Publications by authors named "Isaac Heremans"

Unlabelled: Proteolysis of hydrophobic helices is required for complete breakdown of every transmembrane protein trafficked to the lysosome and sustains high rates of endocytosis. However, the lysosomal mechanisms for degrading hydrophobic domains remain unknown. Combining lysosomal proteomics with functional genomic data mining, we identify Lysosomal Leucine Aminopeptidase (LyLAP; formerly Phospholipase B Domain-Containing 1) as the hydrolase most tightly associated with elevated endocytic activity.

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Hydroxylated fatty acids are important intermediates in lipid metabolism and signaling. Surprisingly, the metabolism of 4-hydroxy fatty acids remains largely unexplored. We found that both ACAD10 and ACAD11 unite two enzymatic activities to introduce these metabolites into mitochondrial and peroxisomal β-oxidation, respectively.

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Article Synopsis
  • Cells can get hurt by bad substances, and this damage might be linked to diseases like Parkinson's and aging.
  • PARK7 is an enzyme that helps protect cells by breaking down a harmful compound created during sugar processing.
  • If PARK7 isn't working, it leads to more damaged proteins and other compounds, which could be important for understanding Parkinson's disease better.
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Anti-GQ1b antibodies can be detected in the serum of patients with Miller Fisher syndrome (MFS) and its incomplete forms such as acute ophthalmoparesis (AO), acute ptosis, acute mydriasis, acute oropharyngeal palsy and acute ataxic neuropathy (AAN), as well as in pharyngeal-cervical-brachial weakness, Bickerstaff brainstem encephalitis (BBE) and in overlap syndromes with Guillain-Barré syndrome (MFS-GBS, BBE-GBS). We searched the laboratory medicine database at University Hospitals Leuven between 2002 and 2017 for serum samples with anti-GQ1b IgG antibodies. We identified eight patients with anti-GQ1b antibodies: 4 MFS, 2 AO, 1 MFS-GBS and 1 AAN.

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