Year: 2024
Type: article
Abstract: Activin/TGF-β signals are transduced intracellularly when its transcription factor dSmad2 (also called Smad on X or Smox) is C-terminally phosphorylated by pathway receptors. Recently, it has been shown that receptor-activated dSmad2 undergoes bulk degradation, however, the mechanism of how this occurs is unknown. Here we investigated if two putative linker phosphorylation sites are involved in dSmad2 degradation. We demonstrate that degradation of activated-dSmad2 occurs independently of threonine phosphorylation at linker sites 252 and 277. We also show that dSmad2 degradation is not carried out by cellular proteasomes.
Source: PubMed Central
Language: English
Topic: TGF-β signaling in diseases
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
Awards: Bridge to the Doctorate at California State University, Los Angeles: CSU-LSAMP-BD Cohort 14, Investigating if Mad linker phosphorylations can control BMP receptor turnover, Bridge to the Doctorate at California State University, Los Angeles: CSU-LSAMP-BD Cohort 13, Research Initiative for Scientific Enhancement, Undergraduate Research Training for Student Enhancement (U-RISE) at Cal State LA
OpenAlex ID: W4394762806