Metastatic suppression by DOC2B is mediated by inhibition of epithelial-mesenchymal transition and induction of senescence.
Sign Up to like & getrecommendations! Published in 2021 at "Cell biology and toxicology"
DOI: 10.1007/s10565-021-09598-w
Abstract: Senescence induction and epithelial-mesenchymal transition (EMT) events are the opposite sides of the spectrum of cancer phenotypes. The key molecules involved in these processes may get influenced or altered by genetic and epigenetic changes during… read more here.
Keywords: mesenchymal transition; senescence; doc2b; inhibition ... See more keywords
Doc2b Protects β-Cells Against Inflammatory Damage and Enhances Function
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DOI: 10.2337/db17-1352
Abstract: Loss of functional β-cell mass is an early feature of type 1 diabetes. To release insulin, β-cells require soluble N-ethylmaleimide–sensitive factor attachment protein receptor (SNARE) complexes, as well as SNARE complex regulatory proteins like double… read more here.
Keywords: cell mass; doc2b; cell; functional cell ... See more keywords
DOC2b Enhances β-Cell Function Via A Novel Tyrosine Phosphorylation-Dependent Mechanism.
Sign Up to like & getrecommendations! Published in 2022 at "Diabetes"
DOI: 10.2337/db21-0681
Abstract: Double C2 Domain Β (DOC2b) protein is required for glucose-stimulated insulin secretion (GSIS) in β-cells, the underlying mechanism of which remains unresolved. Our biochemical analysis using primary human islets, human and rodent clonal β-cells revealed… read more here.
Keywords: doc2b; gsis; enhances cell; mechanism ... See more keywords