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The casein kinase 1 (CK1) family, a major intracellular serine/threonine kinase, is implicated in multiple pathways; however, understanding its regulation has proven challenging. A recent study published in Science identifying allosteric activation of CK1 by the DEAD-box RNA helicase DDX3 expands our understanding of the control of this abundant kinase family.
FBW7 tumor suppressor suppresses the growth and survival of tumor cells by promoting the degradation of several oncoproteins, and induces endothelial differentiation by modulating the NF1/RAS axis. A recent study in this issue of Cell Research showed that FBW7 further regulates endothelial functions via degrading transcription factor KLF2.
In mice treated with antibiotics to deplete commensal microbiota, there is a significant overhaul of host cellular disposition and function with CX3CR1+ mononuclear phagocytic cells carrying pathogenic and non-pathogenic administered bacteria to the (messenteric lymph node) MLN, resulting in T cell stimulation and IgA production.
Two recent papers in Science illustrate how the prokaryotic CRISPR-Cas immune system machinery, which typically targets invasive genetic elements such as viruses and plasmids, can be converted into a sophisticated molecular tool for next-generation human genome editing. The versatile Cas9 RNA-guided endonuclease can be readily reprogrammed using customizable small RNAs for sequence-specific single- or double-stranded DNA cleavage.
Paramyxoviruses evade antiviral immune response using a small nonstructural protein, V, which binds to the host dsRNA sensor MDA5 and prevents it from activating the interferon signaling pathway. A recent crystal structure of the V protein in complex with MDA5, published in Science, revealed that V disrupts the structure of MDA5 and is integrated into the MDA5 protein fold, providing an intriguing new example of viral mimicry as a countermeasure against the host immune system.
Emerging evidence suggests that the ability of p53 to regulate metabolism is important for its tumor suppressor activity. A recent study published in Nature reveals a novel connection between p53 and metabolism: p53 transcriptionally represses the expression of malic enzymes and associated NADPH production, which in turn triggers a positive feedback loop resulting in sustained p53 activation, cellular senescence, and tumor suppression.
The intracellular levels of the p53 tumor suppressor protein are regulated through various pathways and involve numerous regulatory components. A recent study published in Cell Research identifies a proteasome-independent pathway of p53 protein degradation in the nucleolus that is dependent on Def and Calpain3.