ライフサイエンスコーパス: intercellular contact

1 face independent of antibody crosslinking or intercellular contact.

2 vels of H2AX protein under conditions of low intercellular contact.

3 messengers within the first hours following intercellular contact.

4 those in lonesome microwells, which prevent intercellular contact.

5 to activate signals that reinforce stressed intercellular contacts.

6 opy reflected cAMP-induced reorganization of intercellular contacts.

7 signals through SLAM receptors to stabilize intercellular contacts.

8 n of extracellular pH and destabilization of intercellular contacts.

9 lls in a biofilm are specialized to maintain intercellular contacts.

10 exhibits lateral mobility, segregating into intercellular contacts.

11 the cytoplasmic aprons, and formation of new intercellular contacts.

12 owed the immunolocalization of N-cadherin in intercellular contacts.

13 al changes, including establishment of close intercellular contacts.

14 Intercellular contact activated the stromal fibroblasts,

15 s thought to enable metastasis by disrupting intercellular contacts-an early step in metastatic disse

16 inoma cells (HCCs) in a manner that required intercellular contact and involved gap junctions.

17 ol, became unable to disintegrate both their intercellular contacts and adhesive dimers in response t

18 tin-1 during dynamic changes in formation of intercellular contacts and cell polarity accompanying ep

19 Thus, cleavage of Pcdhs may function to link intercellular contacts and intracellular signaling.

20 Dividing cells lose many intercellular contacts and polarized features.

21 ases transmit Hippo signaling in response to intercellular contacts and serum levels to limit cell gr

22 cells (SCs) reside in niches, which, through intercellular contacts and signaling, influence SC behav

23 and that claudin-4 was also restricted from intercellular contacts and tended to accumulate in the c

24 e two-hit conditions: disassembly/absence of intercellular contacts and transforming growth factor-be

25 otile cellular state is achieved once stable intercellular contacts are formed between mature cells.

26 Thus, polycystin-1 is not detected in intercellular contacts at early steps of tubulogenesis,

27 onjugation) requires the formation of secure intercellular contacts before DNA transfer can occur.

28 gnaling pathway mediates its effects through intercellular contact between neighboring cells.

29 Interruption of intercellular contact between platelets and monocytes dr

30 ty and regulate antibody responses depend on intercellular contacts between T cells and antigen-prese

31 Here, we use biotin labeling of intercellular contacts (BLINC), a method for imaging pro

32 ter their internalization upon disruption of intercellular contacts by Ca(2+) depletion of the medium

33 activating and inhibitory signals at direct intercellular contacts called immune synapses.

34 iciently disseminates by cell-cell spread at intercellular contacts called virological synapses (VS),

35 Cellular injury disrupts these intercellular contacts, causing a loss of contact inhibi

36 Tight junctions form continuous intercellular contacts controlling solute movement throu

37 Intercellular contact duration is the predominant factor

38 fficiency: the level of shear stress and the intercellular contact duration.

39 uch mechanisms may mediate the disruption of intercellular contacts during normal tissue remodeling a

40 The intimate intercellular contacts enforced by ILPs consistently pre

41 Immunological synapses are specialized intercellular contacts formed by several types of immune

42 e these findings do not discount the role of intercellular contact in facilitating HIV-1 transmission

43 f membrane-associated complexes at points of intercellular contact in many vertebrate cell types.

44 ithelial sheets or tubes making and breaking intercellular contacts in an oriented manner.

45 PS1 concentrates at intercellular contacts in epithelial tissue; in brain, i

46 Intercellular contacts in multicellular organisms are ma

47 icating that a role for Stat3 is to regulate intercellular contacts in myeloid cells.

48 markedly reduced and almost disappeared from intercellular contacts in PKD3-overexpressed epithelial

49 ed for the stability of force balance across intercellular contacts in tissues.

50 tion that occurs after remodeling of myocyte intercellular contacts indicates the possibility of unan

51 notion that both molecules are required for intercellular contact maturation.

52 ition, the results suggest that CAR-mediated intercellular contacts may regulate proliferation and di

53 npolarized cells, CAR localized to homotypic intercellular contacts, mediated homotypic cell aggregat

54 en fluorescent protein-tagged receptor at an intercellular contact or immune synapse.

55 membrane domains, in a polarized fashion, to intercellular contacts or plasmodesmata.

56 Force transmission through intercellular contacts plays a key role in this process

57 Upon disruption of intercellular contacts, PMP22 was internalized into vesi

58 43 expression is repressed, facilitating the intercellular contact required for chemotaxis, phagocyto

59 l units that mediate protein interactions in intercellular contact, signal transduction and assembly

60 ESCs expressed connexin 43 at intercellular contact sites.

61 We found that intercellular contact stabilizes histone H2AX and gammaH

62 cipate in formation of virological synapses, intercellular contact structures that play a key role in

63 a multiprotein complex localized to sites of intercellular contact that may function to tether microt

64 bind sufficient ligand over the duration of intercellular contact to withstand hydrodynamic stresses

65 Moreover, cell spreading and intercellular contacts together control the subcellular

66 d E-cadherin, involved in the maintenance of intercellular contact, were downregulated in LMP2A tumor

67 DCK cells, presenilin-1 (PS1) accumulates at intercellular contacts where it colocalizes with compone

68 helial galectin-3 to the site of heterotypic intercellular contacts, whereas galectin-3 in MDA-MB-435

69 uitment and maintenance of AJ/TJ proteins at intercellular contacts, whereas myosin II regulates cell

70 the other prerequisite is the uncoupling of intercellular contacts, which induces Rho-dependent nucl