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1 ol, phosphatidylglycerol and an unidentified aminophospholipid.
2 E) display a markedly reduced sensitivity to aminophospholipids.
3 two products of nonenzymatic modification of aminophospholipids.
4                                  Transported aminophospholipids activate the dephosphorylation simila
5 r in the absence of primary amine group from aminophospholipids and amino acids.
6 lets bound annexin-V, indicating exposure of aminophospholipids and were enriched in young platelets
7                                              Aminophospholipid (APL) trafficking across the plasma me
8 ed by compensatory increase in prothrombotic aminophospholipids (aPL) in circulating cell membranes.
9    This protocol measures externalization of aminophospholipids (APLs) to the outside of the plasma m
10                                              Aminophospholipids (APLs), composed of phosphatidylethan
11 g a balance between sphingolipid content and aminophospholipid asymmetry in eukaryotic plasma membran
12 ties can result in sustained exposure of the aminophospholipids at the cell surface, which allows cap
13 t was found to be disrupted in the P4-ATPase AMINOPHOSPHOLIPID ATPASE 3 (ALA3), a lipid flippase that
14 this work, we address the role of ALA10 (for aminophospholipid ATPase), a P4-type ATPase, in a proces
15       Here we show that Arabidopsis thaliana Aminophospholipid ATPase10 (ALA10) is a P4-type ATPase f
16 of repp12 as a single amino acid exchange in Aminophospholipid ATPase3 (ALA3), a phospholipid flippas
17 ses (autoinhibited H+-ATPase, P3A), putative aminophospholipid ATPases (ALA, P4), and a branch with u
18                                              Aminophospholipid ATPases (ALAs) are lipid flippases inv
19 ticipates in maintaining the distribution of aminophospholipids between the inner and outer leaflets
20 )-ATPase, appears to participate directly in aminophospholipid binding or to mediate a crucial intera
21 specific marker for covalent modification of aminophospholipids by myeloperoxidase.
22   Therefore, the properties of nonmethylated aminophospholipids capable of organization into a bilaye
23 idylserine and phosphatidylethanolamine, two aminophospholipids exposed on the outer leaflet of dead
24 f P-selectin, and potentiation of Ca(2+) and aminophospholipid exposure to CRP in SHIP(-/-) platelets
25 cytic pathway without concomitant effects on aminophospholipid exposure.
26 initiation of ciliogenesis in Chlamydomonas, aminophospholipid flippase 2 (ALA2) is rapidly recruited
27 xt-sensitive function for ATP11C, a putative aminophospholipid flippase, in B cell development.
28 zed of these transporters is the erythrocyte aminophospholipid flippase, which selectively transports
29 results from mutations in ATP8B1, a putative aminophospholipid flippase.
30 consistent with the function of Atp8b1 as an aminophospholipid flippase.
31 eimide (NEM), an inhibitor of the endogenous aminophospholipid flippase.
32                                         This aminophospholipid "flippase" selectively transports PS t
33                         Here, we report that aminophospholipid flippases regulate the lipid compositi
34 sing the role of carbonyl-amine reactions of aminophospholipids in aging and age-related diseases.
35 es catalyze the final step of atg8ylation of aminophospholipids in membranes.
36        To determine whether aldehydes modify aminophospholipids in vivo, we quantified levels of pHA-
37 se to apoptotic Neuro2a cells is mediated by aminophospholipid ligands, phosphatidylserine and phosph
38 the formation of F4-neuroprostane-containing aminophospholipids might adversely effect neuronal funct
39 rate that this reactive aldehyde targets the aminophospholipids of LDL in vitro and in vivo.
40 on by transducing intracellular signals from aminophospholipids on apoptotic cells, as well as uniden
41                          Limited exposure of aminophospholipids on the outer leaflet of the plasma me
42 critical [Ca2+]i level necessary to maintain aminophospholipids on the outer surface of the platelet
43  with adenosine triphosphate (ATP)-dependent aminophospholipid (phosphatidyl-serine) translocase acti
44 rnalization of PS but not of the other major aminophospholipid, phosphatidylethanolamine.
45  anomaly in bovine erythrocytes that affects aminophospholipids: phosphatidylethanolamine (PE) shows
46 ising the possibility that aldehyde-modified aminophospholipids play a role in inflammation and vascu
47     Fluorescamine derivatization of external aminophospholipids revealed that PS, but not phosphatidy
48     By contrast, Lys(865) is unimportant for aminophospholipid sensitivity.
49 ed upon specific events required for de novo aminophospholipid synthesis in the yeast Saccharomyces c
50 oxylase (TbPSD), two key enzymes involved in aminophospholipid synthesis, for trypanosome viability.
51 ter leaflet of the membrane bilayer contains aminophospholipids that are normally sequestered to the
52 eptions, most cells restrict the bulk of the aminophospholipids to the inner membrane leaflet by mean
53 lterations (spherocytosis), translocation of aminophospholipids to the outer leaflet of the membrane,
54 teins correct for sporadic incursions of the aminophospholipids to the outer membrane leaflet as a re
55 , and testis, where it mediates transport of aminophospholipids toward the cytoplasmic leaflet.
56 transporters involved in PS externalization, aminophospholipid translocase (APLT) and phospholipid sc
57              PS distribution is regulated by aminophospholipid translocase (APLT), which maintains PS
58  cytosolic leaflet of the plasma membrane by aminophospholipid translocase (APLT).
59 rnalization was accompanied by inhibition of aminophospholipid translocase (APT).
60  is an essential P-type ATPase and potential aminophospholipid translocase (flippase) in the Drs2p fa
61 ntegral membrane P-type ATPase and potential aminophospholipid translocase (or flippase).
62 embrane surface, but can interfere with both aminophospholipid translocase activity and calcium-induc
63 erstood but has been associated with loss of aminophospholipid translocase activity and nonspecific f
64 uld affect PS appearance, either by altering aminophospholipid translocase activity or phospholipid f
65 arance in the plasma membrane outer leaflet, aminophospholipid translocase activity ultimately modula
66 ibited despite DNA fragmentation and loss of aminophospholipid translocase activity, the latter demon
67  RBC and that it correlates with the loss of aminophospholipid translocase activity, the only common
68 de of PS appearance depended on the level of aminophospholipid translocase activity.
69  to severe cellular damage and impairment of aminophospholipid translocase activity.
70 hich can be exacerbated by the inhibition of aminophospholipid translocase activity.
71 ent of spin-labeled PS was used to determine aminophospholipid translocase activity.
72 it is thought that declining activity of the aminophospholipid translocase and calcium-mediated, nons
73 lic Ca2+ in concert with inactivation of the aminophospholipid translocase and is inhibited by calciu
74 tosis, the appearance of PS followed loss of aminophospholipid translocase and was accompanied by non
75 ter the decline in PS inward movement by the aminophospholipid translocase as measured by the uptake
76   The recently cloned gene for the mammalian aminophospholipid translocase belongs to this new subfam
77 s2p/Swa3p is a P-type ATPase and a potential aminophospholipid translocase that localizes to the tran
78 ate-labeled annexin V, (ii) PS uptake by the aminophospholipid translocase using [6-[(7-nitrobenz-2-o
79 activity in concert with inactivation of the aminophospholipid translocase, there is no evidence indi
80 e inner leaflet of the plasma membrane by an aminophospholipid translocase, which has now been cloned
81  support its function as an energy-dependent aminophospholipid translocase.
82 the inactivation of the transmembrane enzyme aminophospholipid-translocase (or flippase) by HNE and a
83  consists of 12 members that encode putative aminophospholipid translocases (ALA1-12).
84                                              Aminophospholipid translocases (APLTs) are defined prima
85 s encoding P-type ATPases that are potential aminophospholipid translocases (APTs): DRS2, NEO1, and t
86                     Our results suggest that aminophospholipid translocases play an important role in
87 alysis of strains harboring deletions of the aminophospholipid translocating P-type ATPases (APLTs).
88                           Cells in which the aminophospholipid translocating protein was inhibited be
89 ype ATPase and is presumably responsible for aminophospholipid translocation activity in eukaryotic c
90                                          The aminophospholipid translocation activity plays an import
91 ies in Saccharomyces cerevisiae suggest that aminophospholipid translocation is a general function of
92 ng lipid content, phospholipid organization, aminophospholipid transport (flippase), and prothrombin
93 d subfamily of P-type ATPases; ATP-dependent aminophospholipid transport is the previously described
94 nositides in the regulation of intracellular aminophospholipid transport.
95                                  Thus, a new aminophospholipid transporter expressed exclusively in s
96  screen, we have discovered an ATP-dependent aminophospholipid transporter that is exclusively expres
97          Six genes, including four candidate aminophospholipid transporters, are refractory to gene d
98  and a computational pipeline, we identified aminophospholipid transporting ATPase 2 (ALA2) and the r
99 s a putative protein homologous to the mouse aminophospholipid-transporting ATPase Atp10c.
100  detected as N-methylpiperazine-amide-tagged aminophospholipids using a precursor scan of the stable
101  method for N-methylpiperazine- amide-tagged aminophospholipids was used to examine the fate of diacy
102  been implicated in exposure of procoagulant aminophospholipids, we have now examined calcium fluxes
103 nal-transducing TREM2 ligands different from aminophospholipids, which appear to be derived from neur
104                                         When aminophospholipids with only saturated and monounsaturat
105 are not useful in determining the changes of aminophospholipids with polyunsaturated fatty acids (PUF
106 on-induced dissociation spectra of nontagged aminophospholipids with PUFAs.

 
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