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 ay aid in the development of drugs targeting sheddases.

11 dependent of ectodomain cleavage by receptor sheddases.

12 ng the importance of identifying EGFR ligand sheddases.

13 a strong incentive to define the responsible sheddases.

14 d from the primary cilium upon activation of sheddases.

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

16 ADAM17 is the prototype 'sheddase', a family of proteases that cleaves other memb

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

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

19 IFN-I inhibits LC ADAM17 sheddase activity in murine and human LCs, and IFNAR blo

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

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

22 r receptor (EGFR) ligands and that LC ADAM17 sheddase activity is reduced in lupus.

23 Sheddase activity is responsible for cleavage of multipl

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

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

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

27 ckade in lupus model mice restores LC ADAM17 sheddase activity, all without consistent effects on LC

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

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

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

31 ating activation of the ADAM metalloprotease/sheddase activity.

32 oproteinases 1 (TIMP1) and TIMP3 control the sheddases ADAM10 and ADAM17, key for NOTCH activation.

33 sor protein and N-cadherin, but not with its sheddases ADAM10 or BACE1 at the cell surface, arguing a

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

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

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

37 vary cells with/without functional GPIbalpha sheddase ADAM17.

38 iRhom2 is also a direct regulator of the sheddase, ADAM17, and the antiviral adaptor protein, sti

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

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

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

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

43 ellular caspases, and the ectodomains of the sheddases, ADAMs 10 and 17.

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

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

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

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

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

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

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

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

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

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

54 M10, a virion-associated cellular ectodomain sheddase, and thus increases the amount of HIV-1 envelop

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

56 study delineated ADAM10 and ADAM17 are Robo4 sheddases, and ectodomain shedding, including negative r

57 Sheddases are specialized proteases that control the abu

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

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

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

61 These proteinases are termed sheddases because they have a transmembrane domain and t

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

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

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

65 hich suggests that neutrophil activation and sheddase cleavage occurred.

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

67 ted ERK kinase to activate the iRhom2-ADAM17 sheddase complex.

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

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

70 latory mechanism in which targeting a single sheddase enables broad regulation of multiple critical s

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

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

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

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

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

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

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

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

79 metalloprotease that serves as the principle sheddase for tumor necrosis factor a (TNFa), interleukin

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

81 Sheddases for EGFR-ligands are therefore key signaling s

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

83 in part by inhibiting UVR-induced LC ADAM17 sheddase function and raise the possibility that anifrol

84 Anti-IFNAR-mediated LC ADAM17 sheddase function restoration is associated with reduced

85 , differentiate between effects on LC ADAM17 sheddase function, LC ADAM17 expression, and LC numbers.

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

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

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

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

90 M17 (a disintegrin and metalloproteinase 17) sheddase in pDCs, which is essential for TNF-alpha cleav

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

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

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

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

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

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

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

98 Although sheddase inhibition prevents autocrine ligand shedding a

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

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

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

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

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

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

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

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

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

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

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

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

111 hrough the transcriptional activation of the sheddase molecule, ADAM 10 (A disintegrin and metallopro

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

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

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

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

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

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

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

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

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

121 (ADAM)10 and ADAM17 are physiologic relevant sheddases of inactive promeprin beta, which influences i

122 have identified MMP-3 and MMP-7 as important sheddases of syndecan-1 shedding in corneal epithelial c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

140 0 (ADAM10), a Ca(2+)-regulated transmembrane sheddase that mediates S2 Notch1 cleavage.

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

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

143 This process is mediated by the ADAM10 sheddase, the activity of which is associated with XKR8-

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

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

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

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