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JNK inhibitory kinase is up‐regulated in retinal ganglion cells after axotomy and enhances BimEL expression level in neuronal cells
Author(s) -
Wakabayashi Taketoshi,
Kosaka Jun,
Oshika Tetsuro
Publication year - 2005
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2005.03389.x
Subject(s) - axotomy , biology , microbiology and biotechnology , protein kinase a , retina , protein kinase c , kinase , neuroscience , regeneration (biology)
Optic nerve transection results in retinal ganglion cell (RGC) death in adult mammals, after the alteration of gene expression of RGCs. To elucidate the molecular mechanism by which axotomy induces RGC death, we isolated the molecules up‐regulated after optic nerve transection. One of these, axomtomy‐related gene (ARG)357, an 895‐amino‐acid protein containing a complete serine–threonine kinase domain, was isolated from a subtraction library of the rat retina. The sequence showed that this gene was a rat homolog of human c‐Jun N‐terminal kinase (JNK) inhibitory kinase and so belonged to the germinal center kinase‐VIII subfamily of Sterile20s protein kinase. We designated ARG357 as rat JNK inhibitory kinase (JIK). Rat JIK was expressed ubiquitously in various tissues and was highly expressed in the retina, with selective expression in RGCs. After axotomy, BimEL and Hrk, which are BH3‐only proteins, and rat JIK were up‐regulated in RGCs. Overexpression of rat JIK in neuronal cells up‐regulated the expression of BimEL, but not that of Hrk. These results indicate that JIK may contribute to axotomy‐induced RGC death by up‐regulating the expression of BH3‐only protein.