ライフサイエンスコーパス: cell debris

1 th dependent on the uptake of dead cells and cell debris.

2 in response to chemotherapy-generated tumor cell debris.

3 c therapies as a result of the generation of cell debris.

4 d CCL5, by human macrophages stimulated with cell debris.

5 d and engulfment of unicellular organisms or cell debris.

6 ced between the co-precipitated proteins and cell debris.

7 This causes a buildup of unengulfed cell debris.

8 capable of phagocytizing extracellular lens cell debris.

9 ced by low doses of cytotoxic agents, clears cell debris.

10 in response to self-DNA, self-RNA, and dead cell debris.

11 tal rippling is a result of scavenging lysed cell debris.

12 ddition to congestion of the swim bladder by cell debris.

13 enveloped viruses from microvesicles and/or cell debris.

14 , vascular smooth muscle cells, and necrotic cell debris.

15 neuron-derived components such as myelin and cell debris.

16 can be formed by pollen, fungal spores, and cell debris.

17 After removal of cells and cell debris, a 0.50 mL sample (e.g., cell culture medium

18 nd growth factors, and they phagocytose dead cell debris, a process that is critical for resolution o

19 Indeed, necrotic cell debris allow macropinocytic breast and prostate can

20 diated by dendritic cell uptake of apoptotic cell debris and associated nucleic acids, whereas the su

21 CRP is known to facilitate the clearance of cell debris and bacteria by phagocytic cells, the role o

22 ber cells demonstrated that they phagocytose cell debris and bacteria.

23 n, buffer exchange, and selective removal of cell debris and by-products of the reactions.

24 end products (RAGE), inhibited responses to cell debris and conditioned medium and reduced the numbe

25 y enhancing macrophage phagocytosis of tumor cell debris and counter-regulating macrophage-secreted p

26 ated increased internalization of irradiated cell debris and dextran macromolecules.

27 known as CLEC9A), a receptor that binds dead-cell debris and facilitates XP of corpse-associated anti

28 of whole, intact apoptotic cells, as well as cell debris and foreign organisms to which these molecul

29 Instead, DCs capture B cell debris and generate T cells specific for EBV latenc

30 of cholesterol (harnessed from extracellular cell debris and generated by de novo synthesis) to assem

31 loss of collagen and matrix, accumulation of cell debris and intense intimal inflammation.

32 tissue homeostasis by scavenging dead cells, cell debris and lipoprotein aggregates via phagocytosis.

33 nt on oxidized LDL (OxLDL), apoptotic cells, cell debris and modified proteins in the vessel wall, ac

34 se of foamy M , and accelerated clearance of cell debris and necrotic cells, which resulted in functi

35 and homogenization and from contamination of cell debris and nuclear DNA.

36 down results in incomplete clearance of germ cell debris and premature follicle cell death.

37 ceptor that binds to F-actin exposed by dead cell debris and promotes cross-presentation of associate

38 taminants, the particle size distribution of cell debris and the physical properties of the resultant

39 Moreover, the removal of necrotic cell debris and the regeneration of endothelial cell str

40 cal environmental substances such as lipids, cell debris, and calcium cause a fluidic balance of proi

41 lmonary vascular congestion, edema, necrotic cell debris, and gross inflammatory infiltration when co

42 chemokines, injury-conditioned medium, dead cell debris, and high mobility group box chromosomal pro

43 obstruction of the airways due to mucus and cell debris, and increased risk of recurrent wheezing.

44 ng due to background HTOs, low-quality cells/cell debris, and multiplets.

45 olve their phagocytic cargo of cell corpses, cell debris, and pathogens.

46 etection of bacteria, clearance of apoptotic cell debris, and removal of autoantigens driving autoimm

47 tissues, where they ingest and degrade dead cells, debris, and foreign material and orchestrate infl

48 This way, apoptotic cells and cell debris as well as doublets or cell clusters could b

49 tides were overproduced and solubilized from cell debris by denaturation and refolding.

50 show that ischemic cell death and uptake of cell debris by macrophages in the heart fuel a fatal res

51 uding autophagy of damaged cells, removal of cell debris by macrophages, and more active cell prolife

52 led fibrocytes, and promotes phagocytosis of cell debris by macrophages.

53 antly enhanced the phagocytosis of apoptotic cell debris by monocyte-derived cells.

54 of cancer cells followed by phagocytosis of cell debris by MPhi.

55 Antigens derived from apoptotic cell debris can drive clonal T-cell deletion or anergy,

56 Cell debris can elevate IOP during the initial culture p

57 Significant levels of cell degeneration and cell debris, characteristic of necrosis, were observed i

58 d phagocytosis pathway and that internalized cell debris co-localizes with alphaVbeta5 and with RAB7

59 positively responds to tissue damage, clears cell debris, directs and modulates the adaptive immune s

60 al cell debris persisted for months, granule cell debris disappeared rapidly.

61 Abnormally liberated iris pigment and cell debris enter the ocular drainage structures, leadin

62 ignificantly more silver was present in the "cell debris" fraction (known to contain the cell wall an

63 a peptide deposits from the normal brain and cell debris from injured brain tissue.

64 Dendritic cells exposed to cell debris from tumors expressing mEGP are similarly co

65 containing mucin goblets together with other cell debris, further indicating apoptosis of the goblet

66 his study, we demonstrate that ovarian tumor cell debris generated by first-line platinum- and taxane

67 ltures is the presence of impurities such as cell debris, host cell DNA, proteins and small-molecule

68 nt mice accumulated excessive surfactant and cell debris in airways (pulmonary alveolar proteinosis)

69 th AIM in facilitating the clearance of dead cell debris in injured kidney, which is a key response i

70 -professional phagocytes to clear large germ cell debris in mid and late oogenesis, providing an exce

71 the main astrocytic phagocytic receptors for cell debris in the above experiments, indicating that as

72 junctival or subretinal haemorrhage and mild cell debris in the anterior vitreous) were generally mil

73 glia are the principal phagocytes that clear cell debris in the central nervous system (CNS).

74 ation entailing the production of endogenous cell debris in the CNS that must be removed by microglia

75 dited to myeloid cells interacting with dead cell debris in the infarct zone(1,2).

76 icenter of the SCI lesion, where they engulf cell debris including abundant myelin debris to become p

77 that enhancing endogenous clearance of tumor cell debris is a new therapeutic target that may complem

78 s intact even after multiple wounding, while cell debris is simultaneously removed using laminar flow

79 By removing the dead cell debris, it can increase the live cell percentage in

80 The tumor-specific antigen, cytokines and cell debris liberated by HIFU enhance response to innate

81 fects of promoting engulfment/degradation of cell debris may go beyond merely removing corpses to act

82 cross-presentation of antigens obtained from cell debris of EBOV-infected cells.

83 Whereas pyramidal cell debris persisted for months, granule cell debris di

84 ng permanent magnet, Further, removal of the cell debris, proteins, and carbohydrates was done using

85 that tubular cells exposed apically to dead cell debris secrete high levels of GM-CSF and induce rep

86 by chemotherapy or targeted therapy ("tumor cell debris") stimulate primary tumor growth when coinje

87 Chemotherapy-generated cell debris stimulates colon carcinoma tumor growth via

88 nduce apoptotic cell death and the resulting cell debris stimulates hepatocellular carcinoma (HCC) tu

89 e lens could result in accumulation of toxic cell debris that could contribute to UV light-induced ca

90 r cells, yet it simultaneously creates tumor cell debris that may stimulate inflammation and tumor gr

91 which results in the build up of a plaque of cell debris that severely impairs feeding.

92 ly high-pressure cultures revealed scattered cell debris throughout the meshwork in greater amounts t

93 Given the importance of clearing apoptotic cell debris to prevent inappropriate exposure of TLRs to

94 ium and delivers it along with the apoptotic cell debris to the lysosomal compartment.

95 extension of microglial cell branches toward cell debris underlies the mechanisms of microglial migra

96 Here, we show that consuming necrotic cell debris via macropinocytosis (necrocytosis) offers a

97 serves as a receptor for apoptotic cells and cell debris, we hypothesize that this regulatory mechani

98 examined host cell types and accumulation of cell debris were observed in infections with the human i

99 This raises the question, which cells remove cell debris when microglial phagocytic activity is impai

100 have posterior nuclear cataracts composed of cell debris, whereas the remaining fiber cells appear ge

101 ived proteases associate with necrotic tumor cell debris, which acts as a vehicle for Ag transfer tha

102 d mainly concentrated around broken cells or cell debris with floating open ends, eDNAs produced via

103 paramount in the clearance of pathogens and cell debris, yet is increasingly recognized as a key com