Current Opinion in Cell Biology, Journal Year: 2025, Volume and Issue: 94, P. 102493 - 102493
Published: March 21, 2025
Language: Английский
The FASEB Journal, Journal Year: 2025, Volume and Issue: 39(2)
Published: Jan. 15, 2025
Abstract The correct synthesis and degradation of proteins are vital for numerous biological processes in the human body, with protein primarily facilitated by ubiquitin‐proteasome system. SKP1‐CUL1‐F‐box (SCF) E3 ubiquitin ligase, a member Cullin‐RING ligase (CRL) family, plays crucial role mediating ubiquitination subsequent 26S proteasome during normal cellular metabolism. Notably, SCF is intricately linked to pathogenesis various diseases, including malignant tumors. This paper provides comprehensive overview functional characteristics complexes, encompassing their assembly, disassembly, regulatory factors. Furthermore, we discuss diverse effects on such as cell cycle progression, DNA replication, oxidative stress response, proliferation, apoptosis, differentiation, maintenance stem characteristics, tissue development, circadian rhythm regulation, immune response modulation. Additionally, summarize associations between onset, prognosis By synthesizing current knowledge, this review aims offer novel perspective holistic systematic understanding complexes multifaceted functions physiology disease pathogenesis.
Language: Английский
Citations
0
Cell Death and Disease, Journal Year: 2025, Volume and Issue: 16(1)
Published: March 1, 2025
Abstract Mitophagy is a selective process that targets the damaged, dysfunctional, or superfluous mitochondria for degradation through autophagy. The SCF FBXL4 E3 ubiquitin ligase complex suppresses basal mitophagy by targeting BNIP3 and BNIP3L, two key cargo receptors, ubiquitin-proteasomal degradation. loss-of-function mutations lead to excessive BNIP3/3L-dependent mitophagy, thereby causing devastating multi-system disorder called mitochondrial DNA depletion syndrome, type 13 (MTDPS13). PPTC7, matrix phosphatase, essential proper function biogenesis. Here, we show proportion of PPTC7 located on outer membrane, where it interacts with BNIP3/3L. decreases BNIP3/3L protein stability in phosphatase activity-independent manner. Using vitro cell culture Pptc7 knockout mouse model, demonstrate deficiency activates high levels Mechanistically, facilitates -mediated Overall, these findings establish as an co-factor suppressor mitophagy.
Language: Английский
Citations
0
ACS Infectious Diseases, Journal Year: 2025, Volume and Issue: unknown
Published: March 19, 2025
Pneumonia caused by Staphylococcus aureus infection has consistently been a significant cause of morbidity and mortality worldwide. Extensive research to date indicates that N6-methyladenosine (m6A) modification plays crucial role in the development progression various diseases. However, it remains unknown whether m6A affects bacterial pneumonia. To explore this question, we assessed levels as well expression methyltransferases (METTL3 METTL14), demethylase fat mass obesity-related protein (FTO), methylation reader proteins YTHDF1 YTHDF2 mice MH-S cells during S. infection. The METTL3 were significantly upregulated aureus-infected cells. siMETTL3 knockdown resulted more severe colonization, lung damage, increased inflammatory cytokines (IL-6, IL-1β, TNF-α), rates following Regulation inflammation was associated with activation MAPK/NF-κB/JAK2-STAT3 signaling pathway. Moreover, exhibited an release superoxides exacerbated oxidative stress lungs infection, which correlated impaired mitochondrial autophagy mediated Pink1/Parkin Our findings provide previously unrecognized evidence protective aureus-induced acute pneumonia, indicating potential therapeutic target for infections.
Language: Английский
Citations
0
Nature Reviews Cardiology, Journal Year: 2025, Volume and Issue: unknown
Published: March 20, 2025
Language: Английский
Citations
0
Current Opinion in Cell Biology, Journal Year: 2025, Volume and Issue: 94, P. 102493 - 102493
Published: March 21, 2025
Language: Английский
Citations
0