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Primary acid-labile subunit deficiency due to recessive IGFALS mutations results in postnatal growth deficit associated with low circulating insulin growth factor (IGF)-I, IGF binding protein-3 levels, and hyperinsulinemia
When these isolated senescence cells were presented with FOXO4-DRI peptide, researchers reported that the peptide appeared to block FOXO4 proteins, allowing p53 to bind with DNA, which led to the nuclear exclusion of p53 and induction of apoptosis of the senescent Leydig cells
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(2022) 30(1):4152.e5
