ABCC1 p.Leu1437Arg
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PMID: 19063607
[PubMed]
Qin L et al: "Residues responsible for the asymmetric function of the nucleotide binding domains of multidrug resistance protein 1."
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Sentence
Comment
55
Additional mutations (W653Y, V680T, P794A, V1432G, L1437R, and C1439S) were introduced into the dh D793E vector by site-directed mutagenesis using a QuikChange II kit (Stratagene, La Jolla, CA).
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ABCC1 p.Leu1437Arg 19063607:55:51
status: NEW56 The forward primers for W653Y, V680T, P794A, V1432G, L1437R, and C1439S were 5'-GCCACATTCACCTATGCCAGGAGC- GAC-3', 5'-GTGGTGGGCCAGACGGGCTGCGGAAAG-3', 5'-TTTA- CCTTCGATGAGGCCCTCTCAGCAGTGGA-3', 5'-AGAAC- CTCAGTGGCGGGCAGCGC-3', and 5'-CAGCGCCAGC- GTGTGAGCCTAGCCCG-3', respectively.
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ABCC1 p.Leu1437Arg 19063607:56:53
status: NEW61 To make V1432G, L1437R, and C1439S mutations, a KpnI-ClaI MRP1 DNA fragment was cloned into pBluescript II KS vector, and PCR mutagenesis was performed as described above.
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ABCC1 p.Leu1437Arg 19063607:61:16
status: NEW148 The Walker A V680T mutation and the signature C V1432G mutation in NBD2 were without effect, while the double L1437R/C1439S signature C mutation essentially inactivated the D793E protein (Figure 3B).
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ABCC1 p.Leu1437Arg 19063607:148:110
status: NEW