ライフサイエンスコーパス: cytoadherence

1 its ability to adhere to endothelial cells (cytoadherence).

2 hat contains kahrp and pfemp3 causes reduced cytoadherence.

3 expression of surface proteins required for cytoadherence.

4 lag3 genes previously assumed to function in cytoadherence.

5 etory (E/S) products can facilitate in vitro cytoadherence.

6 d them for their ability to mediate in vitro cytoadherence.

7 ositively charged protamine sulfate promoted cytoadherence.

8 gulates PfEMP1 expression and the parasite's cytoadherence.

9 Nutrient acquisition, cytoadherence and antigenic variation are among the key

10 acute stress in erythrocytes, which enhances cytoadherence and hemolysis.

11 he glycan contacts, underscoring its role in cytoadherence and in antigenic variation in malaria.

12 ronemal proteins (MICs) are key mediators of cytoadherence and invasion for Toxoplasma gondii.

13 Clinical interventions aimed at reducing cytoadherence and microvascular inflammation may improve

14 Cytoadherence and sequestration of erythrocytes containi

15 to study the components involved in B. bovis cytoadherence and sequestration.

16 A large family of variant proteins mediates cytoadherence and their binding specificity determines p

17 ns, differentiation, cell cycle progression, cytoadherence, and both stimulation and evasion of host

18 strated relationships among knob expression, cytoadherence, and infectivity.

19 Both rosetting and cytoadherence are mediated by the parasite-derived IE su

20 An in vitro cytoadherence assay was used to investigate the presence

21 rapeutics for cerebral, placental, and other cytoadherence-associated malaria illnesses.

22 AHRP and PfEMP3, play important roles in the cytoadherence by mediating the clustering of PfEMP1 in r

23 histidine-rich protein (KAHRP), an essential cytoadherence component.

24 domains) specifically inhibited and reversed cytoadherence down to low concentrations (<10 mug/ml of

25 ylated proteins, including those involved in cytoadherence, drug resistance, signaling, development,

26 Rosetting and cytoadherence have been widely studied as separate entit

27 on the erythrocyte membrane is critical for cytoadherence, however the molecular mechanisms behind t

28 with a link between antigenic variation and cytoadherence in B. bovis and suggest that the VESA1 Ag

29 udies of cytokine activation and erythrocyte cytoadherence in babesiosis and malaria have exploited t

30 oral anthelminthic drug levamisole inhibits cytoadherence in vitro and reduces sequestration of late

31 ein-1-mediated phenomena appears to diminish cytoadherence in vivo and to protect against disease in

32 at the erythrocyte membrane is necessary for cytoadherence in vivo, our findings have implications fo

33 otection in AS children by further weakening cytoadherence interactions.

34 We have also shown that in vitro cytoadherence is a surrogate for the formation of antifi

35 ated that loss of EPCR and TM at sites of IE cytoadherence is detectible in nonfatal CM.

36 locking methods, we found that M. pneumoniae cytoadherence is important for the induction of cytokine

37 heparinase had no significant inhibition on cytoadherence, it is unlikely that sulfated glycoconjuga

38 The attendant increase in cell stiffness and cytoadherence leads to sequestration of infected RBCs in

39 ne protein-1 (PfEMP-1), the parasite's major cytoadherence ligand and virulence factor on the erythro

40 al cell-surface display of the main variable cytoadherence ligand, PfEMP-1 (P. falciparum erythrocyte

41 The first gene characterizing the clag (cytoadherence linked asexual gene) family of Plasmodium

42 s study has shown that the parasite protein, cytoadherence-linked asexual gene 9 (CLAG9), is also ess

43 first report demonstrating up-regulation by cytoadherence of a plasminogen-binding alpha-enolase in

44 Cytoadherence of HB3EC-6 to human microvascular endothel

45 brane protein 1 (PfEMP1), is responsible for cytoadherence of infected cells to host endothelial rece

46 f Plasmodium falciparum malaria is caused by cytoadherence of infected erythrocytes, which promotes p

47 responsible for both antigenic variation and cytoadherence of infected erythrocytes.

48 Therefore, cytoadherence of IT/R29 IE is distinct from rosetting, w

49 ytes by Plasmodium falciparum merozoites and cytoadherence of parasitized erythrocytes (PRBC) to endo

50 ble to inhibit CSA-, CD36-, and TSP-mediated cytoadherence of PE.

51 e invasion of erythrocytes by merozoites and cytoadherence of PRBC to endothelial cells by increasing

52 We have compared the cytoadherence properties of parasitized AS and AA erythr

53 y changes in the permeability, rigidity, and cytoadherence properties of the host erythrocyte.

54 rocyte membrane protein 1 (PfEMP1) family of cytoadherence receptors.

55 that the spiral and dense coat organize the cytoadherence structures in the knob, and anchor them in

56 tope may be targeted to disrupt the parasite cytoadherence system.

57 s restored knob expression and CD36-mediated cytoadherence, thereby showing that the human environmen

58 RBC and the sudden transition from firm RBC cytoadherence to flipping on the endothelial surface.

59 the host cell surface leading to ablation of cytoadherence to host receptors.

60 the more biologically relevant phenomenon of cytoadherence to PBMC, can result in considerable enhanc

61 malaria parasite P. falciparum, and mediates cytoadherence to the host vascular endothelium.

62 s that have the ability to block erythrocyte cytoadherence to the PvDBP.

63 deformability and they also exhibit enhanced cytoadherence to vascular endothelium and other healthy

64 Knobs are required for cytoadherence under flow conditions, and they contain bo

65 Cytoadherence was inhibited by heparin and by treatment

66 ghest inhibitory effect on both invasion and cytoadherence, whereas the positively charged protamine