Results 301 to 310 of about 1,531,875 (388)

The E3 ubiquitin ligase, RNF219, suppresses CNOT6L expression to exhibit antiproliferative activity

open access: yesFEBS Open Bio, EarlyView.
We identified RNF219 as a CCR4‐NOT complex‐interacting E3 ubiquitin ligase that targets the CCR4‐NOT subunit CNOT6L for ubiquitination. RNF219 directly binds to the DUF3819 domain of CNOT1 through its putative α‐helix spanning amino acids 521–542. Our findings also suggest that antiproliferative activity of RNF219 is at least partially mediated by ...
Shou Soeda   +9 more
wiley   +1 more source

CD9‐association with PIP2 areas is regulated by a CD9 salt bridge

open access: yesFEBS Open Bio, EarlyView.
The tetraspanin CD9 has an intracellular salt bridge. If CD9 opens, open‐CD9 moves from PIP2‐rich areas to regions populated by its interaction partner EWI‐2. Hence, the state of the salt bridge regulates the distribution of CD9 and by this CD9‐EWI‐2 complex formation.
Yahya Homsi   +2 more
wiley   +1 more source

Characterization of WAC interactions with R2TP and TTT chaperone complexes linking glucose and glutamine availability to mTORC1 activity

open access: yesFEBS Open Bio, EarlyView.
TTT and R2TP chaperone complexes are required for the assembly and activation of mTORC1. WAC directly interacts with components of TTT, R2TP, and mTORC1, and these interactions are affected by the availability of glucose and glutamine, correlating with changes in mTORC1 activity.
Sofía Cabezudo   +11 more
wiley   +1 more source

Ro 31‐8220 suppresses bladder cancer progression via enhancing autophagy in vitro and in vivo

open access: yesFEBS Open Bio, EarlyView.
The pan‐protein kinase C inhibitor Ro‐31‐8220 demonstrates potent anti‐bladder cancer effects both in vitro and in vivo by suppressing migration/invasion, inducing apoptosis and crucially activating autophagy, where blocking autophagy with chloroquine reduces its cell‐killing efficacy, suggesting its promise as a novel therapeutic candidate requiring ...
Shengjun Fu   +12 more
wiley   +1 more source

Home - About - Disclaimer - Privacy