Ira Milošević

The paper shows that β-adrenergic signaling inhibits MHCII surface deposition in reactive astrocytes via amisyn, reducing exocytosis of lysosome-like vesicles.

This study identifies nucleophagy as the mechanism by which trapped PARP1 is cleared, showing that inhibiting this process re-sensitizes PARPi-resistant cells to PARPi.

The paper investigates dopamine release defects in Parkinson's patient-derived neurons and identifies reduced VMAT2 function as the cause.

The paper shows that oxidative stress causes micronuclear collapse in Parkinson's fibroblasts, leading to DNA export via amphisomes and pro-inflammatory EVs, which can be mitigated by a mitochondria-targeted antioxidant.

This study shows that loss of CLN3 disrupts lysosomal lipid metabolism, leading to nuclear envelope lipid changes, DNA damage, and YAP1-driven apoptosis in Batten disease models.

The paper shows that Intersectin-1 and Endophilin A1 form condensates near synaptic release sites to cluster replacement vesicles, enabling rapid replenishment of neurotransmitter release sites.

The paper shows that synaptic endocytic failure in dopamine neurons leads to the emergence of dopamine-like neurons through protein transfer, supporting dopamine compensation in early Parkinson's disease.

The paper identifies that lysosomal defects up-regulate cholesterol synthesis via mitochondrial respiratory chain interactions and Ca2+ retention, while mitochondrial defects down-regulate it.

The paper shows that a small population of synaptic vesicles contain different neurotransmitter transporters, enabling corelease of various neurotransmitter combinations.

This study shows endophilin-A1 and A2 regulate exocytosis of neurosecretory vesicles by controlling recruitment, priming, and fusion, independent of their endocytic roles.