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It is conceivable that the GAP activity observed in our in vitro assays may be further stimulated in vivo by interactions of TBC1D9B with other proteins (e.g., TMEM55B), by membrane lipids, and/ or via posttranslational modifications that could alter the conformational state and, thereby, the activity of TBC1D9B

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A variety of cellular stresses, including DNA damage can cause the induction of cellular senescence, which represents a multifaceted and highly heterogeneous cellular state characterized by irreversible growth arrest and importantly the secretion of a multitude of factors, including proteases and chemokines 2

But, the model of ER acting on an ERE in the promoter region of said growth factors did not fit the data