Genomes and Genes
Gene Symbol: unc-51
Description: Serine/threonine-protein kinase unc-51
Alias: Serine/threonine-protein kinase unc-51
Species: Caenorhabditis elegans
- Ogura K, Goshima Y. The autophagy-related kinase UNC-51 and its binding partner UNC-14 regulate the subcellular localization of the Netrin receptor UNC-5 in Caenorhabditis elegans. Development. 2006;133:3441-50 pubmed
- Aladzsity I, Tóth M, Sigmond T, Szabo E, Bicsák B, Barna J, et al. Autophagy genes unc-51 and bec-1 are required for normal cell size in Caenorhabditis elegans. Genetics. 2007;177:655-60 pubmed..This function for unc-51 and bec-1 in cell size control and their interaction with these two growth modulatory pathways may represent a link between the hormonal and nutritional regulation of cell growth. ..
- Samara C, Syntichaki P, Tavernarakis N. Autophagy is required for necrotic cell death in Caenorhabditis elegans. Cell Death Differ. 2008;15:105-12 pubmed..Our findings demonstrate that autophagy contributes to cellular destruction during necrosis. Thus, interfering with the autophagic process may protect neurons against necrotic damage in humans. ..
- Tóth M, Simon P, Kovacs A, Vellai T. Influence of autophagy genes on ion-channel-dependent neuronal degeneration in Caenorhabditis elegans. J Cell Sci. 2007;120:1134-41 pubmed..Our findings reveal a role for autophagy genes in neuronal cell loss in C. elegans. ..
- Liang Q, Yang P, Tian E, Han J, Zhang H. The C. elegans ATG101 homolog EPG-9 directly interacts with EPG-1/Atg13 and is essential for autophagy. Autophagy. 2012;8:1426-33 pubmed publisher..epg-9 encodes a protein with significant homology to mammalian ATG101. EPG-9 directly interacts with EPG-1/Atg13. Our study indicates that EPG-9 forms a complex with EPG-1 in the aggrephagy pathway in C. elegans...
- Sato M, Sato K. Degradation of paternal mitochondria by fertilization-triggered autophagy in C. elegans embryos. Science. 2011;334:1141-4 pubmed publisher..Thus, fertilization-triggered autophagy is required for selective degradation of paternal mitochondria and thereby maternal inheritance of mitochondrial DNA. ..
- Ogura K, Okada T, Mitani S, Gengyo Ando K, Baillie D, Kohara Y, et al. Protein phosphatase 2A cooperates with the autophagy-related kinase UNC-51 to regulate axon guidance in Caenorhabditis elegans. Development. 2010;137:1657-67 pubmed publisher..This is the first report of a serine/threonine protein phosphatase functioning in axon guidance in vivo. ..
- Desai C, Garriga G, McIntire S, Horvitz H. A genetic pathway for the development of the Caenorhabditis elegans HSN motor neurons. Nature. 1988;336:638-46 pubmed..Nearly all are pleiotropic, revealing that the genes specifying HSN development also function in the development of other cell types. ..
- Lai T, Garriga G. The conserved kinase UNC-51 acts with VAB-8 and UNC-14 to regulate axon outgrowth in C. elegans. Development. 2004;131:5991-6000 pubmed..Taken together, our results suggest that VAB-8 and UNC-14 are substrates that mediate the function of UNC-51 in axon outgrowth. ..
- Erdélyi P, Borsos E, Takacs Vellai K, Kovacs T, Kovacs A, Sigmond T, et al. Shared developmental roles and transcriptional control of autophagy and apoptosis in Caenorhabditis elegans. J Cell Sci. 2011;124:1510-8 pubmed publisher..The identification of apoptosis and autophagy as compensatory cellular pathways in C. elegans might help us to understand how dysregulated PCD in humans can lead to diverse pathologies, including cancer, neurodegeneration and diabetes. ..
- Miedel M, Graf N, Stephen K, Long O, Pak S, Perlmutter D, et al. A pro-cathepsin L mutant is a luminal substrate for endoplasmic-reticulum-associated degradation in C. elegans. PLoS ONE. 2012;7:e40145 pubmed publisher..elegans. This transgenic line will facilitate high-throughput genetic or pharmacological screens for ERAD modifiers using widefield epifluorescence microscopy. ..
- Schipanski A, Lange S, Segref A, Gutschmidt A, Lomas D, Miranda E, et al. A novel interaction between aging and ER overload in a protein conformational dementia. Genetics. 2013;193:865-76 pubmed publisher..These data suggest that targets aimed at increasing UPR capacity in neurons are valuable tools for therapeutic intervention. ..