ArticleJournal of molecular histology2012
Transient global cerebral ischemia induces up-regulation of MLTKα in hippocampal CA1 neurons.
Article in Journal of molecular histology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 7 citations in OpenAlex.
- Spatiotemporal pattern of TRAF3 expression after rat spinal cord injury.Journal of molecular histology · 2014Article
- Article
- Neuroprotective properties of Melissa officinalis after hypoxic-ischemic injury both in vitro and in vivo.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2012Article
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6 authors at 1 institution in 1 country.
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Abstract
MLTK (mixed-lineage kinase-like mitogen-activated protein triple kinase) is a member of the mitogen-activated protein kinase family and functioned as a mitogen activated kinase kinase kinase. MLTKα, one of the alternatively spliced forms of MLTK, could activate the c-Jun N-terminal kinase pathway, which involved in cellular stress responses and apoptosis. But the role of MLTKα in neural apoptosis was still unclear. Here, we performed a transient global cerebral ischemia model (TGCI) in adult rats and detected the dynamic changes of MLTKα in hippocampal CA1 neurons and brain cortex. We found the MLTKα expression was increased shortly after TGCI and peaked after 8 h. In spatial distribution, MLTKα was widely located in neurons rather than astrocytes and microglia. Moreover, there was a concomitant up-regulation of active caspase-3. Taken together, we hypothesized the up-regulation of MLTKα played an essential role in the apoptosis of hippocampal CA1 neurons.
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