Publications by authors named "C Enrich"

Introduction: HIV-1 exploits dendritic cells (DCs) to spread throughout the body via specific recognition of gangliosides present on the viral envelope by the CD169/Siglec-1 membrane receptor. This interaction triggers the internalization of HIV-1 within a structure known as the sac-like compartment. While the mechanism underlying sac-like compartment formation remains elusive, prior research indicates that the process is clathrin-independent and cell membrane cholesterol-dependent and involves transient disruption of cortical actin.

View Article and Find Full Text PDF

Cholesterol is an essential lipid that ensures the functional integrity of mammalian cells. Most cells acquire cholesterol via endocytosis of low-density lipoproteins (LDL). Upon reaching late endosomes/lysosomes (LE/Lys), incoming ligands, including LDL-derived cholesterol, are distributed to other organelles.

View Article and Find Full Text PDF

Senescent cells are commonly detected in tumors after chemo and radiotherapy, leading to a characteristic cellular phenotype that resists apoptotic cell death. In this study, we used multiple melanoma cell lines, molecular markers, and therapies to investigate the key role of the BCL-2 family proteins in the survival of senescent cells. We first used BH3 profiling to assess changes in apoptotic priming upon senescence induction.

View Article and Find Full Text PDF
Article Synopsis
  • Accumulation of lipid-laden macrophages is vital in forming atherosclerotic plaques, and reduced ZEB1 levels in these cells lead to larger plaques and increased cardiovascular risk.
  • Male mice lacking ZEB1 in myeloid cells show significant lipid build-up and metabolic issues, indicating that ZEB1 deficiency worsens atherosclerosis.
  • Targeted delivery of ZEB1 using nanoparticles can reverse lipid accumulation and reduce plaque formation, suggesting that ZEB1 could be an important therapeutic target for atherosclerosis.
View Article and Find Full Text PDF

Acute inflammation can either resolve through immunosuppression or persist, leading to chronic inflammation. These transitions are driven by distinct molecular and metabolic reprogramming of immune cells. The anti-diabetic drug Metformin inhibits acute and chronic inflammation through mechanisms still not fully understood.

View Article and Find Full Text PDF