ライフサイエンスコーパス: GASP

1 d, including GDF-associated serum protein-1 (GASP-1) and GASP-2, which are capable of inhibiting the

2 eceptor (GPCR)-associated sorting protein-1 (GASP-1).

3 ic analysis the hypothesis that the lrp-1141 GASP mutation confers a fitness gain by enhancing amino

4 ged culture of an rpoS strain had acquired a GASP mutation in lrp.

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

7 Here, we show that GASP-1 and GASP-2 act by blocking the initial signaling event (name

8 these findings suggest that both GASP-1 and GASP-2 are important modulators of GDF-11 and MSTN activ

9 Included are the antagonists GASP-1 and GASP-2, which are unique in that they specifically antag

10 ree and myostatin-bound states of GASP-1 and GASP-2.

11 GDF-associated serum protein-1 (GASP-1) and GASP-2, which are capable of inhibiting the activities o

12 Included are the antagonists GASP-1 and GASP-2, which are unique in that they specifi

13 All of these findings suggest that both GASP-1 and GASP-2 are important modulators of GDF-11 and

14 However, when we compete GASP mutants against wild-type cells in a chain of micro

15 Each locus is capable of conferring GASP on the rpoS819 parent, and they can provide success

16 nus common to the D(3) and D(2) that confers GASP-1 binding.

17 Disruption of the D2-GASP interaction facilitates recovery of D2 responses, s

18 ponses, suggesting that modulation of the D2-GASP interaction is important for the functional down-re

19 Disruption of the DOR-GASP interaction through receptor mutation or overexpres

20 l Antimicrobial Surveillance Programme (Euro-GASP) in 2020, and made comparisons with Euro-GASP data

21 ASP) in 2020, and made comparisons with Euro-GASP data from 2013 and 2018.

22 antage in stationary phase (GASP); we expect GASP cells to maintain a proliferative state and dominat

23 semble that of the D(2) and D(3) facilitated GASP-1 binding and promoted post-endocytic degradation o

24 The first GASP mutation was identified as a loss-of-function allel

25 ni can expose determinants with affinity for GASP binding and consequently target receptors for degra

26 All four GASP mutations isolated thus far allow for faster growth

27 ing techniques for pharmacophore generation (GASP) and ligand-receptor docking (GOLD).

28 henotypes (Lifelines/DAG [Dutch Asthma GWAS]/GASP [Genetics of Asthma Severity & Phenotypes] cohorts)

29 tingtin-interacting protein 1 [HIP1], HIP14, GASP-1, and Nedd4) that decrease insulin secretion from

30 not interact with GASP-1, not only inhibited GASP-1 binding but slowed degradation after endocytosis.

31 or the lrp GASP phenotype, and hence the lrp GASP phenotype is due to more global physiological chang

32 play a role, it is not necessary for the lrp GASP phenotype, and hence the lrp GASP phenotype is due

33 Here we have identified three new GASP loci from an aged rpoS819 strain: sgaA, sgaB, and s

34 ith megalin is mediated by the PDZ domain of GASP binding to the DSDV motif found at the carboxyl-ter

35 x, suggesting that the C-terminal domains of GASP-1 are the primary mediators for asymmetric complex

36 xpression of a dominant negative fragment of GASP inhibited receptor trafficking to lysosomes and pro

37 A close homolog of GASP, i.e., membrane-associated guanylate kinase with in

38 The interaction of GASP with megalin is mediated by the PDZ domain of GASP

39 al standpoint describing the interactions of GASP antagonists with myostatin.

40 shRNA knockdown of GASP-1 delayed post-endocytic degradation of both the D(

41 myostatin-free and myostatin-bound states of GASP-1 and GASP-2.

42 Additionally, C-terminal truncations of GASP-1 result in less potent myostatin inhibitors that f

43 the growth advantage in stationary phase, or GASP, phenotype.

44 itable growth advantage in stationary phase (GASP) compared with overnight cultures.

45 ress a growth advantage in stationary phase (GASP) phenotype, enabling them to grow and displace the

46 ss the growth advantage in stationary phase (GASP) phenotype.

47 have a growth advantage in stationary phase (GASP); we expect GASP cells to maintain a proliferative

48 Genetics of Asthma Severity and Phenotypes [GASP] initiative and the Unbiased BIOmarkers in PREDicti

49 vironmental Satellite Aerosol/Smoke Product (GASP) Aerosol Optical Depth (AOD), followed by the CTM o

50 A genetic algorithm similarity program (GASP) approach (virtual ligand screening) identified thr

51 ng the Genetic Algorithm Similarity Program (GASP) method.

52 om the Genome Annotation Assessment Project (GASP) showed that GeneWise provided reasonably accurate

53 as the Genome Annotation Assessment Project (GASP), was launched in May 1999.

54 of the Genome Annotation Assessment Project (GASP).

55 of the Genome Annotation Assessment Project (GASP).

56 is both necessary and sufficient to promote GASP-1 binding and receptor degradation.

57 s named glycoprotein 330-associated protein (GASP), appears to be a truncated mouse counterpart of th

58 coupled receptor-associated sorting protein (GASP).

59 coupled receptor-associated sorting protein (GASP).

60 The GPCR-associated sorting protein, GASP, has been shown to preferentially sort a number of

61 Our studies have revealed GASP-1, which is 100 times more potent than GASP-2, pref

62 GASP-1, which is 100 times more potent than GASP-2, preferentially binds myostatin in an asymmetrica

63 In addition, these data demonstrated that GASP-1 can mediate post-endocytic degradation of dopamin

64 Here, we show that GASP-1 and GASP-2 act by blocking the initial signaling

65 The GASP family of proteins may modulate lysosomal sorting a

66 of gene finding and used as a basis for the GASP competition.

67 To date, most studies of the GASP phenotype have focused on identifying alleles that

68 This GASP allele, lrp-1141, encodes a mutant protein lacking

69 As a consequence of this GASP interaction, D2 responses in rat brain fail to rese

70 mutations in their C termini in fact bind to GASP and are targeted for degradation.

71 lacking a recycling signal, does not bind to GASP and is therefore not targeted for degradation.

72 cks the terminal valine is unable to bind to GASP, illustrating the PDZ domain-dependent interaction

73 atin in an asymmetrical 1:1 complex, whereas GASP-2 binds in a symmetrical 2:1 complex.

74 ity under nutrient-limited conditions, while GASP cells dominate nutrient-rich regions.

75 emble the D(4), which does not interact with GASP-1, not only inhibited GASP-1 binding but slowed deg