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The molecular signaling that controls these phases involves intricate cascades of growth factors, transcription factors, and structural proteins

[25] The fusion proteins formed by these translocations lack the DNA-binding domain, causing the protein to lose function

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10.1002/prp2.211 Pharmacol

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UFL1 phosphorylation by AKT is required for UFL1-mediated breast tumor growth Given that AKT1 interacts with UFL1, which possesses a canonical AKT consensus phosphorylation motif (Fig