Kasturi Haldar

This study identifies a Plasmodium falciparum redox survival mechanism involving K13 that enables artemisinin-induced death in resistant strains.

The paper investigates how GLDC variants affect mitochondrial energy metabolism in the brain, showing reduced GLDC levels and altered metabolic pathways in mutant mice.

The paper shows that a triple combination of HDAC inhibitor and excipients improves microglial function in a mouse model of Kabuki Syndrome by restoring chromatin marks and cognitive responses.

This study demonstrates that gene therapy using rAAV9-GLDC prevents disease and death in a mouse model of non-ketotic hyperglycinemia.

This study uses human and mouse models to show that Kabuki syndrome mutations cause an imbalance in excitatory and inhibitory synapses, leading to synaptic dysfunction and intellectual disability.

This study shows a triple combination of HDAC inhibitor, caging agent, and PEG extends efficacy of a single dose of HDACi for chronic pain treatment in rats.

The paper develops a prediction model for prenatal disease outcomes in GLDC mutations using combined human and murine genomic analyses and in vivo evidence.

The paper develops a mutation score and clinical severity scale to predict neurological disease severity in glycine decarboxylase mutations.

This study shows that chronic administration of a triple HDACi formulation is well-tolerated in mice, preserving brain and lung function while improving drug delivery to the brain and lungs.

The paper investigates kelch13 polymorphisms in asymptomatic Plasmodium falciparum infections in Cameroon and finds associations with increased PfHRP2 levels but not gametocyte presence.

This case report describes an infant with aggressive tibial pseudarthrosis as the primary symptom of neurofibromatosis, diagnosed through exome sequencing after initial clinical suspicion.