Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.108 (TAT)
 2,389 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

MS results from destruction of the protective myelin sheath surrounding axons, which prevents the transmission of nerve impulses. Precursors of oligodendrocytes, the cells capable of myelinating axons, are preserved in demyelinating lesions; however, why these precursors do not differentiate into mature oligodendrocytes and remyelinate axons is unknown. Contactin is a noncanonical Notch receptor ligand that mediates oligodendrocyte differentiation. In this issue of the JCI, Nakahara et al. show that Contactin is abundantly expressed on demyelinated axons in human chronic MS lesions and that Notch1 is activated in oligodendrocyte precursor cells (see the related article beginning on page 169). However, Notch1 intracellular domain coassociates with the nuclear transporter Importin beta but fails to show evidence of nuclear translocation. These cytoplasmic aggregates also contain TAT-interacting protein 30 kDa (TIP30), a proapoptotic factor, which inhibits nuclear transport and, consequently, Notch1-mediated oligodendrocyte differentiation and remyelination. These data target TIP30 as a new pathogenic factor in MS.
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PMID:Revisiting Notch in remyelination of multiple sclerosis lesions. 1910 51