Michael B. Datto

TL;DR: A four-tiered system to categorize somatic sequence variations based on their clinical significances is proposed, with variants with strong clinical significance and variants with potential clinical significance in tier I; tier III, variants of unknown clinical significance; and tier IV, variants deemed benign or likely benign.

TL;DR: It is demonstrated that a single extracellular antiproliferative signal, TGF-beta, can act through multiple signaling pathways to elicit a growth arrest response, suggesting that p21 can respond to both intracellular and extacellular signals for cell cycle arrest.

TL;DR: A role for Smad3 in mediating the antiproliferative effects of TGF-β is established and smad3 is implicate as a potential effector for T GF-β in modulating immune system function.

TL;DR: A 10-base pair sequence is defined that is required for the activation of the p21 promoter and is sufficient to drive TGF-β-mediated transcription from a previously nonresponsive promoter in the case of p21.

TL;DR: Results show that Smad3 contributes to bleomycin-induced lung injury and thatSmad3 may serve as a novel target for potential therapeutic treatment of lung fibrosis.