Yinjie Yang

TL;DR: It is shown that phosphorylation of the autophagy-adaptor protein p62 markedly increases p62's binding affinity for Keap1, an adaptor of the Cul3-ubiquitin E3 ligase complex responsible for degrading Nrf2, and that inhibitors of the interaction between phosphorylated p62 and Keap 1 have potential as therapeutic agents against human HCC.

TL;DR: The expression of mutant but not wild-type CALR induces the thrombopoietin-independent growth of UT-7/TPO cells, and it is proposed that mutant CALR promotes myeloproliferative neoplasm development by activating c-MPL and its downstream pathway.

TL;DR: It is shown that ALFY binds selectively to LC3C and the GABARAPs through a LIR in its WD40 domain, indicating that residues outside the LIR‐binding hydrophobic pockets confer specificity to the interactions with Atg8 homolog proteins.

TL;DR: This study demonstrates that mutant, but not wild-type, CALR interacts to form a homomultimeric complex and proposes a model in which the constitutive activation of the MPL downstream pathway by mutant CALR multimers induces the development of MPN.

TL;DR: A model in which mutant CALR induces MPL activation on the cell surface to promote MPN development is proposed, and it is found that Mutant CALR and MPL interact on thecell surface.