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1 ne and associated with disrupted TLR9 at the submembrane.
2 esting that they may translocate against the submembrane actin cortex.
3                    KCC2 interaction with the submembrane actin cytoskeleton via 4.1N is known to cont
4  extracellular environment with the parasite submembrane actomyosin motor.
5  gold particles/microgram 2 cytoplasm in the submembrane and the central region of intracapillary neu
6 t elevation in K(ATP) p(open) may arise from submembrane ATP depletion by the Na(+)-K(+) ATPase, as t
7 ump interacts with KATP current (IK-ATP) via submembrane ATP depletion in isolated giant membrane pat
8 can be observed with widely varying apparent submembrane [ATP] ([ATP](sub)).
9 ional sample preparation does not reveal the submembrane axonemal structure, which holds key implicat
10             On a long-range scale (>250 nm), submembrane barriers, or skeleton fences that hinder lon
11 ulses (10-100 ms) lead to the development of submembrane Ca(2+) gradients, as previously described.
12                We demonstrate that a rise in submembrane Ca(2+) induces a large decrease in T-type cu
13 dually increased as the cell repolarized and submembrane [Ca(2+)] decreased further.
14 6 pA/pF) followed by decay to the point that submembrane [Ca(2+)] reached ~10 muM.
15                              NCAM2-dependent submembrane [Ca(2+)] spikes colocalize with the bases of
16 ll surface of mouse cortical neurons induces submembrane [Ca(2+)] spikes, which depend on the L-type
17  We then used this relationship to infer the submembrane [Ca(2+)](i) ([Ca(2+)](sm)) sensed by NCX dur
18 X current (INCX) was used to infer the local submembrane [Ca]i ([Ca]sm) that is sensed by NCX dynamic
19 it has become clear that cyclic variation of submembrane [Ca2+] and activation of the Na+-Ca2+ exchan
20  to more negative potentials by increases in submembrane [Ca2+] from 1 to 60 microM.
21 to embrace the impact of cyclic variation in submembrane [Ca2+] on pacemaker function.
22                                              Submembrane [Ca2+]i changes were examined in rat chromaf
23         This information was used to examine submembrane [Ca2+]i elevations arising out of Ca2+ influ
24                                              Submembrane [Ca2+]i elevations fall rapidly after termin
25                   In contrast to influx, the submembrane [Ca2+]i elevations produced by release of in
26 ities of transient and nonuniform changes in submembrane calcium concentration produced by voltage-ga
27  and illustrate the functional importance of submembrane calcium microdomains.
28 at PDE2 mediates NP/cGMP-driven decreases of submembrane cAMP levels.
29 pled exocytosis apparently requires elevated submembrane cation concentrations that dissipate rapidly
30                    A model consisting of two submembrane (caveolar and extracaveolar) microdomains an
31             In control rabbits, the ratio of submembrane/central gold was always greater than one and
32                                 The ratio of submembrane/central gold was greater in complement-treat
33                         Collybistin promotes submembrane clustering of gephyrin and is essential for
34                                              Submembrane colocalization of NCX1 and cardiac RyR (cRyR
35 y transmission of energetic signals into the submembrane compartment synchronizing K(ATP) channel act
36                  This complex localizes in a submembrane compartment where cAMP synthesis occurs.
37 s, but may control cAMP levels in restricted submembrane compartments that are defined by small volum
38 rane lipid composition varies greatly within submembrane compartments, different organelle membranes,
39 likely due to restricted cAMP diffusion from submembrane compartments.
40 oteolytic processing of SOAF from sperm head submembrane compartments.
41 in family are ubiquitous constituents of the submembrane cortex, especially in epithelial cells.
42 and then interact with specific sites on the submembrane cortex.
43  and beta-Spectrin are major components of a submembrane cytoskeletal network connecting actin filame
44                       Dystrophin is a large, submembrane cytoskeletal protein, absence of which cause
45  might serve to anchor NMDA receptors to the submembrane cytoskeleton and aid in the assembly of sign
46 n does not depend on membrane trafficking or submembrane cytoskeleton and has no effect on GJ conduct
47 n, and associated molecules form a periodic, submembrane cytoskeleton in the axons of neurons.
48         These results suggest that an apical submembrane cytoskeleton of intermediate filaments is ex
49 ments may function as a novel element of the submembrane cytoskeleton of spines.
50 on of "extracellular matrix-surface membrane-submembrane cytoskeleton" assembly of the NK-sensitive T
51 ated proteins that are key components of the submembrane cytoskeleton.
52 s used for optical imaging of exocytosis and submembrane depolarization-evoked [Ca(2+)](i).
53 ed that GLP-1 activates PLC, which increases submembrane diacylglycerol and thereby activates PKC, re
54 calize the enzyme to specific subcellular or submembrane domains.
55          In contrast, ANP elicited sustained submembrane elevations in [cGMP](i), which were converte
56  interactions enhance the functioning of the submembrane exocytic machinery.
57 e membrane by altering the properties of the submembrane F-actin and/or its attachment to the membran
58  Cytoskeletal rearrangements, as assessed by submembrane F-actin rims, result in poorly deformable ne
59                                          For submembrane fluorescence-marked actin, the intensity, of
60 ws that a 30 min incubation of spinach PS II submembrane fragments at pH 6.3 in the presence of 10 mi
61 cardiomyocyte and neuronal excitability at a submembrane junction, suggesting a pathway conferring su
62                Here, we discuss how receptor submembrane localization and the formation of alternate
63 oncluded that both substrate specificity and submembrane location are critical to phosphatase-mediate
64 l development and originates from sperm head submembrane matrices.
65 ty of collybistin to translocate gephyrin to submembrane microaggregates in transfected mammalian cel
66                                     All five submembrane MX helices of the membrane-intact junctional
67 , it is necessary to accurately estimate the submembrane Na(+) concentration ([Na(+)]sm).
68                     However, larger rises in submembrane [Na+] ([Na+]sm) local to Na+-Ca2+ exchangers
69  suggest that micromolar [Ca(2+) ]i , in the submembrane or junctional cleft space, is not required t
70 y restricting its distribution to a discrete submembrane pool.
71 ithin the membrane (the sarcoglycans), and a submembrane protein (utrophin).
72 oviding a mechanism for assembly of distinct submembrane protein complexes.
73 in some cells result in local proteolysis of submembrane proteins, leading to generation of membrane
74 istribution of actin from the central to the submembrane region and the microvilli and result in more
75 neutrophils by altering the stiffness of the submembrane region and/or by preventing the microvilli f
76 fening required F-actin formation within the submembrane region but not microtubule rearrangement in
77 phils also contained more F-actin within the submembrane region than circulating neutrophils when exa
78 xes depend on the Na(+) concentration in the submembrane region, it is necessary to accurately estima
79 on of end-binding protein 3 (EB3) in the AIS submembrane region.
80 rger in the interior of the cell than in the submembrane region.
81  dynamic KCNQ1 vesicles were observed in the submembrane region.
82 olocalizes with GLUT4 in perinuclear but not submembrane regions visualized by confocal total interna
83                        Inclusion of adjacent submembrane residues of L0, the linker between TMD0 and
84 g of these receptors, for recruitment of the submembrane scaffold protein gephyrin to postsynaptic si
85 whirlin (L-whirlin), a PDZ domain-containing submembrane scaffold protein, is present at the tips of
86               Zonula occludens-1 (ZO-1) is a submembrane scaffolding protein that may display proinva
87 ough the cell, and the ongoing nonfunctional submembrane signalling activity or noise.
88 sts that specific AKAPs direct the kinase to submembrane sites to facilitate phosphorylation and modu
89 from cell populations, single cells, and the submembrane space of a single cell.
90 r, revealed a diffusional barrier within the submembrane space, preventing direct reception of cytoso
91 with different dynamic Ca(2+) signals in the submembrane space, the cytosol, and the nucleus.
92 lations, single cells, and the intracellular submembrane space, we have demonstrated in a model liver
93 and the remaining 80% probably occurs in the submembrane space.
94 orylation and regulation were facilitated by submembrane targeting of protein kinase A (PKA), through
95 t CTLA-4 proteins were localized in Tregs in submembrane vesicles that rapidly recycled to/from the c