ライフサイエンスコーパス: CD95 ligand

1 s are refractory to the cytotoxic effects of CD95 ligand.

2 ral early activation markers but not CD95 or CD95 ligand.

3 uce expression of the death receptor ligand, CD95 ligand.

4 of the mutant protein or impaired binding to CD95 ligand.

5 a predominant feature of defects in CD95 or CD95 ligand.

6 athway is required for optimal activation of CD95 ligand.

7 acellular apoptotic signal upon binding with CD95 ligand.

8 1q23, near the gene for the TNF homolog Fas/CD95 ligand [5].

9 iochemical events that lead to expression of CD95 ligand, a required step for TCR-induced apoptosis.

10 resembling that seen with defects in CD95 or CD95-ligand (also known as FAS and FASLG, respectively),

11 ymphocytes through the induced expression of CD95 ligand and its receptor.

12 tocompatibility complex (MHC) molecules, and CD95 ligand and secretes immunosuppressive factors, the

13 d T cells followed by an interaction between CD95 ligand and the CD95 receptor also expressed on this

14 e that up-regulation of SNARK in response to CD95 ligand and tumor necrosis factor alpha depends on a

15 e, SEB triggered increased levels of soluble CD95 ligand, and down-regulation of IgSC responses and i

16 rmore, ELL-12 had no effect on expression of CD95 ligand, and inhibition of the Fas signaling pathway

17 TNFR2, CD36, CD40, CD47, CD80, CD86, PD-L1, CD95 ligand, and type I interferon receptor), we report

18 increased the sensitivity of tumor cells to CD95 ligand- and TRAIL-induced apoptosis.

19 nds, such as tumor necrosis factor-alpha and CD95 ligand, but was independent of receptor-interacting

20 hemotherapy, which can cause upregulation of CD95 ligand by both tumor and nontumor cells.

21 ulated c-myc prevented the downregulation of CD95 ligand by maintaining its transcription, but caused

22 rability is independent of the expression of CD95 ligand by target RPE cells and implies that immune

23 Inducible expression of Fas ligand (CD95 ligand) by activated T cells and the resulting apop

24 apoptosis of CD40-activated CLL cells via a CD95 ligand (CD95-L)-dependent mechanism.

25 gering of perforin or Fas ligand (FasL)/Fas (CD95 ligand/CD95) cytotoxicity in our influenza-specific

26 FasL/Fas (CD95 ligand/CD95)-mediated cytolysis requires de novo pr

27 e expression of CD95 (Fas) by XS52 DC and of CD95 ligand (CD95L) (Fas ligand) by activated HDK-1 T ce

28 Here, we report that serum levels of CD95 ligand (CD95L) are higher in patients with TNBC tha

29 we report that DCs that are transfected with CD95 ligand (CD95L) cDNA, called 'killer' DCs, deliver d

30 e-tested siRNAs and shRNAs targeting CD95 or CD95 ligand (CD95L) induce a form of cell death characte

31 CD95 ligand (CD95L) is expressed by immune cells and tri

32 Here we describe high extrinsic CD95 ligand (CD95L)-mediated apoptosis in CD10-/CD21lo m

33 , the perforin/granzyme- and Fas ligand/Fas (CD95 ligand (CD95L)/CD95)-mediated pathways.

34 cells were obtained from eyes of normal and CD95 ligand (CD95L)deficient mice and tested for their c

35 adhesion and transmigration upon binding of CD95-ligand (CD95L) that is presented by endothelial cel

36 O-1) and are therefore potential targets for CD95-ligand (CD95L)-mediated injury.

37 Constitutive expression of CD95 ligand contributes to the privileged status.

38 eneic C57BL/6, and allogeneic B6Smn.C3H-gld (CD95 ligand-deficient) mice were used as donors for BALB

39 ALB/c recipients, and syngeneic C3H/HeJ-gld (CD95 ligand-deficient) mice were used for normal C3H/HeJ

40 Signaling through CD95, induced by murine CD95 ligand expressed on fibroblasts, resulted in the pr

41 o not appear to be required for constitutive CD95 ligand expression in Sertoli cells.

42 Similarly, B6-gld corneas deficient in CD95 ligand expression showed acute destruction beneath

43 tal C57BL/6 or C57BL/6 gld/gld (deficient in CD95 ligand expression) mice.

44 ty of TCR to stimulate apoptosis by inducing CD95 ligand expression, TCR signals at the time of CD95

45 critical transcription factors that regulate CD95 ligand expression, we demonstrate a cyclosporin A-s

46 n the regulation of T cell receptor-mediated CD95 ligand expression.

47 phosphatase are required for TCR-stimulated CD95 ligand expression.

48 ell death of Fas+ cells by tissue-associated CD95 ligand (Fas ligand, FasL) is an important component

49 s is dependent on the presence of functional CD95-ligand (Fas-ligand) molecules on donor cells.

50 CD95 ligand (FasL) mRNA was detected in both immature an

51 The CD95 ligand (FasL) transmembrane protein is found on act

52 , and the T cell death genes, CD95 (Fas) and CD95 ligand (FasL), were inhibited.

53 In immune privileged sites such as the eye, CD95 ligand (FasL)-induced apoptosis controls dangerous

54 was associated with inhibition of Fas (Apo-1/CD95) ligand (FasL) expression, whereas Fas signaling wa

55 engagement that are important for regulating CD95 ligand gene expression.

56 cell activation-induced transcription of the CD95 ligand gene is regulated coordinately by this respo

57 in the expression of CD95 (lpr mutation) and CD95-ligand (gld mutation) were used as recipients and c

58 oding the apoptosis effector proteins, human CD95 ligand (hFasL) or human tumor necrosis factor-relat

59 s appear important for optimal expression of CD95 ligand in activated T cells, mutational analysis su

60 ty is preserved when death cytokines such as CD95 ligand induce autoregulatory mature T cell apoptosi

61 n activator was found to be required for the CD95 ligand-induced motility and invasiveness.

62 multiple apoptosis-resistant tumor cells by CD95 ligand induces increased motility and invasiveness,

63 n of Fas by specific Abs or Fas ligand (FasL/CD95 ligand) induces rapid apoptotic cell death in a var

64 sion protein and blocking antibodies against CD95 ligand inhibit stress-induced reduction in lymphocy

65 In contrast, neither CD95/CD95 ligand interactions nor TNF-alpha appear to play a

66 Perforin- and Fas ligand (APO-1/CD95 ligand)-mediated cytotoxicity have been proposed as

67 requirement of receptor internalization for CD95 ligand-mediated DISC amplification, caspase activat

68 f death-inducing ligands (in particular Fas [CD95] ligand), microenvironmental factors (in particular

69 val (MST)=44 days, P=0.0004] and gld (mutant CD95-ligand, MST=37 days, P=0.02) donor spleen cells enh

70 r) (CD95 receptor mutant) and FasL(gld/gld) (CD95 ligand mutant) mice, cell death was significantly s

71 -stimulated apoptosis requires expression of CD95 ligand on activated T cells followed by an interact

72 Inducible expression of CD95 ligand on activated T lymphocytes contributes to bo

73 effect was also dependent on the presence of CD95-ligand on donor cells and CD95 on recipient cells.

74 Heterozygous mutations in CD95, CD95 ligand or caspase-10 underlie most cases of autoimm

75 factor-related apoptosis-inducing ligand, or CD95 ligand or knockdown of death receptors fail to resc

76 Cell fate following Fas (CD95) ligand or agonistic anti-Fas antibody stimulation

77 ograft survival is not dependent on the CD95/CD95-ligand pathway; therefore the deletion of allospeci

78 E grafts, through constitutive expression of CD95 ligand, promote their own survival at heterotopic s

79 gulate this expression, we have examined the CD95 ligand promoter to determine which regions are requ

80 Two sites within the CD95 ligand promoter, identified through DNase I footpri

81 eporter construct containing elements of the CD95 ligand promoter.

82 otherapeutic drugs and/or those that use the CD95-ligand/receptor system to trigger apoptosis.

83 on of this gene that is critical for optimal CD95 ligand reporter activity in stimulated T cells.

84 We have identified a soluble form of CD95 ligand (S2) that is cytotoxic to type II cells but

85 In contrast, CD95 ligand stimulation of cells unable to internalize C

86 acities to tether the T cell inhibitor FasL (CD95 ligand) to the surfaces of B7 (CD80 and CD86)-posit

87 ith induced expression of Fas-ligand (APO-1, CD95-ligand), whose gene is a putative c-Jun/AP-1 target

88 the expression of both CD95 (APO-1/Fas) and CD95 ligand within 12 h.