ライフサイエンスコーパス: calcein-AM

1 unting cells in tissue colabeled with PI and Calcein AM.

2 , Oregon green carboxylic acid diacetate, or Calcein AM.

3 Redox-active iron was monitored using calcein-AM.

4 ct, respectively, on blocking SPGP efflux of calcein-AM.

5 and preferentially inhibited SPGP efflux of calcein-AM.

6 etrogradely labeled RGCs was determined with calcein-AM 24 hours after plating.

7 s was determined by live cell staining using calcein AM (5 microM).

8 led that one analog inhibited SPGP efflux of calcein-AM, although not as potently as ditekiren.

9 sured variables included cellular viability (calcein AM and annexin-V/propidium iodide), reactive oxy

10 small cell lung cancer cell line H69 AR in a calcein AM and daunorubicin cell accumulation assay.

11 lucose-6-phosphate dehydrogenase (G6DP), and calcein AM and ethidium homodimer (calcein AM/EthD-1)] h

12 Cell viability was measured using calcein Am and ethidium homodimer-1.

13 ide-containing derivatives promote uptake of calcein AM and have very slow passive, absorptive, and s

14 Thioamide 31-S promoted uptake of calcein AM and inhibited efflux of vinblastine with IC(5

15 Live/dead (calcein AM and propidium iodide) testing revealed that a

16 (10), and their ability to promote uptake of calcein AM and vinblastine in multidrug-resistant cells.

17 (10), for their ability to promote uptake of calcein AM and vinblastine in multidrug-resistant MDCKII

18 aining 2 microM calcein-acetoxymethyl ester (calcein-AM) and 4 microM ethidium homodimer.

19 odide [PI]); cytosol (CellTracker Red CMTPX, calcein AM); and membranes (octadecyl rhodamine B chlori

20 Proliferation was determined using calcein-AM, and cytotoxicity was evaluated by MTT assay.

21 transfected into Jurkat cells, labeled with Calcein-AM, and migration to SCF assessed in the presenc

22 ing P-gp overexpressing PLHC-1/dox cells and calcein-AM as model substrate.

23 Cell viability was measured by calcein AM assay, and 2',7'-dichlorofluorescein diacetat

24 With the calcein-AM assay, LA-N-1 cell survival was 10%, 55%, and

25 luated for P-glycoprotein inhibition using a calcein-AM assay.

26 bodipy-FL)-verapamil, bodipy-FL-vinblastine, calcein-AM, bodipy-FL-prazosin, bisantrene, and bodipy-F

27 ters export canonical MDR susbtrates such as calcein-AM, bodipy-verapamil, bodipy-vinblastine, and mi

28 , 7, 8, and 15 pi were labeled in vitro with calcein-AM (C-AM) and infused intravenously into syngene

29 times more of the ABC transporter substrates calcein-AM, CellTrace RedOrange, BoDipy-verapamil and Bo

30 Cell-to-cell transfer of the fluorescent dye calcein-AM confirmed cytoplasmic communication via nanot

31 (7)) were labeled with rhodamine-dextran and calcein AM, cultured with cells from one mouse liver in

32 er selective loading of the endothelium with calcein AM, direct transfer of dye from the endothelium

33 Using calcein-AM efflux assay, we identified compound 28 (IC50

34 tility, and ABC-transporter inhibition via a calcein-AM efflux assay.

35 6DP), and calcein AM and ethidium homodimer (calcein AM/EthD-1)] have been adopted to verify the feas

36 as assayed by BrdU uptake and cell counts of calcein AM/ethidium bromide-stained cells.

37 nduced apoptosis was further confirmed using calcein AM/ethidium homodimer-1 dye and cleavage of poly

38 olayers, more than 30% of clone A cells lost calcein AM fluorescence compared to fewer than 5% of CX-

39 Cell volume was measured with the use of calcein AM fluorescent dye, detected by confocal microsc

40 measured in low-passage human SC cells using calcein AM fluorescent dye; images were captured with a

41 l cells from RCs was possible after 5 min of Calcein AM incubation.

42 lly, the TMR analogues facilitated uptake of calcein-AM into CR1R12 and MDCK-MDR1 cells and are activ

43 luorescent calcein for over 60 minutes after calcein-AM is removed from the extracellular space.

44 rect observation and by adoptive transfer of calcein-AM-labeled bone marrow-derived leukocytes from s

45 The cell volume of calcein AM-loaded keratocytes and myofibroblasts was det

46 Using the calcein AM method, at day 2, 10 nmol/l rapamycin caused

47 ted with 4-hour calcein acetoxymethyl ester (calcein-AM) microcytotoxicity assay, electron microscopy

48 osome pool, of LeMDR1 were active in pumping calcein AM out of the cell.

49 ompetitive inhibitor of daunorubicin (MRP1), calcein AM (P-gp), and pheophorbide A (BCRP) transport.

50 Cell death was measured by using a calcein-AM/propidium iodide cell-survival assay.

51 roblasts, and B lymphoblastoid cell lines in calcein-AM retention NK assays with allogeneic NK effect

52 odamine-stained glucose-signal amplifier and calcein-AM-stained pancreatic beta-cell capsules, is dev

53 as assessed by phase-contrast microscopy and calcein AM staining and quantified with imaging software

54 Pulse-chase labelling experiments with calcein AM suggested that the Golgi and ER pools, but no

55 Calcein AM, the cell-permeable derivative of calcein, sh

56 lthough cyclosporine A and reserpine blocked calcein-AM transport by MDR1, these drugs had either min

57 pite dramatic reduction in rhodamine 123 and calcein-AM transport, the linker-shortened mutant P-gp p

58 Cells labelled with calcein AM under conditions that slow vesicular transpor

59 IgG was toxic to keratinocytes, as judged by calcein-AM uptake.

60 Living cells, determined by metabolism of calcein-AM viewed with fluorescein filters, were counted

61 The viability dye calcein AM was unchanged in AD terminals compared to con

62 f the traceable-fluorescent LeMDR1 substrate calcein AM were examined in both Leishmania mexicana and