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1 d, including GDF-associated serum protein-1 (GASP-1) and GASP-2, which are capable of inhibiting the
3 ic analysis the hypothesis that the lrp-1141 GASP mutation confers a fitness gain by enhancing amino
5 ious work identified the rpoS819 allele as a GASP mutation allowing cells to take over stationary-pha
6 in during carbon starvation, as it may allow GASP mutants to outcompete the parental cells when growi
8 these findings suggest that both GASP-1 and GASP-2 are important modulators of GDF-11 and MSTN activ
11 GDF-associated serum protein-1 (GASP-1) and GASP-2, which are capable of inhibiting the activities o
18 ponses, suggesting that modulation of the D2-GASP interaction is important for the functional down-re
20 antage in stationary phase (GASP); we expect GASP cells to maintain a proliferative state and dominat
21 semble that of the D(2) and D(3) facilitated GASP-1 binding and promoted post-endocytic degradation o
23 ni can expose determinants with affinity for GASP binding and consequently target receptors for degra
26 tingtin-interacting protein 1 [HIP1], HIP14, GASP-1, and Nedd4) that decrease insulin secretion from
27 not interact with GASP-1, not only inhibited GASP-1 binding but slowed degradation after endocytosis.
28 or the lrp GASP phenotype, and hence the lrp GASP phenotype is due to more global physiological chang
29 play a role, it is not necessary for the lrp GASP phenotype, and hence the lrp GASP phenotype is due
31 ith megalin is mediated by the PDZ domain of GASP binding to the DSDV motif found at the carboxyl-ter
32 x, suggesting that the C-terminal domains of GASP-1 are the primary mediators for asymmetric complex
33 xpression of a dominant negative fragment of GASP inhibited receptor trafficking to lysosomes and pro
42 ress a growth advantage in stationary phase (GASP) phenotype, enabling them to grow and displace the
44 have a growth advantage in stationary phase (GASP); we expect GASP cells to maintain a proliferative
45 vironmental Satellite Aerosol/Smoke Product (GASP) Aerosol Optical Depth (AOD), followed by the CTM o
48 om the Genome Annotation Assessment Project (GASP) showed that GeneWise provided reasonably accurate
53 s named glycoprotein 330-associated protein (GASP), appears to be a truncated mouse counterpart of th
58 GASP-1, which is 100 times more potent than GASP-2, preferentially binds myostatin in an asymmetrica
59 In addition, these data demonstrated that GASP-1 can mediate post-endocytic degradation of dopamin
68 cks the terminal valine is unable to bind to GASP, illustrating the PDZ domain-dependent interaction
71 emble the D(4), which does not interact with GASP-1, not only inhibited GASP-1 binding but slowed deg
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