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1                                              DTDST imports sulfate for the modification of glycosamin
2                                              DTDST is both necessary and sufficient to induce FN matr
3 sis 1B phenotype have null mutations on both DTDST alleles.
4  sulfate transport function of the different DTDST mutations are grouped according to the general phe
5 aring the sulfate transport capacity of each DTDST mutation with the chondrodysplasia in which it has
6 ase-causing mutations of DTDST, we expressed DTDST-mediated sulfate transport in mammalian HEK-293 ce
7 strophic dysplasia sulfate-transporter gene (DTDST).
8  clinically distinct, the associated genes ( DTDST, CLD and PDS, respectively) emanate from a well co
9 Here, we report that AOII patients also have DTDST mutations, which lead to defective uptake of inorg
10 esis type IB, is also caused by mutations in DTDST, these results demonstrate a phenotypic series of
11 e proteoglycans is reduced in the absence of DTDST.
12                                 Knockdown of DTDST ablates FN matrix, whereas its overexpression incr
13 To characterize disease-causing mutations of DTDST, we expressed DTDST-mediated sulfate transport in
14 he sulfate transport activity of 11 reported DTDST mutations.
15                                 We show that DTDST is upregulated by dexamethasone stimulation of HT1
16 ntrinsic sulfate transport properties of the DTDST protein may influence the phenotype in individuals
17 he mutations on the residual activity of the DTDST protein.
18                     To determine whether the DTDST mutations found in individuals with these chondrod
19 e diastrophic dysplasia sulfate transporter (DTDST) gene encodes a transmembrane protein that transpo
20 e diastrophic dysplasia sulfate transporter (DTDST) gene have been linked to four chondrodysplasias o
21   Diastrophic dysplasia sulfate transporter (DTDST) is a sulfate/chloride antiporter whose function i
22  transport at rates only 39-62% of wild-type DTDST.
23  transport nearly equal to that of wild-type DTDST.
24 es of 17 and 32%, respectively, of wild-type DTDST.
25 mal sulfate transport function and wild-type DTDST.
26 ein was reduced when compared with wild-type DTDST.
27  influence the phenotype in individuals with DTDST mutations.

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