ライフサイエンスコーパス: ER export

1 the recruitment of COPII to the membranes or ER export.

2 Lst1p, suggesting a unique role for Lst1p in ER export.

3 was sufficient for COPII binding but not for ER export.

4 at is responsible for cargo selection during ER export.

5 ces in the N terminus supply information for ER export.

6 ze the possible role of kinase regulation in ER export.

7 n analyzed their role in cargo selection and ER export.

8 t-negative mutant of Sar1 (Sar1pdn) blocking ER export.

9 dispersion of Sec16A from ERES and impaired ER export.

10 aling that dimerization was not required for ER export.

11 n controls membrane constriction to regulate ER export.

12 uired in a number of instances for efficient ER export.

13 at AMPARs sample the gating cascade prior to ER export.

14 ks ERES membranes to regulate COPII-mediated ER export.

15 phosphatidylinositols (PtdIns) in regulating ER export.

16 Ins4P) is required to promote COPII-mediated ER export.

17 bligatory role for the beta2 AChR subunit in ER export.

18 structural determinants of alpha4beta2 AChR ER export.

19 y unappreciated role for Nm23H2 in mammalian ER export.

20 s -4 and -1) that was required for efficient ER export.

21 mbly at steady state and reduced kinetics of ER export.

22 important regulator of COPII-mediated EphA2 ER export.

23 thus PLD is temporally regulated to support ER export.

24 vation is required to support COPII-mediated ER export.

25 13/31 COPII complexes to ER export sites and ER export.

26 FA) to cause Golgi collapse and H89 to block ER export.

27 component SEC24C for endoplasmic reticulum (ER) export.

28 ocal zones of ER complexity compartmentalize ER export and correspond to sites of new dendritic branc

29 The combined effects of reduced ER export and endocytosis significantly deplete Pmel17 w

30 Both ER export and ER Golgi intermediate compartment (ERGIC)-

31 both proteins are required in HeLa cells for ER export and for normal tER organization.

32 tinual fatty acid synthesis was required for ER export and for normal tER site structure, whereas inh

33 ive protein kinase A inhibitor, blocked both ER export and hypo-osmotic-, brefeldin A-, or nocodazole

34 s as a molecular chaperone, increasing gH/gL ER export and incorporation into virions.

35 d-type proinsulin improves, accelerating its ER export and increasing wild-type insulin production.

36 These results demonstrate that ER export and initiation of COPII vesicle formation in m

37 A C-terminal valine residue functioned in ER export and interacted with coat complex (COP)II, whil

38 We demonstrate that US11 itself undergoes ER export and proteasomal degradation and utilize this s

39 es the exit signal, and thereby prevents the ER export and surface expression of the channel.

40 Association with hERG 1a facilitated 1b ER export and surface expression.

41 st that TR gO acts as a chaperone to promote ER export and the incorporation of gH/gL complexes into

42 aperones released the CNX-bound receptors to ER export and, furthermore, were able to rescue the Cys(

43 anisms underlying the endoplasmic reticulum (ER) export and cell surface transport of nascent G prote

44 viously suggested to play important roles in ER-export and subunit co-assembly respectively in this f

45 between cell volume, endoplasmic reticulum (ER) export, and stimulated Golgi-to-ER transport.

46 exit-site (ERES) assembly and COPII-mediated ER export are currently unknown.

47 f ERGIC and Golgi proteins into the ER after ER export arrest.

48 Q-SNAREs into COPII vesicles, implying their ER export as a preassembled complex.

49 ther with the sensitivity of BFA remnants to ER export blockade, suggests that presence of matrix pro

50 ze large COPII-coated endoplasmic reticulum (ER) export carriers.

51 activity and Cdc14 nuclear release for Chs2 ER export, cells ensure that septum formation is conting

52 plasmic reticulum (ER) membranes and becomes ER export competent only upon coexpression with Gn.

53 the connecting [C]-peptide) is folded in the ER, exported, converted to human insulin, and secreted.

54 Alternatively, disruption of procollagen I ER export could activate the unfolded protein response (

55 The ER export delay and cell surface retention are also obse

56 er with the previously identified N-terminal ER export diacidic motif, account for the differential l

57 localize adjacent to endoplasmic reticulum (ER) export domains, and resident Golgi transmembrane pro

58 Star acts as an endoplasmic reticulum (ER) export factor for all three.

59 ished as either competent or incompetent for ER export has not been elucidated.

60 rons to examine the role of SEC24C-dependent ER export in axonal targeting of SERT.

61 These data suggest that hERG undergoes ER export in COPII vesicles and endosomal recycling prio

62 We have characterized the organization of ER export in the malaria parasite, Plasmodium falciparum

63 ing cargo export in live cells, we show that ER export in vivo is also characterized by the formation

64 Blocking ER export in vivo stabilized the interaction between Vma

65 ER export is accelerated by the alternatively spliced C2

66 This ER export is blocked by brefeldin A and wortmannin but i

67 ents show that the site of the new Golgi and ER export is determined by the location of the new basal

68 These results indicate that efficient ER export is not sufficient to enable normal cell-surfac

69 inhibited without disrupting COPII-dependent ER export machinery (by brefeldin A treatment or express

70 d oxidative folding exceeded the capacity of ER export machinery.

71 e residue at position +2 downstream from the ER export motif ((607)RI(608) in SERT).

72 enesis identified an acidic-residue putative ER export motif responsible for the I-II loop-mediated i

73 Loss of an ER export motif upon cleavage of GIRK2 abolishes surface

74 We also verified that the presence of two ER export motifs (in concatemers of SERT and GABA transp

75 interaction through mutation of the putative ER export motifs of Sed5p and the cargo-binding A-site o

76 eir cytoplasmic tails, which themselves lack ER export motifs.

77 Consistent with a function for Nm23H2 in ER export, Nm23H2 localized to a reticular network that

78 We investigated where endoplasmic reticulum (ER) export occurs in dendrites using an in vitro permeab

79 We conclude that, when nicotine accelerates ER export of alpha4beta2 nAChRs, this suppresses ER stre

80 ER export of BiP occurs via COPII-dependent transport to

81 The effect of these three mutations on ER export of DAT was demonstrated in porcine aortic endo

82 nt of protein folding and leads to efficient ER export of even misfolded species.

83 BiP, therefore, prevents the ER export of folded but alpha(1)-unassembled beta subuni

84 the F(X)(6)LL motif plays a general role in ER export of G protein-coupled receptors (GPCRs).

85 Thus, ER export of membrane proteins is not necessarily limite

86 p26Delta cells revealed a role for Svp26p in ER export of only a subset of type II membrane proteins.

87 This prevents premature ER export of partially folded receptors.

88 fibroblasts of this individual revealed that ER export of procollagen was inefficient and that ER tub

89 endoplasmic reticulum (ER) quality control, ER export of secretory cargo, and programmed cell death.

90 Furthermore, ER export of the complexes is dependent of the interacti

91 , impaired (pre)proinsulin oxidation affects ER export of the mutant as well as that of coexpressed w

92 We show that efficient ER export of the p24 family of proteins is a major drive

93 n the C terminus were also found to regulate ER export of the receptors.

94 t transmembrane domain are essential for the ER export of the transporter.

95 component SEC24D, which is important in the ER export of wild type DAT, also blocked the rescue effe

96 In the absence of Pma1-D378N, ER export of wild-type Pma1 is not affected by eps1 dele

97 negative effect on cell growth by preventing ER export of wild-type Pma1.

98 that acts to promote endoplasmic reticulum (ER) export of gH/gL and that gO is not stably incorporat

99 and ARF1 regulate the endoplasmic reticulum (ER) export of proteins in COPII and COPI vesicles, respe

100 thesized proteins and directs them either to ER export or ER-associated degradation (ERAD).

101 motifs important for endoplasmic reticulum (ER) export or endocytotic trafficking.

102 o the cell periphery via the classical Golgi/ER export pathway.

103 protein is sufficient to confer an enhanced ER export rate.

104 s due to cycling via the ER and preferential ER export rather than their stable assembly in a matrix

105 s and therefore does not appear to act as an ER export receptor.

106 e; SVP26, encoding an endoplasmic reticulum (ER) export receptor for ALP; and AP-3 subunit genes.

107 this stress-induced pathway by depleting the ER-export receptors leads to aggregation of the ER-retai

108 We show here that Chs2 ER export requires the direct reversal of the inhibitory

109 of the ER indicate that in the absence of an ER export signal, molecules are inefficiently captured i

110 l GPI-APs and provides a protein-independent ER export signal.

111 suggests that the NPF motif is the dominant ER export signal.

112 nnels or a G protein-coupled receptor, these ER export signals increased the number of functional pro

113 Kir3.2 and Kir3.4, but not Kir3.1, contain ER export signals that are important for plasma membrane

114 Here, we describe two ER export signals that profoundly altered the steady-sta

115 about the identity of endoplasmic reticulum (ER) export signals and how they are used to regulate the

116 olgi is not the exclusive product of the new ER export site.

117 Duplication of the endoplasmic reticulum (ER) export site follows exactly the same time course.

118 Here, we show that these areas correspond to ER export sites (ERESs), distinct ER domains where glyco

119 of Sec23/24 and Sec13/31 COPII complexes to ER export sites and ER export.

120 We show that ER export sites are assembled regularly throughout the e

121 eatment led to a rapid loss of Sec13-labeled ER export sites but betaCOP localization to the Golgi wa

122 terize the three-dimensional organization of ER export sites in vivo and in vitro.

123 l protein kinase, in recruitment of COPII to ER export sites, as well as in stimulated but not consti

124 d occupy the space between cis cisternae and ER export sites, whereas the COPIb vesicles bud exclusiv

125 rough the generation of transitional tubular ER export sites.

126 ntly inhibited binding of exogenous Sec13 to ER export sites.

127 e distribution of this critical component at ER export sites.

128 f the NMDA receptor subunit NR1 to remodeled ER export sites.

129 s us to specifically control the assembly of ER export sites.

130 In mitosis, when ER export stops, Golgi proteins redistributed into the E

131 segregated from other cargo proteins during ER export, suggesting that ER membranes produce more tha

132 of biosynthetic cargo to prevent or enhance ER export suggests that interactions of cargo with the C

133 The mechanism for triggering Chs2 ER export thus far is unknown.

134 capture, or may be specifically employed in ER export to control deployment of nascent proteins.

135 l into COPII-enriched ER exit sites prior to ER export via a process that requires Sar1-GTPase.

136 i complex after mitosis failed to occur when ER export was blocked.

137 An in vitro assay for ER export was used to demonstrate preferential packaging

138 ed LRP6 molecules undergo palmitoylation and ER export, while unsuccessfully folded proteins are, wit