A1 Vertaisarvioitu alkuperäisartikkeli tieteellisessä lehdessä
Superior cervical ganglion-10 protein as a molecular effector of c-Jun N-terminal kinase 1: implications for the therapeutic targeting of Jun N-terminal kinase in nerve regeneration
Tekijät: Westerlund N, Zdrojewska J, Courtney MJ, Coffey ET
Kustantaja: INFORMA HEALTHCARE
Julkaisuvuosi: 2008
Journal: Expert Opinion on Therapeutic Targets
Tietokannassa oleva lehden nimi: EXPERT OPINION ON THERAPEUTIC TARGETS
Lehden akronyymi: EXPERT OPIN THER TAR
Vuosikerta: 12
Numero: 1
Aloitussivu: 31
Lopetussivu: 43
Sivujen määrä: 13
ISSN: 1472-8222
DOI: https://doi.org/10.1517/14728222.12.1.31
Tiivistelmä
Background: Cell stress and tissue injury lead to c-Jun N-terminal kinase (JNK) activation, which is known to contribute to cell death. Paradoxically, strong evidence supports an important role for JNK in the regeneration of neuronal processes, subsequent to injury. Objective: Recent research revealed the growth cone-associated protein superior cervical ganglion-10 protein as a candidate effector for the regeneration pathway mediated by JNK1. This implies that neuroprotective strategies targeting JNK may have negative effects on neuronal regeneration, unless JNK1 function is spared, and that the mechanistic relationships between JNK1 and neuronal regeneration deserve increased attention. Results: This review proposes a model reconciling the microtubule regulatory properties of superior cervical ganglion protein 10 with its role as a JNK effector of regeneration and highlight remaining issues to be resolved.
Background: Cell stress and tissue injury lead to c-Jun N-terminal kinase (JNK) activation, which is known to contribute to cell death. Paradoxically, strong evidence supports an important role for JNK in the regeneration of neuronal processes, subsequent to injury. Objective: Recent research revealed the growth cone-associated protein superior cervical ganglion-10 protein as a candidate effector for the regeneration pathway mediated by JNK1. This implies that neuroprotective strategies targeting JNK may have negative effects on neuronal regeneration, unless JNK1 function is spared, and that the mechanistic relationships between JNK1 and neuronal regeneration deserve increased attention. Results: This review proposes a model reconciling the microtubule regulatory properties of superior cervical ganglion protein 10 with its role as a JNK effector of regeneration and highlight remaining issues to be resolved.
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