Publications by authors named "M Lazarou"
Article Synopsis
- Plasmodium, the parasite that causes malaria, first infects liver cells (hepatocytes) before causing symptoms during the blood stage of infection, residing in a specialized compartment called the parasitophorous vacuole (PV).
- The study focuses on how the host's autophagy processes and a specific transcription factor, TFEB, play crucial roles in the development of Plasmodium's liver stages.
- Researchers discovered that certain ATG8 family proteins, particularly GABARAP, help recruit a complex (FLCN-FNIP) that inhibits TFEB, and that blocking this complex activates TFEB, revealing new details about the interaction between the parasite and host cell signaling during the liver infection phase
Article Synopsis
- Selective autophagy helps cells get rid of harmful stuff to keep them healthy.
- Scientists found that certain special receptors can start this cleanup process using different strategies.
- Understanding how these receptors work could lead to new treatments for diseases.
Article Synopsis
- Mitophagy, the process that removes damaged mitochondria, needs to be tightly controlled to keep cells healthy, with the SCF ubiquitin ligase complex playing a key role by degrading mitophagy receptors BNIP3 and NIX.
- Mutations in the FBXL4 gene can lead to mitochondrial diseases due to increased mitophagy, showing that proper regulation is crucial.
- The phosphatase PPTC7 is essential for linking BNIP3 and NIX to FBXL4 for their degradation, and it helps to prevent excessive mitophagy by responding adaptively to changes in cell conditions.
Mitophagy preserves overall mitochondrial fitness by selectively targeting damaged mitochondria for degradation. The regulatory mechanisms that prevent PTEN-induced putative kinase 1 (PINK1) and E3 ubiquitin ligase Parkin (PINK1/Parkin)-dependent mitophagy and other selective autophagy pathways from overreacting while ensuring swift progression once initiated are largely elusive. Here, we demonstrate how the TBK1 (TANK-binding kinase 1) adaptors NAP1 (NAK-associated protein 1) and SINTBAD (similar to NAP1 TBK1 adaptor) restrict the initiation of OPTN (optineurin)-driven mitophagy by competing with OPTN for TBK1.
View Article and Find Full Text PDFActivation of PINK1 and Parkin in response to mitochondrial damage initiates a response that includes phosphorylation of RAB7A at Ser72. Rubicon is a RAB7A binding negative regulator of autophagy. The structure of the Rubicon:RAB7A complex suggests that phosphorylation of RAB7A at Ser72 would block Rubicon binding.
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