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Sabrina ABSALON

BOSTON

En résumé

I am working in Jeff Dvorin's Lab:
Dr. Dvorin’s research focuses on the molecular pathogenesis of the human malaria parasite Plasmodium falciparum. The major goal of the Dvorin lab is to identify fundamental biological processes within the parasite life cycle. One of these fundamental processes is the regulated and efficient egress from human erythrocytes that occurs during asexual replication. The parasite relies on egress for a sequential round of invasion; this allows exponential expansion of the parasite during the blood-stage of malaria. Parasite egress requires a calcium-mediated signal, but the proteins that mediate the critical calcium-dependent steps of parasite egress have not been fully identified or characterized. Using genetic, cell biological, and novel molecular biology techniques, the Dvorin lab is interested in multiple aspects of parasite egress from an infected human erythrocyte.

Mes compétences :
Malaria
Research
Scientific
Scientific research

Entreprises

  • Children's Hospital Boston - Research fellow

    2011 - maintenant I am working in Jeff Dvorin's Lab:
    Dr. Dvorin’s research focuses on the molecular pathogenesis of the human malaria parasite Plasmodium falciparum. The major goal of the Dvorin lab is to identify fundamental biological processes within the parasite life cycle. One of these fundamental processes is the regulated and efficient egress from human erythrocytes that occurs during asexual replication. The parasite relies on egress for a sequential round of invasion; this allows exponential expansion of the parasite during the blood-stage of malaria. Parasite egress requires a calcium-mediated signal, but the proteins that mediate the critical calcium-dependent steps of parasite egress have not been fully identified or characterized. Using genetic, cell biological, and novel molecular biology techniques, the Dvorin lab is interested in multiple aspects of parasite egress from an infected human erythrocyte.

  • Harvard Medical School - Postdoctoral Research Fellow

    2008 - 2011 miR-26b Induces Pathologies Found in Alzheimer's Disease

    Although accumulation of toxic β-amyloid peptides is the chief defining feature of Alzheimer's disease (AD), many other pathologies are present, including accumulation of abnormally phosphorylated tau protein, cell cycle re-entry, and apoptosis. Absalon et al. propose that these other pathologies stem from increased levels of microRNA miR-26b, which they detected in temporal cortex in early stages of AD. Increasing miR-26b levels in cultured rat cortical neurons decreased levels of retinoblastoma protein (Rb) and p27, which normally prevent cell cycle entry by preventing transcription of cell cycle proteins. Consequently, increasing miR-26b levels also increased expression of cell cycle proteins, ultimately resulting in apoptosis. Additionally, because p27 forms a complex that localizes cyclin-dependent kinase 5 (Cdk5) to the nucleus, decreasing p27 allowed Cdk5 to exit the nucleus and phosphorylate cytoplasmic targets, including AD-associated sites on tau. Cell cycle entry, nuclear exit of Cdk5, and apoptosis also occur when neurons are treated with H2O2, but intriguingly, inhibiting miR-26b increased neuronal survival after H2O2 treatment.

  • Harvard Medical School - Post-doctoral fellow

    2008 - 2011

  • Institut Pasteur - Phd student

    Paris 2005 - 2007 I investigated 3 principal topics related to flagellum formation and function in trypanosomes (a uniflagellated protozoan responsible for sleeping sickness in Africa,): (1) the role of IntraFlagellar Transport (IFT) in flagellum assembly, (2) the mode of regulation of expression of flagellar genes and (3) the role of the flagellum in cell morphogenesis.

Formations

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