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Jj. Cassiman

Researcher at Katholieke Universiteit Leuven

Publications -  70
Citations -  2968

Jj. Cassiman is an academic researcher from Katholieke Universiteit Leuven. The author has contributed to research in topics: Proteoglycan & Chromosomal translocation. The author has an hindex of 26, co-authored 70 publications receiving 2912 citations.

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Molecular cloning of a phosphatidylinositol-anchored membrane heparan sulfate proteoglycan from human lung fibroblasts.

TL;DR: The characterization of human lung fibroblast cDNAs that encode the message for these core proteins and the effect of bacterial phosphatidylinositol-specific phospholipase C suggest that the hydrophobic proteoglycan is membrane-anchored through aospholipid tail.
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Marginal zone B-cell lymphomas of different sites share similar cytogenetic and morphologic features

TL;DR: It is concluded that MZBCL represent a distinct entity of B-NHL with characteristic morphologic and immunophenotypic features and particular chromosomal abnormalities, and that a close histogenetic relationship between extranodal, nodal, and splenic MzBCL is likely, although the clinical presentation may vary.
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Partial primary structure of the 48- and 90-kilodalton core proteins of cell surface-associated heparan sulfate proteoglycans of lung fibroblasts. Prediction of an integral membrane domain and evidence for multiple distinct core proteins at the cell surface of human lung fibroblasts.

TL;DR: The specific reactivity of the polyclonal antiserum confirms the identity of the 48K5 clone and distinguishes the 48- and the 90-kDa core proteins, which do share the 6G12-defined epitope and at least one additional antigenic determinant with the48K5 cDNA-encoded protein, from the 125-, 64-, and 35-k da core proteins of cell surface HSPG of human lung fibroblasts which do not react with either
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D90A heterozygosity in the SOD1 gene is associated with familial and apparently sporadic amyotrophic lateral sclerosis

TL;DR: Two families with ALS and one apparently sporadic ALS patient who are heterozygous for the D90A mutation are described, and one patient had the unusual phenotype of focal nonprogressing motor neuron disease.