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Mechano-metabolic feedback connects tissue fluidity to mitochondrial DNA–dependent immunity in breast cancer
Abstract Why some tumors respond to immunotherapy (“hot” tumors) while others remain resistant (“cold” tumors) is a central challenge in oncology. Elevated RAB5A-dependent endocytosis drives tissue fluidization during the transition to invasive breast carcinoma, but its immunological consequences are unclear. Here we show that RAB5A-driven fluidization induces a mechano-metabolic stress response that disrupts the AMPK–AKAP1–DRP1 mitochondrial fission pathway, causing mitochondrial elongation.
De Novo Gene Transcription of Connexin Mediates Cytoplasmic Fluid Exchange and Flocking Transitions in Physiological and Cancerous Epithelial Systems
Quantitative RT-PCR Analysis Quantitative RT-PCR analysis was performed as previously described.[3] Total RNA was extracted using the RNeasy Mini kit (Qiagen) and quantified by NanoDrop to assess both concentration and quality of the samples. 1 microgram of RNA was retrotranscribed using “High-Capacity cDNA Reverse Transcription Kit – Thermofisher.” RT minus was made to check the absence of genomic DNA.
Muscle diffusion tensor imaging in facioscapulohumeral muscular dystrophy
AD axial diffusivity CSS Clinical Severity Score DMD Duchenne muscular dystrophy DWI diffusion weighted imaging EPG extended phase graph FA fractional anisotropy FSHD facioscapulohumeral muscular dystrophy FF fat fraction MD mean diffusivity MESE multi-echo T2 spin-echo mDTI muscle diffusion tensor imaging mMRI muscle magnetic resonance imaging NMDs neuromuscular disorders qMRI quantitative MRI RD radial diffusivity ROI region of interest STIR Short Tau Inversion Recovery 6-MWT 6-Minute Walk...
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