ABCC1 p.Asp720Asn
| Predicted by SNAP2: | A: N (87%), C: N (72%), E: N (57%), F: D (80%), G: N (72%), H: D (85%), I: D (80%), K: D (66%), L: D (53%), M: D (71%), N: D (66%), P: D (91%), Q: D (75%), R: D (80%), S: N (72%), T: N (78%), V: N (53%), W: D (85%), Y: D (85%), |
| Predicted by PROVEAN: | A: N, C: N, E: N, F: N, G: N, H: N, I: N, K: N, L: N, M: N, N: N, P: N, Q: N, R: N, S: N, T: N, V: N, W: N, Y: N, |
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[hide] Multidrug resistance-associated protein MRP-1 regu... Development. 2005 Jul;132(14):3197-207. Yabe T, Suzuki N, Furukawa T, Ishihara T, Katsura I
Multidrug resistance-associated protein MRP-1 regulates dauer diapause by its export activity in Caenorhabditis elegans.
Development. 2005 Jul;132(14):3197-207., [PMID:15983401]
Abstract [show]
Multidrug resistance-associated proteins (MRPs), when overexpressed, confer drug resistance to cancer cells by exporting anti-cancer agents through the cell membrane, but their role in animal development has not been elucidated. Here we show that an MRP homolog regulates larval development in the nematode Caenorhabditis elegans. C. elegans forms a special third-stage larva called a dauer larva under conditions inappropriate for growth. By contrast, we found that mutants in mrp-1, an MRP homolog gene, form dauer larvae even under conditions appropriate for growth, in the background of certain mutations that partially block the insulin signaling pathway. A functional mrp-1::GFP gene was shown to be expressed in many tissues, and the wild-type mrp-1 gene must be expressed in multiple tissues for a wild-type phenotype. Human MRP1 could substitute for C. elegans MRP-1 in dauer larva regulation, and an inhibitor of the human MRP1 transport activity impaired this function, showing that export activity is required for normal dauer larva regulation. Epistasis studies revealed that MRP-1 acts in neither the TGF-beta nor the cGMP signaling pathway. mrp-1 mutations enhanced the dauer-constitutive phenotype of mutants in the insulin signaling pathway more strongly than that in other pathways. Thus, MRP-1, through its export activity, supports the induction of the normal (non-dauer) life cycle by the insulin signaling pathway.
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No. Sentence Comment
112 ut151 and ut155 had missense mutations in NBD1 (T636I and D720N; amino acids that are conserved in human MRP1), whereas ut153 had a mutation at the splice acceptor site of the fourth intron (AG to AA) (Fig. 2A).
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ABCC1 p.Asp720Asn 15983401:112:58
status: NEW