ライフサイエンスコーパス: exofacial

1 This indicates that it is the exofacial alpha2 domain that is involved in the enhancem

2 ntigens, many of which are created by single exofacial amino acid substitutions, have varying immunog

3 ric distribution of lipid species across the exofacial and cytofacial aspects of the bilayer.

4 Our results also confirm the exofacial and cytosolic localization of N- and C-termina

5 r exit indicating that WZB117 and CB bind at exofacial and endofacial sugar binding sites, respective

6 t a long distance effect on the formation of exofacial antigen epitopes.

7 the TM1 helix (Ile(29)-Gly(50)), as well as exofacial Asn(27) and Asn(28), resulted in functional im

8 dings may be explained by differences in the exofacial binding of substrates, as shown by inhibition

9 The primary defect with exofacial C326 substitutions was the loss of hepcidin bi

10 tional assays, we showed that 6A10 inhibited exofacial CA activity in CA XII-expressing cancer cells.

11 In well-superfused myocytes, exofacial CA activity is superfluous, most likely becaus

12 These results corroborate the notion that exofacial CA is critical for cancer cell physiology and

13 prostate cancer cells, both of which express exofacial CA IX.

14 Effects of intracellular and extracellular (exofacial) CA (CAi and CAe) are distinguished using memb

15 Exofacial carbonic anhydrase activity increases with exp

16 Accordingly, inhibition of exofacial CAs has been proposed as a general therapeutic

17 and, concomitantly, the chemical activity of exofacial cholesterol was increased.

18 lies outside the inner helical bundle in the exofacial configuration of Glut1.

19 omology modeling suggest a structure for the exofacial configuration of the Glut1 glucose transporter

20 A model has been proposed for the exofacial configuration of the Glut1 glucose transporter

21 ernal solvent when the transporter is in its exofacial configuration.

22 w resolution model has been proposed for the exofacial conformation of the Glut1 glucose transporter

23 3) The GLUT1 exofacial conformer lacks a CB binding site.

24 2) GLUT1 and GLUT4 exofacial conformers present multiple, adjacent glucose

25 redox inactivation of adjacent thiols in the exofacial domain of VLA-4 after its ligation to stromal

26 ccess transporter that successively presents exofacial (e2) and endofacial (e1) substrate-binding sit

27 s indicated that ligand binding involves the exofacial end of transmembrane domain (TM) 4, whereas G

28 C124A and C202A mutations, located near the exofacial end of transmembrane helix 3 and in EL2, respe

29 ls, several plasma membrane proteins such as exofacial enzymes, receptors, and ion channels recycle b

30 V (amino acids 1417-1434) only bound to this exofacial epitope if the DRG neurones and cardiac myocyt

31 This approach uses antibodies targeting exofacial epitopes on native GLUT4.

32 Quantification of the exofacial expression of obscurin kinase proteins indicat

33 utive residues predicted to lie close to the exofacial face of the membrane resulted in sensitivity t

34 membrane helices and the conformation of the exofacial glucose binding site of GLUT1 are proposed tha

35 tion of the 12 transmembrane helices and the exofacial glucose-binding site of Glut1 are proposed tha

36 membrane helices and the conformation of the exofacial glucose-binding site of Glut1 is presented tha

37 1) The WZB117 binding envelopes of exofacial GLUT1 and GLUT4 conformers differ significantl

38 We identify an exofacial GLUT3 inhibitor SA47 and elucidate its mode of

39 r three cysteine mutants clustered along the exofacial half of the helix (M129C, T130C, S133C) and fi

40 ane-impermeant MTSET remains confined to the exofacial half of the helix along a single, discrete fac

41 rs: glucose, forskolin, and phloretin at the exofacial infundibulum; forskolin, and phloretin at an e

42 B, was non-competitive and inhibition by the exofacial inhibitor, 4,6-O-ethylidene-alpha-glucose, was

43 ve as a framework for the discovery of GLUTs exofacial inhibitors for therapeutic development.

44 Reasoning that exofacial inhibitors of GLUT1/3 may be favored for thera

45 t can be probed for screening and validating exofacial inhibitors.

46 c peptides derived from the second and third exofacial, interhelical regions of band 3 completely inh

47 ulus in the epitrochlearis muscle, using the exofacial label ATB-[3H]BMPA, showed that adenosine deam

48 limited by ATP-binding Walker motifs, and an exofacial large side cavity of yet unknown function.

49 ncreases concentration of cholesterol on the exofacial layer, typical of aging or Alzheimer's disease

50 esterol distribution that is depleted on the exofacial leaflet but enhanced on the cytofacial leaflet

51 d-based quenchers that are restricted to the exofacial leaflet of the plasma membrane only reduce the

52 ubset of membrane lipids from the lumenal or exofacial leaflet to the cytofacial aspect of the bilaye

53 membrane, 2) that the barrier resides in the exofacial leaflet, 3) that both sphingomyelin and glycos

54 increasing PS levels in the plasma membrane exofacial leaflet, and that this is sufficient to facili

55 holipid translocation to the plasma membrane exofacial leaflet; this leads to unequal lateral packing

56 and NH(3) was 18-90-fold higher than for the exofacial liposomes (P(f(ex)) = 2.4 +/- 0.4 x 10(-4) cm/

57 ing published lipid compositions we prepared exofacial liposomes containing phosphatidylcholine, sphi

58 In exofacial liposomes lacking glycosphingolipids or sphing

59 ontrast, the apparent proton permeability of exofacial liposomes was 4-fold higher than cytoplasmic l

60 e cells stably expressing myc epitope at the exofacial loop (GLUT4).

61 chymotryptic cleavage sites in the adjacent exofacial loop 7-8.

62 a horseradish peroxidase (HRP) in the fourth exofacial loop in either the presence or absence of R107

63 tep process, orchestrated by key residues in exofacial loop regions, as well as in membrane-spanning

64 other molecules exposed on the cell surface (exofacial membrane).

65 which involves the sequential function of an exofacial metalloprotease and the cytoplasmic proteasome

66 Carbonic anhydrase members in this class of exofacial molecules facilitate tumor metabolism by facil

67 GLUT4 vesicle movements and translocation of exofacial Myc-tagged GLUT4-green fluorescent protein to

68 siae using variants of a Type III (naturally exofacial N terminus (Nexo)) transmembrane fusion protei

69 s fusion inserts with exclusively N terminus exofacial (Nexo) topology, serving as a model type III m

70 ere are two positively charged cavities (one exofacial, one endofacial) delimited by ATP-binding Walk

71 In lipid vesicles mimicking the exofacial (outer) membrane leaflet, PFO-membrane binding

72 inward-facing amino acid side chains in the exofacial parts of transmembrane helices 4 and 7 contrib

73 Much has been learned about the role of exofacial phosphatidylserine (PS) in apoptosis and blood

74 Exofacial phosphatidylserine (PS) is an important ligand

75 mediated, in part, by receptors that bind to exofacial phosphatidylserine (PS) on cells or cellular d

76 s-[2-(3)H] (D-mannose-4-yloxy)-2-propylamine exofacial photolabeling technique, was reduced by approx

77 yl]-1,3-bis(D-mannos-4-yloxy)-2-propyl amine exofacial photolabeling technique.

78 ell surface recruitment of GLUT4 assessed by exofacial photolabeling with [3H]-ATB bis-mannose was re

79 These data demonstrate that the exofacial portion of transmembrane segment 11 is accessi

80 These data demonstrate that the exofacial portion of transmembrane segment 7 is accessib

81 in the presence or absence of ligand, by an exofacial proteolytic activity producing a membrane-anch

82 l, generating membrane-derived vesicles with exofacial PS.

83 ithin M9 (residues 342-363) and the adjacent exofacial re-entrant loop 5 between M9 and M10 (EL5; res

84 Earlier, we identified two nonglycosylated exofacial regions of erythrocyte band 3 termed 5ABC and

85 Two nonglycosylated exofacial regions of human band 3 in the RBC membrane we

86 ond Cys residue that was introduced into the exofacial segment of TM III, within the sequence Leu-142

87 s residue (Cys-532(7.42)) located within the exofacial segment of transmembrane domain (TM) VII, clos

88 two distinct regions of the M3 receptor, the exofacial segments of TM V and VI and the cytoplasmic en

89 he concept that agonist activation pulls the exofacial segments of TMs VII and III closer to each oth

90 ster groups (5-Bn) of 21 oriented toward the exofacial side and the 4-position phenylethynyl group si

91 (289), Val(290), and Phe(291)), all near the exofacial side of the cell membrane, produced transporte

92 d to critical residues in TM3 and TM7 on the exofacial side of the human P2Y1 receptor.

93 These results suggest that residues on the exofacial side of TM3 and TM7 are critical determinants

94 tants or continuous surface labeling with an exofacial specific antibody demonstrated that GLUT4 did

95 ation pathway of Glut1, probably between the exofacial substrate-binding site and the outer vestibule

96 eriments indicated that Cys165 lies near the exofacial substrate-binding site or directly in the suga

97 e inner helical bundle predicted to form the exofacial substrate-binding site.

98 e antigen of 80 kDa that is expressed on the exofacial surface of erythrocytes infected by early-to-l

99 se these polarized lipids are present in the exofacial surface of the bilayer, we propose that the li

100 by phosphatidylserine (PS) displayed at the exofacial surface of the plasma membrane; however, neith

101 ructs containing inserted surface-accessible exofacial tags, which allow visualization of only those

102 (-SH) naturally present on the cell surface (exofacial thiols) can be used to enhance cellular associ

103 osomal escape through contacts with cellular exofacial thiols, in addition to facilitating cellular u

104 te specific phospholipid substrates from the exofacial to the cytosolic leaflet of membranes to gener

105 by flipping specific phospholipids from the exofacial to the cytosolic leaflet.

106 three basic domains of the receptors (i.e., exofacial, transmembrane, and cytoplasmic segments) that

107 nd intracellular domains, with a funnel-like exofacial vestibule (infundibulum), followed by a 15 A-l