Maximiliano Gabriel Gutierrez

The paper investigates how Mtb remodels antigen storage compartments in macrophages using a split fluorescent protein reporter and subcellular spatial proteomics.

This study investigates the functional consequences of catalytic activity loss in LRRK2, showing impaired proteostasis and altered interactome in guanosine nucleotide-depleted Lrrk2.

The paper shows that endolysosomal damage leads to intraluminal protein condensates that prevent cytosolic leakage and sequester therapeutic oligonucleotides.

A single-donor iPSC-derived alveolar chip with epithelial, endothelial and macrophage cells models early Mycobacterium tuberculosis infection and shows ATG14-deficient macrophages die more without extra bacterial replication.

This study shows Mycobacterium tuberculosis remodels its lipidome to survive phosphate starvation by using phosphorus-free lipids and host-derived phosphate sources.

The paper shows ATG9A and ARFIP2 work together to regulate PI4P levels for lysosomal repair during damage and bacterial infection.

The paper analyzes ancient Borrelia genomes to document the evolutionary transition from tick-borne to louse-borne transmission and shows rapid reductive evolution.

This paper uses 3D imaging to show that M. tuberculosis ESX-1 affects granuloma architecture in infected mice.

This study shows that using a human plasma-like medium enhances M. tuberculosis replication in iPSC-derived macrophages by altering lipid metabolism and organelle function.

This study identifies LRRK2-G2019S-dependent lysosomal membrane repair defects in macrophages leading to increased cell death.

The paper shows increased DYRK1A dosage causes mitochondrial dysfunction and congenital heart defects in Down syndrome, which can be mitigated by a DYRK1A inhibitor.

The paper finds elevated levels of LRRK2 and α-synuclein in CSF of infectious meningitis patients, suggesting a link between neuroinflammation and infection.

This study shows that Mycobacterium tuberculosis forms intracellular cords in human lymphatic endothelial cells, evading xenophagy via the ESX-1 system and PDIM lipid.