期刊
ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, VOL 35
卷 35, 期 -, 页码 501-521出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-cellbio-100617-062644
关键词
axon regeneration; neuronal development; MAP3K; DLK; LZK; JNK; p38; DLK-1; Wallenda; neuronal death; axon degeneration; cytoskeleton; astrocytes; Alzheimer disease models; HSV infection; adipogenesis; insulin beta-cells
资金
- NINDS NIH HHS [R01 NS093588, R01 NS093055, P30 NS047101, R37 NS035546] Funding Source: Medline
- RRD VA [I01 RX002483] Funding Source: Medline
The dual leucine zipper-bearing kinase (DLK) and leucine zipper-bearing kinase (LZK) are evolutionarily conserved MAPKKKs of the mixed-lineage kinase family. Acting upstream of stress-responsive JNK and p38 MAP kinases, DLK and LZK have emerged as central players in neuronal responses to a variety of acute and traumatic injuries. Recent studies also implicate their function in astrocytes, microglia, and other nonneuronal cells, reflecting their expanding roles in the multicellular response to injury and in disease. Of particular note is the potential link of these kinases to neurodegenerative diseases and cancer. It is thus critical to understand the physiological contexts under which these kinases are activated, as well as the signal transduction mechanisms that mediate specific functional outcomes. In this review we first provide a historical overview of the biochemical and functional dissection of these kinases. We then discuss recent findings on regulating their activity to enhance cellular protection following injury and in disease, focusing on but not limited to the nervous system.
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