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1 ignaling mechanisms-autocrine, paracrine and juxtacrine.
2  cell proliferation, caspase activation, and juxtacrine activity assays by using a 3D spheroid cultur
3 ite of blastocyst apposition, and which is a juxtacrine adhesion factor for blastocysts, could be one
4 spects of cellular arrangement, analogous to juxtacrine and paracrine signaling during animal develop
5 ion, and the modeling of cell communication (juxtacrine and paracrine signaling).
6 opreserved primary human hepatocytes through juxtacrine and paracrine signals in polymeric scaffolds.
7                  The two forms are active as juxtacrine and paracrine/autocrine growth factors, respe
8  an integration of the endocrine, paracrine, juxtacrine, and autocrine signaling pathways.
9                    Autocrine, paracrine, and juxtacrine are recognized modes of action for mammalian
10                                   However, a juxtacrine assay where fixed SUM149 cells and MCF10A AR
11                                           In juxtacrine assays, the CD9-induced EGFR hyperactivation
12  ligand; they also suggest a potential Notch juxtacrine/autocrine loop in gliomas.
13                                              Juxtacrine binding between numerous adhesion, signaling,
14 binations of diverse biochemical stimuli and juxtacrine cell interactions, we present evidence that a
15 econd role may be to inhibit activation of a juxtacrine cell relay, thereby confining chordin's actio
16 fferentiation are often tightly regulated by juxtacrine (cell-cell contact) signalling.
17  such positive feedback, in combination with juxtacrine communication, provides a novel mechanism for
18 s and G protein-coupled receptors, mimicking juxtacrine communication, while Saccharomyces SATURN (ad
19 linositol (GPI)-linked ephrin-A1 ligand in a juxtacrine configuration.
20 putational model that involves an inter-cell juxtacrine coupling, yielding simulation results that sh
21 1, we have reconstituted key features of the juxtacrine EphA2-ephrinA1 signaling system while maintai
22 simplified rule to represent the concepts of juxtacrine epidermal growth factor receptor (EGFR) activ
23 g that chondromodulin is not a member of the juxtacrine family of growth factors, despite some simila
24  between expression of TNF cytotoxicity in a juxtacrine fashion and detection of trimer.
25  structure and mediate TNF cytotoxicity in a juxtacrine fashion without releasing mature TNF.
26 s, and this was used to discriminate between juxtacrine from paracrine signalling.
27 in keratocyte cells and, possibly, autocrine-juxtacrine functions in epithelium and endothelium.
28 hich in its full-length form was as active a juxtacrine growth factor as was the wild type HB-EGF in
29                               HB-EGF TM is a juxtacrine growth factor that mediates cell-cell contact
30 studies were designed to test the effects of juxtacrine HB-EGF signaling upon cell survival and epith
31 Del-1 function in the HSC niche represents a juxtacrine homeostatic adaptation of the hematopoietic s
32 s activated EGFR as a result of an autocrine/juxtacrine interaction with HB-EGF which, in turn, resul
33  regulate glucagon release from alpha-cells, juxtacrine interactions are the least studied.
34 itive B-lineage precursors in BM by inducing juxtacrine interactions between the IL-7 and c-Met recep
35 ugh a combination of paracrine crosstalk and juxtacrine interactions involving direct physical contac
36 ls selectively modulate PMN-MC paracrine and juxtacrine interactions to influence MC and/or PMN adhes
37 h NRG3 and CRD-NRG1 cluster on axons through juxtacrine interactions with ErbB4 present on GABAergic
38 w biomaterials modulate PMN-MC paracrine and juxtacrine interactions.
39 r on the EphA2 receptor without the need for juxtacrine interactions.
40  change its properties, such as converting a juxtacrine into a paracrine signaling molecule.
41 nd Jagged-1/Notch3 interaction constitutes a juxtacrine loop promoting proliferation and disseminatio
42                     Thus, TWEAK can act in a juxtacrine manner to initiate cellular responses, and th
43 ting that TGF-beta 1 acts in an autocrine or juxtacrine manner to regulate epithelial proliferation.
44 neuroendocrine system, acting in a paracrine/juxtacrine manner.
45 T to fine-tune RET signaling, establishing a juxtacrine mechanism controlling kidney development.
46 stimulating proliferation via a paracrine or juxtacrine mechanism.
47 RG that may activate erbB-2 and erbB-3 via a juxtacrine mechanism.
48 d complex nature of concurrent paracrine and juxtacrine mechanisms of CAF-driven resistance that may
49 spontaneous [Ca(2+)](i) signals, while other juxtacrine mechanisms, regulated by PKA and glucose, sup
50 ate SMC growth via autocrine, paracrine, and juxtacrine mechanisms.
51                                         This juxtacrine-mediated model provides insight into the func
52 e present evidence supporting a new model of juxtacrine-mediated regulation of glucagon secretion whe
53 signal via ErbB3/4 receptors in paracrine or juxtacrine mode.
54 e on axons where they interact with ErbB4 in juxtacrine mode.
55 only a subclass of EGFR ligands can act in a juxtacrine mode.
56                                        This "juxtacrine" mode of communication has been well studied
57 pelling evidence in support of non-canonical juxtacrine Notch signaling within platelet aggregates th
58                  The paracrine antiviral and juxtacrine NOTCH3 pathways converge as STAT1 facilitates
59 l myelination: an initial phase dependent on juxtacrine Nrg1 signaling and a later phase that can be
60     It is possible that myelination requires juxtacrine Nrg1 signaling provided by the membrane-bound
61  may regulate the ability of EDA to act as a juxtacrine or paracrine factor.
62 f-1, thereby determining the mode of action, juxtacrine or paracrine, of the pref-1 protein.
63 GF to reproduce these findings suggests that juxtacrine or tightly coupled paracrine interactions und
64            Peptidergic signaling can involve juxtacrine, paracrine, endocrine, and neuronal signaling
65 ted pericytes produce VEGF that may act in a juxtacrine/paracrine manner as a survival and/or stabili
66                          To investigate this juxtacrine pathway, we mimic receptor-ligand binding wit
67  by age-dependent PDGF-AB-mediated paracrine/juxtacrine pathways that may be essential in the transla
68 cells is governed by age-dependent paracrine/juxtacrine platelet-derived growth factor (PDGF) pathway
69 y main mechanisms (intrinsic, paracrine, and juxtacrine) proposed to regulate glucagon release from a
70 he speed of such waves in both diffusive and juxtacrine relay systems.
71 red SMCs elicited a series of proatherogenic juxtacrine responses associated with increased foam cell
72                  We further created JUPITER (juxtacrine sensor for protein-protein interaction), a ge
73 ecific regulation of autocrine/paracrine and juxtacrine signaling accounted for the differential effi
74 to the two-dimensional (2D) cell membrane in juxtacrine signaling affects the accuracy of ligand sens
75 ical terms, which is particularly suited for juxtacrine signaling and mechanosensing studies.
76 ely controls their ability to participate in juxtacrine signaling and thus, only a subclass of EGFR l
77 t NOTCH activation in GBM CSLCs is driven by juxtacrine signaling between tumor cells and their surro
78  Disp1, unlike Smo, is not required for this juxtacrine signaling by Shh.
79 cally joining cells or by facilitating other juxtacrine signaling events.
80 urthermore, we identify a mechanism by which juxtacrine signaling from LFs to triple negative breast
81                                 Although its juxtacrine signaling geometry (EphA2's cognate ligand ep
82                                              Juxtacrine signaling is an important class of signaling
83 red precursor that can activate the EGFR via juxtacrine signaling or can be released and act as a sol
84                        We show that EphA7, a juxtacrine signaling receptor, is expressed on myocytes
85 ints on the dynamics of processes relying on juxtacrine signaling systems, such as axon guidance medi
86  is distinct from the classical EphA4-ephrin juxtacrine signaling through contact-dependent cell-cell
87 st cancer (BrCa) cells utilize paracrine and juxtacrine signaling to drive chemotherapy and radiation
88 esonance energy transfer studies showed that juxtacrine signaling typically occurred in trans at the
89  while still anchored to the membrane (i.e., juxtacrine signaling).
90 uronal differentiation of adult NSCs through juxtacrine signaling, findings that advance our understa
91 ns capable of participating in bidirectional juxtacrine signaling.
92 ay play an important role in KL/Kit-mediated juxtacrine signaling.
93  (autocrine/paracrine) and contact-mediated (juxtacrine) signaling molecules were evaluated for two c
94 hort-range patterning of the Delta/Notch (or juxtacrine) signaling pathway.
95 mediated by autocrine/paracrine, rather than juxtacrine, signaling.
96 etween cell division, cell fate choices, and juxtacrine signalling can affect the macroscopic orderin
97    The analysis presented here suggests that juxtacrine signalling dominates.
98 lly, a model with a simple representation of juxtacrine signalling is considered.
99 te a novel method to model morphogenesis and juxtacrine signalling, provide insights into the molecul
100 ation involves coupling of transcription via juxtacrine signalling.
101 eneous protein and receptor distributions in juxtacrine signalling.
102  signalling by transmembrane ligands, called juxtacrine signalling.
103 ctors, such as insulin and somatostatin, and juxtacrine signals between EphA4/7 on alpha-cells and ep
104 ever, recent evidence shows that a number of juxtacrine signals can lead to the opposite phenomenon o
105 ojections that glia extend when they receive juxtacrine signals from axons.
106                                              Juxtacrine signals from myelinating glia direct their se
107               Cell-cell interactions promote juxtacrine signals in specific subcellular domains, whic
108             Specifically, the integration of juxtacrine signals, such as CD40 and antigen, results in
109 cell fate decisions in response to competing juxtacrine signals.
110  is mediated, at least in part, by autocrine/juxtacrine stimulation by HB-EGF.
111  The latter then results in autocrine and/or juxtacrine stimulation of collagen gene expression.
112                   These results suggest that juxtacrine stimulation takes place in human tumor cells
113 wth factor, which serves as an autocrine and juxtacrine stimulus of proliferation.
114 ytes have been implicated, but their role in juxtacrine (that is, cell-cell contact dependent) signal
115 gulate the conversion of HB-EGF from being a juxtacrine to a paracrine/autocrine growth factor.
116 t fibroblast subtypes under the influence of juxtacrine Wnt signals.

 
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