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These elevations are consistent with their accumulation in fibrotic lungs and their potential involvement in mTORC1-driven fibroblast activation [133, 134]

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(11) demonstrated that interferon-gamma (IFN-) could upregulate CUL5 expression and disrupt the binding of Cdc37/Hsp90 to HER2, consequently inducing tumor cell senescence and promoting HER2 degradation

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this is when the body has the opportunity to repair itself