ライフサイエンスコーパス: sheddase

1 mediated by a cell surface metalloprotease ("sheddase").

2 a converting enzyme (TACE)/ADAM 17 as a MUC1 sheddase.

3 ), a transmembrane metalloprotease, as a GHR sheddase.

4 helial cell line and identify TACE as a MUC1 sheddase.

5 or effectively blocks both TACE and the CD44 sheddase.

6 igodendrocyte precursor cells via the ADAM10 sheddase.

7 y reduced by an inhibitor of ADAM17, a known sheddase.

8 eddases and suggested that ADAM17 is a major sheddase.

9 but were unable to activate TACE, the TNFR1 sheddase.

10 a strong incentive to define the responsible sheddases.

11 d from the primary cilium upon activation of sheddases.

12 dependent of ectodomain cleavage by receptor sheddases.

13 ng the importance of identifying EGFR ligand sheddases.

14 ls expressed high levels of the FcepsilonRII sheddase a disintegrin and metalloproteinase 10, which i

15 VECs in response to TSST-1 that includes the sheddase, a disintegrin and metalloproteinase 17 (ADAM17

16 various growth factor environments influence sheddase activity and cell migration in the invasive dis

17 This sheddase activity is attributed to the ADAM (a disintegr

18 We have found that mesothelin sheddase activity is mediated by a TNF-alpha converting

19 Sheddase activity is responsible for cleavage of multipl

20 Furthermore, the pervanadate-regulated sheddase activity is sensitive to TIMP-2 but not TIMP-1,

21 nhibition reduces cell migration by blocking sheddase activity while additionally preventing the comp

22 However, inhibition of l-selectin sheddase activity with KD-IX-73-4 had no effect on the n

23 e suggest that ARTS-1 does not possess TNFR1 sheddase activity.

24 tiated tumor growth and survival is to block sheddase activity.

25 ylserine (PS) is pivotal for ADAM17 to exert sheddase activity.

26 ating activation of the ADAM metalloprotease/sheddase activity.

27 post-translational BMPR-II cleavage via the sheddases, ADAM10 and ADAM17 in pulmonary artery smooth

28 from metastatic prostate cancer cells by the sheddase ADAM17 in response to TGF-beta.

29 ssential for ATP-dependent activation of the sheddase ADAM17, which is responsible for liberation and

30 vary cells with/without functional GPIbalpha sheddase ADAM17.

31 that is independent of the major L-selectin sheddase, ADAM17, but results in significant elevation o

32 he latter being dependent on the EGFR ligand sheddase, ADAM17.

33 y evident in the absence of the major HB-EGF sheddase, ADAM17.

34 he presence of angiotensin-converting enzyme-sheddase ADAM9 (a disintegrin and metalloproteinase doma

35 substrate selectivity of two major cellular sheddases, ADAMs 10 and 17.

36 peripheral-blood leukocytes, indicating the sheddase also plays a role in the constitutive cleavage

37 study identifies ADAM10 as the in vivo CD23 sheddase and an important regulator of B cell developmen

38 anes and, if so, to identify the responsible sheddase and determine whether activation of the PDGFRbe

39 We conclude that the CD44 sheddase and TACE are distinct enzymes, and that Ab- and

40 MMPs act as cell-surface sheddases and can affect cell signalling initiated by gr

41 the cell surface is mediated by one or more sheddases and likely regulates 4-1BB-4-1BBL interactions

42 AMs 9, 10, and 17 as candidate collagen XVII sheddases and suggested that ADAM17 is a major sheddase.

43 TIMP3 is known to inhibit ADAM17 (DLK1 sheddase) and MMP14 (implicated in extracellular matrix

44 st of a multidomain oligomeric transmembrane sheddase, and of its zymogen.

45 transforming growth factor-alpha (TGF-alpha) sheddase, and we also demonstrated enhanced shedding of

46 ymes are considered to be candidate TNFalpha sheddases as well.

47 In a transfected cell-based sheddase assay, ADAM33 functioned as a negative regulato

48 Thus, here we present a sheddase-based mechanism of rapidly acquired resistance

49 bstrate that is not only cleaved by multiple sheddases but is also processed by three different I-CLi

50 AM17), has emerged as the best candidate TNF sheddase, but other proteinases can also release TNF.

51 active sheddases or activation of different sheddases by distinct stimuli.

52 hich suggests that neutrophil activation and sheddase cleavage occurred.

53 mbrane cleavage at the previously identified sheddase cleavage site, Thr517.

54 ent from endogenous AXL was dependent on the sheddase disintegrin and metalloprotease 10 (ADAM10) and

55 e therefore evaluated the role of TACE as a "sheddase" during lung morphogenesis by analyzing the dev

56 maturation of the multi-substrate ectodomain sheddase enzyme ADAM17 (TACE) in macrophages.

57 a central inhibitor of matrix-degrading and sheddase families of metalloproteinases.

58 In addition, ADAM17 emerged as the major sheddase for neuregulins beta1 and beta2 in mouse embryo

59 as TNFalpha-converting enzyme, is the major sheddase for the EGF receptor ligands and is considered

60 This study identifies the principal sheddase for the PDGFRbeta and provides new insights int

61 tor, but Ca++ influx activated an additional sheddase for these epidermal growth factor receptor liga

62 mice to address whether TACE is the relevant sheddase for TNF in adult mice.

63 vious studies identified ADAM17 as principal sheddase for transforming growth factor (TGF)-alpha and

64 nto the identity and regulation of the major sheddases for collagen XVII in keratinocytes and skin an

65 Sheddases for EGFR-ligands are therefore key signaling s

66 Here, we uncovered the sheddases for six EGFR ligands using mouse embryonic cel

67 our understanding of context-dependent ADAM "sheddase" function and our ability to predictably target

68 Identification of the primary sheddase has allowed the characterization of a novel mec

69 roteinase 10 (ADAM10) is the major ephrin-B2 sheddase in fibroblasts.

70 t TACE is the major endotoxin-stimulated TNF sheddase in mouse myeloid cells in vivo, thereby further

71 , and we demonstrate a crucial role for this sheddase in the proteolytic cleavage of MIC by means of

72 and 10 are the most prominent collagen XVII sheddases in primary keratinocytes because (a) collagen

73 ), which demonstrates a novel role for this "sheddase" in regulating an actin-based structure.

74 functional activity of a metalloproteinase (sheddase) in the small intestine compared with the colon

75 ase the soluble form of HB-EGF (s-HB-EGF) by sheddases, including matrix metalloproteinases (MMP) and

76 s factor alpha-converting enzyme (pro-HB-EGF sheddase), increased phosphorylation of EGF receptor and

77 ants in calcyon and inhibitors for the major sheddases indicate that the stimulatory effects of calcy

78 Although sheddase inhibition prevents autocrine ligand shedding a

79 Combining the INCB7839 second-generation sheddase inhibitor with lapatinib prevented the growth o

80 inhibitors of L-selectin shedding and other sheddase inhibitors did not affect PSGL-1 release, sugge

81 ent in TNF-alpha converting enzyme (TACE), a sheddase involved in the processing of several substrate

82 n and metalloprotease 17 (ADAM17) is a major sheddase involved in the regulation of a wide range of b

83 alloproteinase (ADAM) 17 is one of the major sheddases involved in a variety of physiological and pat

84 cting those of other metalloproteases (e.g., sheddases) involved in the release of cell-associated mo

85 n epidermal growth factor receptor-2 (HER-2) sheddase is described.

86 Identification of EGFR ligand sheddases is a crucial step toward understanding the mec

87 One of the TRANCE sheddases is induced by the tyrosine phosphatase inhibit

88 RvE1 enhances HCEC migration through MMP and sheddase-mediated EGFR transactivation.

89 of soluble cytokine receptors, which include sheddase-mediated proteolytic cleavage of cell-surface r

90 strate that intervening with endogenous ADAM sheddase modulatory mechanisms holds potential as a gene

91 ectodomain can be cleaved by three different sheddases, namely ADAM10, ADAM17, and BACE1.

92 lloproteinase (ADAM)10, which is the primary sheddase of CD23, as well as protein expression of both

93 ADAM10 emerged as the main sheddase of EGF and betacellulin, and ADAM17 as the majo

94 ADAM 10 is the main sheddase of epidermal growth factor (EGF) and HER-2/neu

95 einase (ADAM)10 is the primary physiological sheddase of ICOSL in mice and humans.

96 pha-converting enzyme (TACE, or ADAM17) is a sheddase of L-selectin; however, Adam17 gene targeting (

97 se 17 (ADAM17) is a primary and nonredundant sheddase of L-selection by activated neutrophils in vivo

98 e P2X7R signaling pathway activate ADAM10 as sheddase of many ADAM17 substrates in Adam17-/- fibrobla

99 nvasive proteinase, functions as a principal sheddase of PTK7.

100 We identified ADAM10 and ADAM17 as major sheddases of Tim-3 as shown by ADAM-specific inhibitors

101 Targeting the sheddases of VEGFR2 or NRP-1 might offer new opportuniti

102 PSGL-1 may be shed by an as yet unidentified sheddase or removed by some other mechanism.

103 ncreased expression of constitutively active sheddases or activation of different sheddases by distin

104 protease inhibitor, indicating the role of a sheddase other than ADAM17.

105 ECM) degradation, but it also functions as a sheddase releasing non-ECM substrates such as receptor a

106 yme (TACE) is the first discovered mammalian sheddase responsible for cleavage of several important s

107 nction experiments to identify ADAM10 as the sheddase responsible for constitutive and ionomycin-stim

108 n and metalloprotease-17 (ADAM17) is a major sheddase responsible for the regulation of a wide range

109 eness to IL-6 via the activation of an IL-6R sheddase, resulting in an immediate production of functi

110 inase 17 (ADAM17), the principal EGFR ligand sheddase, results in postnatal skin barrier defects in m

111 to produce soluble RANKL, but definite RANKL sheddase(s) and the physiologic function of RANKL sheddi

112 Neither the sheddase(s) responsible for TMEFF2 shedding nor the phys

113 rotease shown to be capable of acting like a sheddase, similar to members of the rhomboid family, whi

114 g and causes the down-regulation of a major "sheddase," suggesting that induced shedding may be regul

115 ADAM17 is an ectodomain sheddase that can modulate the signaling activity of sev

116 strate that ADAM17 is the principal TGFalpha sheddase that is activated by Src in a manner that does

117 aining protein 10 (ADAM10) is a cell surface sheddase that regulates physiologic processes, including

118 converting enzyme (TACE or ADAM17) is a key sheddase that releases TNFalpha from its inactive cell-b

119 TACE functions as a membrane sheddase to release the ectodomain portions of many tran

120 nificantly reduced, due to inhibition of the sheddase-tumor necrosis factor-alpha-converting enzyme b

121 ed that ADAM17 is nevertheless the principal sheddase when both ADAMs 10 and 17 are present.

122 juxtamembrane cleavage and is mediated by a sheddase, which probably belongs to the subtilisin-like