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

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

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

5 indicate cellular mechanisms for preventing autocrine signaling.

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

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

8 intaining the stemness of stem cells through autocrine signaling.

9 R ensures stable ligand retention and robust autocrine signaling.

10 eptive and protumorigenic) via paracrine and autocrine signaling.

11 significance of EVs in hematopoiesis through autocrine signaling.

12 pericyte-to-myofibroblast transition through autocrine signaling.

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

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

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

16 3 (IRF3) independent of interferon paracrine/autocrine signaling.

17 ased from dendrites to produce paracrine and autocrine signaling.

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

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

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

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

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

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

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

25 r results define a paradigm of intracellular autocrine signaling and may explain resistance to antago

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

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

28 ulates cellular levels of WUS mostly through autocrine signaling, and ERfs regulate the spatial expre

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

30 We next identify a novel autocrine signaling axis in OCCC cells whereby tumor-cel

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

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

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

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

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

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

37 These cells are regulated by autocrine signaling by parathyroid hormone-related prote

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

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

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

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

42 iscovered that alphavbeta8-mediated TGF-beta autocrine signaling can occur without TGF-beta1 release

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

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

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

46 Enhanced autocrine signaling could further activate tumor cells e

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

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

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

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

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

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

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

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

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

56 egulatory loop caused by JNK-regulated FGF21 autocrine signaling in adipocytes that promotes increase

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

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

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

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

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

62 ith an increased dependency upon FGF19/FGFR4 autocrine signaling in HNSCC, revealing a therapeutic ta

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

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

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

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

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

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

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

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

71 FGF19/FGFR4 autocrine signaling is one of the main targets for multi

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

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

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

75 elaxin and its associated GPCR RXFP1 form an autocrine signaling loop essential for OC in vivo tumori

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

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

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

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

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

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

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

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

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

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

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

87 These autocrine-signaling loops initiate and maintain the diff

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

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

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

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

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

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

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

95 e results suggest that 12-S-HETE might be an autocrine signaling molecule exported by ABC transporter

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

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

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

99 city mechanism mediated by the synthesis and autocrine signaling of IGF peptides in pyramidal neurons

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

115 nthesize and secrete dopamine, suggesting an autocrine signaling process underlying these results.

116 In general, IL-10 autocrine signaling promotes the survival of malignant B

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

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

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

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

121 e show, analytically and by simulation, that autocrine signaling suffices to cause both strong and we

122 Autocrine signaling systems are commonly studied under c

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

124 1/CXCR-4 identifies VEGF- and bFGF-regulated autocrine signaling systems that are essential regulator

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

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

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

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

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

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

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

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

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

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

135 Autocrine signaling through the Epidermal Growth Factor

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

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

138 rom increased oxoeicosanoid biosynthesis and autocrine signaling through the oxoeicosanoid receptor O

139 This pivot in lipid mediators induced autocrine signaling through the PGI2 receptor and expres

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

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

142 Autocrine signaling through VEGF/VEGFR2 and Akt provides

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

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

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

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

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

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

149 The autocrine signaling was also inhibited with neutralizati

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

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

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

153 Our findings indicate potential autocrine signaling where NF2 loss leads to secretion/ac

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

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