ライフサイエンスコーパス: autocrine signaling

1 e growth factors as well as their receptors (autocrine signaling).

2 indicate cellular mechanisms for preventing autocrine signaling.

3 n in part by interfering with TGF-alpha/EGFR autocrine signaling.

4 ve than anti-ligand antibodies in inhibiting autocrine signaling.

5 pericyte-to-myofibroblast transition through autocrine signaling.

6 ades forming a positive feedback loop of the autocrine signaling.

7 minished, and thus dependent on ATP-mediated autocrine signaling.

8 receptor complex, the latter enhancing IL-15 autocrine signaling.

9 on fix the parameters needed to define Notch autocrine signaling.

10 growth of several tumor types driven by IL6 autocrine signaling.

11 3 (IRF3) independent of interferon paracrine/autocrine signaling.

12 ased from dendrites to produce paracrine and autocrine signaling.

13 insulin-like growth factor II production and autocrine signaling.

14 ll migrations, here Slit and Robo may act by autocrine signaling.

15 intaining the stemness of stem cells through autocrine signaling.

16 f transcription (STAT) 3 protein, suggesting autocrine signaling.

17 ation by IFNs was shown to involve TNF-alpha autocrine signaling.

18 NF-kappaB activity, but independent of IL-1 autocrine signaling.

19 tes that was enhanced in HF, consistent with autocrine signaling.

20 ent with a model in which Crim1 enhances the autocrine signaling activity of Vegfa in VECs at least i

21 taining exon 6), which enhances the TGFbeta1 autocrine signaling and induces fibroblasts to transdiff

22 his suggested that B cells use the A(3)R for autocrine signaling and self-regulation.

23 hese results underscore the role of aberrant autocrine signaling and transcriptional networking durin

24 TGF-alpha/EGFR autocrine signaling appears to play an important role in

25 et kinase activity, strongly suggesting that autocrine signaling broadly promotes tumorigenesis.

26 in reducing VEGFR2 phosphorylation caused by autocrine signaling, but VEGFR2 phosphorylation was comp

27 Conversely, disruption of autocrine signaling by added inhibitors of these pathway

28 that is able to globally diminish diffusible autocrine signaling by applying continuous media flow to

29 However, recent studies have demonstrated autocrine signaling by complement activation in intracel

30 oss of PTEN function or the establishment of autocrine signaling by growth factors and cytokines.

31 umor formation and confirms the existence of autocrine signaling by PDGF-A and -B.

32 ibitory drugs to address the contribution of autocrine signaling by Raf-induced EGF family proteins t

33 ially dependent on endogenous production and autocrine signaling by TNF-alpha.

34 activation and that this modulation of EGFR autocrine signaling can be accomplished at multiple regu

35 ine in IL15RA-expressing cells stimulated an autocrine signaling cascade that promoted cell prolifera

36 They also provide evidence for an autocrine-signaling cascade involving IL-6, LIF, and MCP

37 being platelet-derived growth factor (PDGF) autocrine signaling characterized by coexpression of PDG

38 Enhanced autocrine signaling could further activate tumor cells e

39 omas of the head and neck (SCCHNs) depend on autocrine signaling driven by HER2/3 dimerization and hi

40 versatile regulation of the spatial range of autocrine signaling enables autocrine cells to perceive

41 l apoptosis, indicative of autonomous VEGF-C autocrine signaling essential for LEC survival.

42 airs we identified are consistent with known autocrine signaling events in cancer cells.

43 Thus, ATP may function as an autocrine signaling factor promoting Cl- secretion in no

44 tified in valve progenitor cells a potential autocrine signaling feedback loop between PN and HA thro

45 nt of the self-sustaining TGF-beta and SDF-1 autocrine signaling gives rise to tumor-promoting CAF my

46 F) rivaled that observed under conditions of autocrine signaling (i.e., where tumor cells expressing

47 us mechanisms, including potentially through autocrine signaling in a dynamically changing extracellu

48 Selective inhibition of TGFbeta-3-mediated autocrine signaling in continuous cocultures of endocard

49 A model of autocrine signaling in cultures of suspended cells is de

50 otes biofilm growth in a manner analogous to autocrine signaling in eukaryotes.

51 We next characterized PDGF autocrine signaling in five glioblastoma cell lines.

52 ansfer we investigated the functions of PDGF autocrine signaling in gliomagenesis by transferring the

53 unction approach, we show that CSF1-mediated autocrine signaling in MAMs is downstream of FLT1 and ca

54 ta PDGF receptor profiling further suggested autocrine signaling in several brain tumor cell lines.

55 emokines, implicating abnormal paracrine and autocrine signaling in the initiation of breast tumorige

56 role for neuronal VEGF in both paracrine and autocrine signaling in the maintenance of neurons and en

57 The functional significance of PDGF autocrine signaling in these cells was demonstrated by t

58 fferentiation in bacteria typically involves autocrine signaling in which all cells in the population

59 e signaling with host macrophages as well as autocrine signaling involving the tumor cells themselves

60 We suggest that LPA-initiated autocrine signaling is a potentially important mechanism

61 A new model mechanism, using autocrine signaling, is outlined by which tissue and org

62 ings underline a new, previously undescribed autocrine signaling loop between Notch1 and NRG1 that co

63 Disruption of this autocrine signaling loop by blocking ligand-induced rece

64 in vivo studies to determine whether a CSF-1 autocrine signaling loop functions in human breast cance

65 d in our study suggested the existence of an autocrine signaling loop in ACC with potential therapeut

66 uggested the involvement of a C3/C3 receptor autocrine signaling loop in regulating tumor growth.

67 together, these results demonstrate that an autocrine signaling loop involving MCP-1 and IL-6 contri

68 We show here that Notch signaling induced an autocrine signaling loop that activates Akt in breast ep

69 and are an important component of the Wnt5A autocrine signaling loop, the activation of which leads

70 IL-1beta stimulates its own synthesis in an autocrine signaling loop.

71 g IDO by transcriptional deregulation of the autocrine-signaling loop IDO-AHR-IL6, which blocks kynur

72 In addition, our algorithm predicts new autocrine signaling loops that can be verified experimen

73 We show that BRCA1-IRIS activates two autocrine signaling loops, brain-derived neurotrophic fa

74 These cells increasingly acquire two autocrine signaling loops, mediated by TGF-beta and SDF-

75 These autocrine-signaling loops initiate and maintain the diff

76 difficulty of experimental investigation of autocrine signaling makes especially valuable an applica

77 te tumor cell proliferation, suggesting that autocrine signaling may often sustain tumor growth.

78 g an inflammatory response and the TNF-alpha autocrine signaling mechanism alone is not sufficient to

79 type-A ET1 receptors (ETA) and recruited an autocrine signaling mechanism distinct from that of ISO,

80 ion of DP1, suggesting a possible intracrine/autocrine signaling mechanism.

81 This autocrine-signaling mechanism may prove to be an attract

82 vn expression is amplified and maintained by autocrine signaling mediated by the E-twenty six (ETS)-f

83 ation inhibitory factor (MIF) in ccRCC as an autocrine-signaling molecule with elevated expression in

84 ceived as a basis for malignant cell growth, autocrine signaling networks are currently known to be a

85 ing that signaling through Gq and PLCbeta by autocrine-signaling neuropeptide receptors is a dominant

86 activity due to the secretion and subsequent autocrine signaling of TNF-alpha.

87 ignaling, as the activation does not involve autocrine signaling or in any other way require active S

88 port the presence of a constitutively active autocrine signaling pathway consistent with IL-10 in the

89 The identification of this VEGF autocrine signaling pathway has important implications f

90 These findings present evidence for an autocrine signaling pathway in cartilage involving Gas-6

91 factor (VEGF) in its ability to stimulate an autocrine signaling pathway in metastatic breast carcino

92 breast carcinoma cells by sustaining a VEGF autocrine signaling pathway that involves activation of

93 ductular bicarbonate secretion depends on an autocrine signaling pathway that involves CFTR, apical r

94 and and its receptor, which may establish an autocrine signaling pathway with important roles in the

95 stimulated their growth through an activin A autocrine signaling pathway, a hypothesis confirmed by a

96 nism, which likely involves activation of an autocrine signaling pathway.

97 IL-6 has been implicated in autocrine signaling pathways promoting tumor progression

98 has become apparent of several paracrine and autocrine signaling pathways that regulate stem cell pro

99 nscriptional regulation via paracrine and/or autocrine signaling pathways.

100 of the endocrine, paracrine, juxtacrine, and autocrine signaling pathways.

101 tes to malignancy through the acquisition of autocrine signaling, receptor overexpression, or mutatio

102 s and other cells, suggesting involvement in autocrine signaling since these cells express the mu3 op

103 EGFR inhibitors, suggesting a required EGFR autocrine signaling step for enzyme expression.

104 of the VM-inhibiting miRNAs, suggesting that autocrine signaling stimulating VM is regulated by ZEB1-

105 Autocrine signaling systems are commonly studied under c

106 patially distributed and recursive nature of autocrine signaling systems makes their experimental ana

107 1/CXCR-4 identifies VEGF- and bFGF-regulated autocrine signaling systems that are essential regulator

108 culture assays are routinely used to analyze autocrine signaling systems, but quantitative experiment

109 UPR-dependent induction of NF-kappaB and IL6 autocrine signaling that promotes a protumorigenic infla

110 Thus, Ras utilizes autocrine signaling through EGFR to increase radioresist

111 h radioresistance is dependent on Ras-driven autocrine signaling through EGFR.

112 Recent studies have suggested that autocrine signaling through epidermal growth factor rece

113 otease inhibitor batimastat, indicating that autocrine signaling through ligand shedding was responsi

114 small cell lung cancer (SCLC) is mediated by autocrine signaling through multiple G protein-coupled n

115 the ductal tumor cells, suggesting decreased autocrine signaling through pathways mediated by the pri

116 th factor alpha and amphiregulin and require autocrine signaling through the EGFR for proliferation a

117 ld be the result of their ability to inhibit autocrine signaling through the EGFR.

118 Autocrine signaling through the Epidermal Growth Factor

119 We used this technique to investigate autocrine signaling through the epidermal growth factor

120 We show here that Ras-driven autocrine signaling through the epidermal growth factor

121 s unregulated HGF-MET signaling and enhanced autocrine signaling through VEGF and PDGF.

122 b-mediated VEGF blockage may reflect ongoing autocrine signaling through VEGF-VEGFR2-NRP1, which is a

123 Autocrine signaling through VEGF/VEGFR2 and Akt provides

124 This interplay of paracrine and autocrine signaling underlies the spatial and temporal p

125 duced by thymineless stress was regulated by autocrine signaling via Fas-FasL interactions.

126 ctivated expression of HGF, resulting in its autocrine signaling via MET.

127 ce interferon-beta (IFN-beta) and subsequent autocrine signaling via the type I IFN receptor and the

128 -term, but not short-term, survival requires autocrine signaling via TNF-alpha and is facilitated by

129 To further prove that autocrine signaling was accounting for the activation, w

130 The autocrine signaling was also inhibited with neutralizati

131 Furthermore, HSulf-1-mediated inhibition of autocrine signaling was associated with reduced cyclin D

132 In all of the cases, PDGF autocrine signaling was evident because treatment with 1

133 Media exchange experiments indicated that autocrine signaling was not likely responsible for red-l

134 nostimulants is complicated by paracrine and autocrine signaling, which obscures the origin of a prop

135 hich suggests that there is paracrine and/or autocrine signaling within the LC.