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RTK and mTORC1 - Coggle Diagram

- - - - Lipid messenger recruits the survival kinase Akt
        
        Akt phosphorylates the TSC complex, causing the TSC complex to detach and shut down
        
        With TSC shut down, the protein Rheb loads up GTP and docks onto mTORC1, turning it on
        
        mTORC1 phosphorylates 4E-BP1 (releasing the break on protein synthesis) and activates S6K1 (boosting ribosome production)
        
        This drives the translation of growth genes like MYC and CCND1 (CyclinD1)
        
        Increases HIF1A translation
        
        Glucose uptake is increased via GLUT1, providing materials needed for rapid cell division
        
        SREBF1/2 transcription factors are activated
        
        Activated SREBF1/2 turns on genes required to synthesise lipids and cholesterol to build new cell membranes
- - - - Because Akt is unable to inhibit the TSC complex, it remains fully active
        
        If cell is low on energy, AMPK activates and further stimulates TSC
        
        Active TSC acts as a GAP, converting Rheb-GTP to Rheb-GDP inactivating Rheb
        
        mTORC1 is completely off
        
        4E-BP1 becomes unphosphorylated, stopping translation machinery
        
        Production of c-Myc and CyclinD1 stops, stopping the cell cycle
        
        mTORC1 releases the ULK1 complex
        
        ULK1 is then free to initiate autophagy
        
        The cell stops transcribing lipid-synthesis genes (SREBF1)
        
        Cell focuses on transcribing lysosomal and survival genes via the TFEB transcription factor
        
        Cell is able to consume its own waste to survive