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1                                              PNEC cell lines should be generally useful for genetic a
2                                              PNECs can be colabeled with alveolar cells during lung d
3                                              PNECs express mAsh1, a basic helix-loop-helix (bHLH) tra
4                     Associated with aberrant PNEC innervation, the authors discovered that GABA hyper
5                                 In addition, PNECs expressed NT4 as a target-derived mechanism underl
6 tion: endoderm-derived NECs were retained as PNECs, while the carotid body evolved via the aggregatio
7 te NE tumors and derived prostate NE cancer (PNEC) cell lines from a transgenic mouse model using a c
8 survival, we established prostate NE cancer (PNEC) cell lines from CR2-TAg prostate tumors and metast
9 xposure elevated the level of NT4 and caused PNEC hyperinnervation and nodose neuron hyperactivity.
10 s function in pulmonary neuroendocrine cell (PNEC) differentiation has not been fully addressed.
11 l for primary pulmonary neuroendocrine cell (PNEC) hyperplasia/neoplasia using v-Ha-ras driven by the
12 ophages, and pulmonary neuroendocrine cells (PNEC).
13  of solitary pulmonary neuroendocrine cells (PNECs) and neuroepithelial bodies (NEBs) along the main
14              Pulmonary neuroendocrine cells (PNECs) are proposed to be the first specialized cell typ
15              Pulmonary neuroendocrine cells (PNECs) are the only innervated airway epithelial cells.
16 expressed in pulmonary neuroendocrine cells (PNECs), a rare, innervated epithelial population.
17 cells, and 'pulmonary neuroendocrine cells' (PNECs) - are obscure.
18            Treatment of nude mice containing PNEC tumor xenografts with (i) amiloride, a diuretic tha
19 argeted inactivation of Ctnnb by Nkx2.1-cre, PNEC differentiation was not interrupted.
20 wed that nitrosamine treated rodents develop PNEC hyperplasia but non-NE lung tumors, with variable o
21  that SCLC can originate from differentiated PNECs.
22 rcinomas, with rascal mRNA in differentiated PNECs and tumor cells.
23 area covered by NEBs composed of 20 or fewer PNECs was significantly enlarged after naphthalene treat
24 ormation, Wnt signaling is not essential for PNEC differentiation; however, its over-activation promo
25 stablish the foundation of investigating how PNECs contribute to lung homeostasis, injury/repair, and
26                                 Importantly, PNECs have long been speculated to constitute the cells
27 as enabled us to manipulate gene activity in PNECs.
28 (CGRP) locus that encodes a major peptide in PNECs.
29 used to ablate multiple tumor suppressors in PNECs that were simultaneously labeled for following the
30 ested that early deletion of Nkx2.1 inhibits PNEC differentiation, while late repression does not.
31 lung development, and following lung injury, PNECs can contribute to Clara cells and ciliated cells.
32 r, these studies provide unique insight into PNEC lineage and function and establish the foundation o
33 al crest-derived, but endoderm-derived, like PNECs, whose endodermal origin we confirm.
34                          Targeting the nerve-PNEC axis may be a valid treatment strategy for mucus ov
35 s overproduction and changes along the nerve-PNEC axis without any defects in inflammation.
36 tem that permits tracing the early events of PNEC transformation has not been available.
37 dence for NT4-dependent neural regulation of PNEC secretion of GABA in a neonatal disease model.
38 rrent model, we observed that elimination of PNECs has no apparent consequence on Clara cell recovery
39 ion in mouse lung results in an inability of PNECs to cluster into sensory organoids and triggers inc
40 o identify the location, size, and number of PNECs and NEBs in the airways.
41 g using this tool revealed the plasticity of PNECs.
42                          Although studies of PNECs have suggested their involvement in a number of lu
43 arly life allergen exposure by orchestrating PNEC innervation and secretion of GABA.
44  In particular, we prove that summing up PEC/PNEC ratios might serve as a justifiable CA-approximatio
45 ation; however, its over-activation promotes PNEC features.
46  To what extent neural innervation regulates PNEC secretion and function is unknown.
47                                We found that PNECs were the only cellular source of GABA in airways.
48 s, and as xenografted tumors, indicated that PNECs express consistent features ex vivo and in vivo an
49                  We demonstrate in vivo that PNECs act as precise airway sensors that elicit immune r
50                                          The PNEC number per square millimeter was also increased mor
51              These findings suggest that the PNEC and neuropeptide abnormalities documented in a wide
52                                   Similar to PNEC in normal lung, Uchl1(positive) cells were innervat
53               NECs have also been likened to PNECs, which differentiate in situ within lung airway ep
54 NT4 as a target-derived mechanism underlying PNEC innervation during development.
55                                           WD-PNECs and WD-PBECs were generated from nasal and bronchi
56                                           WD-PNECs may provide an authentic surrogate model with whic
57 ogenesis and proinflammatory responses in WD-PNECs compared with WD-PBECs that reproduce many hallmar
58 l-differentiated primary pediatric nasal (WD-PNECs) and bronchial epithelial cells (WD-PBECs).

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