launch the project, and then the project fails. How to prevent this and what approach to choose? I have launched dozens of complex projects and during the talk we will analyze which approaches have worked for me and which have not.
Software Delivery At the Speed of AI: Inflectra Invests In AI-Powered QualityInflectra
In this insightful webinar, Inflectra explores how artificial intelligence (AI) is transforming software development and testing. Discover how AI-powered tools are revolutionizing every stage of the software development lifecycle (SDLC), from design and prototyping to testing, deployment, and monitoring.
Learn about:
• The Future of Testing: How AI is shifting testing towards verification, analysis, and higher-level skills, while reducing repetitive tasks.
• Test Automation: How AI-powered test case generation, optimization, and self-healing tests are making testing more efficient and effective.
• Visual Testing: Explore the emerging capabilities of AI in visual testing and how it's set to revolutionize UI verification.
• Inflectra's AI Solutions: See demonstrations of Inflectra's cutting-edge AI tools like the ChatGPT plugin and Azure Open AI platform, designed to streamline your testing process.
Whether you're a developer, tester, or QA professional, this webinar will give you valuable insights into how AI is shaping the future of software delivery.
PHP Frameworks: I want to break free (IPC Berlin 2024)Ralf Eggert
In this presentation, we examine the challenges and limitations of relying too heavily on PHP frameworks in web development. We discuss the history of PHP and its frameworks to understand how this dependence has evolved. The focus will be on providing concrete tips and strategies to reduce reliance on these frameworks, based on real-world examples and practical considerations. The goal is to equip developers with the skills and knowledge to create more flexible and future-proof web applications. We'll explore the importance of maintaining autonomy in a rapidly changing tech landscape and how to make informed decisions in PHP development.
This talk is aimed at encouraging a more independent approach to using PHP frameworks, moving towards a more flexible and future-proof approach to PHP development.
UiPath Test Automation using UiPath Test Suite series, part 3DianaGray10
Welcome to UiPath Test Automation using UiPath Test Suite series part 3. In this session, we will cover desktop automation along with UI automation.
Topics covered:
UI automation Introduction,
UI automation Sample
Desktop automation flow
Pradeep Chinnala, Senior Consultant Automation Developer @WonderBotz and UiPath MVP
Deepak Rai, Automation Practice Lead, Boundaryless Group and UiPath MVP
Key Trends Shaping the Future of Infrastructure.pdfCheryl Hung
Keynote at DIGIT West Expo, Glasgow on 29 May 2024.
Cheryl Hung, ochery.com
Sr Director, Infrastructure Ecosystem, Arm.
The key trends across hardware, cloud and open-source; exploring how these areas are likely to mature and develop over the short and long-term, and then considering how organisations can position themselves to adapt and thrive.
De-mystifying Zero to One: Design Informed Techniques for Greenfield Innovati...
Signaling events triggered by inactivation of the TSC1-2 Complex: Implications for TSC/LAM pathology and treatment
1. Signaling events triggered by inactivation of the TSC1-2 Complex Implications for TSC/LAM pathology and treatment
2. X TSC1-TSC2 Rheb mTORC1 Other effectors?? (B-Raf) 2. Aberrantly high mTORC1 signaling OFF ON UNKNOWN Amino Acids cell growth cell proliferation cyclin D c-Myc etc… TIF-IA UBF ribosome biogenesis cap-dependent translation 4E-BP1 S6K1/2 eIF4E eIF4B SKAR S6 1. Constitutive Rheb -mTORC1 signaling Pol I cell survival Growth Factors PI3K Akt others GSK3 FOXO NF B PTEN eIF2B cell proliferation
3. X TSC1-TSC2 Rheb mTORC1 Other effectors?? (B-Raf) 2. Aberrantly high mTORC1 signaling Growth Factors PI3K Akt others GSK3 FOXO NF B PTEN cell survival eIF2B OFF ON UNKNOWN Amino Acids cell growth cell proliferation cyclin D c-Myc etc… TIF-IA UBF ribosome biogenesis cap-dependent translation 4E-BP1 S6K1/2 eIF4E eIF4B SKAR S6 1. Constitutive Rheb -mTORC1 signaling Pol I
4. X TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation ribosome biogenesis cap-dependent translation 4E-BP1 S6K1/2 eIF4E Pol I Growth Factors PI3K Akt others GSK3 FOXO NF B PTEN 2. Aberrantly high mTORC1 signaling 1. Constitutive Rheb -mTORC1 signaling cell proliferation OFF ON UNKNOWN cell survival eIF2B
5. cap-dependent translation X TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation Growth Factors PI3K Akt others GSK3 cell survival FOXO NF B ribosome biogenesis PTEN 4E-BP1 S6K1/2 eIF4E Pol I 2. Aberrantly high mTORC1 signaling 1. Constitutive Rheb -mTORC1 signaling OFF ON UNKNOWN eIF2B
6. GSK3 is constitutively phosphorylated on S9 in TSC cells and tumors Tsc2+/+ v. Tsc2-/- MEFs pGSK3 (S9) IHC Tsc2+/- Liver Hemangioma
7. 15 min pretreatment : w = 100 nM wortmannin; r = 20 nM rapamycin Reconstituted Tsc2-/- MEFs PI3K-independent / mTOR-dependent Phosphorylation of GSK3 in TSC-deficient cells
8. S6K1 is the GSK3 kinase in TSC null cells -5 -4 -3 -2 -1 P +1 GSK3 R A R T S S 21 F GSK3 R P R T T S 9 F eIF4B R S R T G S 422 E rS6 R R R L S S 236 L
9. S6K1 IP-kinase assays from serum-starved cells S6K1 is the GSK3 kinase in TSC null cells In Vitro S6K1 siRNA knockdown in serum-starved TSC null cells In Vivo
10. S6K1 is the GSK3 kinase and S6K2 is the S6 kinase in TSC null MEFs S6K1 v. S6K2 siRNA knockdown in serum-starved TSC null cells
11. cap-dependent translation TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation Growth Factors PI3K Akt GSK3 ribosome biogenesis 4E-BP1 S6K1 eIF4E Pol I X eIF2B
12. cap-dependent translation X TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation Growth Factors PI3K Akt ribosome biogenesis 4E-BP1 S6K1 eIF4E Pol I X GSK3 eIF2B 1) GSK3 activity is lower in serum-starved TSC cells. 2) Rapamycin activates GSK3 in TSC cells. 3) Aberrant regulation of GSK3 contributes to the proliferation properties of TSC1/2 null cells.
13. GSK3 kinase activity is reduced in Tsc2-/- cells and is activated by rapamycin Serum starved littermate-derived MEFs IP Kinase Assay
14. Constitutive inhibition of GSK3 contributes to the serum-free proliferation of Tsc2-/- cells 48h-no serum 48h-no serum
15. Constitutive inhibition of GSK3 contributes to the serum-free proliferation of Tsc2-/- cells Serum-starved Tsc2 null cells
16. cap-dependent translation X TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation GSK3 ribosome biogenesis eIF2B 4E-BP1 S6K1 eIF4E Pol I neuronal polarity/survival metabolic processes
17. GSK3 is phosphorylated in TSC “giant cells” H&E pS6 Tuber SEGA Vimentin pGSK3 (S9) Merge Mustafa Sahin
18. H&E Periodic acid Schiff (PAS) Cardiac rhabdomyomas are common in newborns with TSC Comprised of vacuolated myocytes filled with glycogen S6K1 GSK3 glycogen synthase
19. GSK3 inhibition can enhance the survival of smooth muscle cells under hypoxic conditions
20. GSK3 is constitutively phosphorylated in Tsc2-/- smooth muscle cells Serum-starved ELT3 Cells Alex Lipovsky
21. cap-dependent translation X TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation Growth Factors PI3K Akt others GSK3 cell survival FOXO NF B ribosome biogenesis PTEN 4E-BP1 S6K1/2 eIF4E Pol I 2. Aberrantly high mTORC1 signaling 1. Constitutive Rheb -mTORC1 signaling eIF2B
23. X TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation Growth Factors PI3K Akt GSK3 cell survival FOXO NF B 4E-BP1 S6K1/2 eIF4E TORC2 HIF1 VEGF Effects of mTORC1 inhibitors on tumors with loss of TSC1-2? RAP VEGFR PI3K Akt TORC1 Angiogenesis Endothelial Cell TORC2 Tumor Cell
24. X TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation 4E-BP1 S6K1/2 eIF4E VEGFR PI3K Akt TORC1 Angiogenesis Endothelial Cell TORC2 Tumor Cell PI3K Akt GSK3 cell survival FOXO NF B TORC2 Effects of mTORC1 inhibitors on tumors with loss of TSC1-2? RAP 12h rap allows reactivation of Akt
25. X TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation Growth Factors PI3K Akt GSK3 cell survival FOXO NF B 4E-BP1 S6K1/2 eIF4E TORC2 VEGFR PI3K Akt TORC1 Angiogenesis Endothelial Cell TORC2 Tumor Cell Effects of mTORC1 inhibitors on tumors with loss of TSC1-2? RAP
26. mTORC1 inhibitors block the “feedback loop” and allow reactivation of PI3K-Akt signaling. Are they effective LAM/TSC therapeutics?
27. mTORC1 inhibitors can enhance survival of TSC null cells RAD001 rescues lethality of dTsc1 -/- larvae Radimerski et al. 2002 Genes Dev Rap restores IGF1-induced survival of Tsc2 -/- MEFs Harrington et al. 2004 J. Cell Biol. Rap protects Tsc2 -/- MEFs from DNA damage- induced cell death Ghosh et al. 2006 Cancer Cell
28. Before Rapamycin for 2.5 Mos Rapamycin’s effects on TSC SEGAs Franz et al. 2006 Ann Neurol 4 Mos off Rapamycin Rapamycin an additional 8 Mos
29. X TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation Growth Factors PI3K Akt GSK3 cell survival FOXO NF B 4E-BP1 S6K1/2 eIF4E TORC2 HIF1 VEGF VEGFR PI3K Akt TORC1 Angiogenesis Endothelial Cell TORC2 Tumor Cell Effects of mTORC1 inhibitors on tumors with loss of TSC1-2? RAP
30. X TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation Growth Factors PI3K Akt GSK3 cell survival FOXO NF B 4E-BP1 S6K1/2 eIF4E TORC2 VEGFR PI3K Akt TORC1 Angiogenesis Endothelial Cell TORC2 Tumor Cell Effects of mTORC1 inhibitors on tumors with loss of TSC1-2? RAP RAP
31.
32. X TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation Growth Factors PI3K Akt GSK3 cell survival FOXO NF B 4E-BP1 S6K1/2 eIF4E TORC2 VEGFR PI3K Akt TORC1 Angiogenesis Endothelial Cell TORC2 Tumor Cell Effects of mTORC1 inhibitors on tumors with loss of TSC1-2? RAP RAP
33. X TSC1-TSC2 Rheb mTORC1 cell growth cell proliferation Growth Factors PI3K Akt GSK3 cell survival FOXO NF B 4E-BP1 S6K1/2 eIF4E TORC2 VEGFR PI3K Akt TORC1 Angiogenesis Endothelial Cell TORC2 Tumor Cell Effects of mTORC1 inhibitors on tumors with loss of TSC1-2? RAP RAP RAP ? ?
34. Rapamycin increases basal and growth factor-stimulated activation of Akt in Tsc2-/- smooth muscle cells Serum-starved ELT3 Cells Alex Lipovsky
