ライフサイエンスコーパス: membrane flow

1 s to clarify the possible role of tension in membrane flow.

2 hanism to regulate the rate of intracellular membrane flow.

3 ess that has been proposed to occur via bulk membrane flow.

4 ibration of membrane tension by impeding the membrane flow.

5 uring motility, and generation of retrograde membrane flow.

6 brane tension propagation through long-range membrane flows.

7 reveal an endocytic loop formed by circular membrane flow and anterograde movement of lipid vesicles

8 pathways in eukaryotic cells and coordinate membrane flow and cargo transport through the Golgi stac

9 nt mechanism, which is distinct from default membrane flow and remains poorly understood.

10 Thus, membrane flow and tension equilibration may be adapted t

11 er, in contrast to default recycling by bulk membrane flow, and is distinguishable in several ways fr

12 plied to membranes can create tethers, drive membrane flow, and set the diameter of the tubules.

13 Our work demonstrates how membrane flows are an integral part of Cdc42-driven patt

14 imbalance between the endocytic and exocytic membrane flow at the front of a migrating cell.

15 crucial for the establishment of retrograde membrane flow, because inhibition of endocytosis blocks

16 heir participation in opposite directions of membrane flow between the endoplasmic reticulum and Golg

17 an1 domain protein Lem2 acts as a barrier to membrane flow between the nucleus and other parts of the

18 ain membrane proteins does not occur by bulk membrane flow but is instead mediated by a specific endo

19 We conclude that bafilomycin A1 slows bulk membrane flow, but it causes additional inhibition of re

20 Membrane tension gradients drive membrane flows, but there is controversy over how rapidl

21 there is controversy over how rapidly plasma membrane flow can relax tension gradients.

22 h upon CRISPR knockout led to reduced plasma membrane flow directionality despite increased actin flo

23 alysis explains the phenomenon in terms of a membrane flow driven by liberated reaction energy, leadi

24 Membrane flow drives polar bodies and the ICSI site into

25 Upon stimulation, massive membrane flow from an endosomal compartment of tubuloves

26 direct effects, such as either by regulating membrane flow from other compartments or by modulating P

27 e or a transient manifestation of continuous membrane flow from specialized ER exit domains (ERES).

28 However, as compensatory membrane flow from the contiguous endoplasmic reticulum

29 orrelation, which suggests that compensatory membrane flow from the ER buffers T(INM) without prevent

30 ow-temperature-sensitive step that regulates membrane flow from VTCs to the Golgi complex and back to

31 protein Lnp1 acts as a secondary barrier to membrane flow, functionally compensating for lack of Lem

32 ind that, to a marked degree, the pattern of membrane flow in the cell is encoded and recapitulated b

33 of VHA-c1 and VHA-c3 in tissues with active membrane flow, including root cap, vascular strands, and

34 Lem2 deletion increases membrane flow into and out of the nuclear envelope in re

35 ism comes from the slip that occurs when the membrane flows over the cytoskeleton.

36 t, despite intense efforts to understand how membrane flow relates to Golgi form and function, this o

37 ipated by three viscous mechanisms including membrane flow, slip between the two monolayers that form

38 sorptive phenomena in which a tension-driven membrane flow supplements diffusive transfer of Golgi me

39 ed by local Cdc42 GTPase activity results in membrane flows that deplete low-mobility membrane-associ

40 tion of Sec2 and Sec4 are diverted to direct membrane flow to autophagosome formation.

41 as well as a general decrease in the rate of membrane flow to the cell surface.

42 el in which Atg9 multimerization facilitates membrane flow to the PAS for phagophore formation.