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1 PNEC cell lines should be generally useful for genetic a
2 PNEC-enriched cultures were generated from human induced
3 PNECs are an extraordinarily rich and diverse signaling
4 PNECs can be colabeled with alveolar cells during lung d
5 PNECs express mAsh1, a basic helix-loop-helix (bHLH) tra
11 tion: endoderm-derived NECs were retained as PNECs, while the carotid body evolved via the aggregatio
13 te NE tumors and derived prostate NE cancer (PNEC) cell lines from a transgenic mouse model using a c
14 survival, we established prostate NE cancer (PNEC) cell lines from CR2-TAg prostate tumors and metast
15 xposure elevated the level of NT4 and caused PNEC hyperinnervation and nodose neuron hyperactivity.
18 l for primary pulmonary neuroendocrine cell (PNEC) hyperplasia/neoplasia using v-Ha-ras driven by the
21 of solitary pulmonary neuroendocrine cells (PNECs) and neuroepithelial bodies (NEBs) along the main
27 ated to form pulmonary neuroendocrine cells (PNECs), a putative cell of origin for neuroendocrine-pos
29 th increased pulmonary neuroendocrine cells (PNECs), excess PNEC-derived neuropeptides are responsibl
30 ells to form pulmonary neuroendocrine cells (PNECs), putative precursors to small cell lung cancers (
33 proposed Predicted No-Effect Concentration (PNEC) and the Environmental Quality Standard (EQS) for M
38 ms (algae, invertebrates and fish) to derive PNEC values for the 14 metals most commonly observed in
39 wed that nitrosamine treated rodents develop PNEC hyperplasia but non-NE lung tumors, with variable o
44 lmonary neuroendocrine cells (PNECs), excess PNEC-derived neuropeptides are responsible for pulmonary
45 KRAS or EGFR genes did not induce or expand PNECs, but tumors resembling early-stage SCLC grew in im
46 area covered by NEBs composed of 20 or fewer PNECs was significantly enlarged after naphthalene treat
48 ormation, Wnt signaling is not essential for PNEC differentiation; however, its over-activation promo
50 stablish the foundation of investigating how PNECs contribute to lung homeostasis, injury/repair, and
51 ion methods, and little is known about human PNEC function in response to asthma-relevant stimuli.
52 ate a previously unrecognized role for human PNEC in mediating a direct neuroendocrine response to ae
53 eveloped and characterized an in vitro human PNEC model and investigated the neuroendocrine response
58 used to ablate multiple tumor suppressors in PNECs that were simultaneously labeled for following the
59 ll lung cancers (SCLCs), and we can increase PNECs by reducing levels of retinoblastoma (RB) proteins
60 essor genes TP53 and RB1 allowed the induced PNECs to form subcutaneous growths in immune-deficient m
61 ested that early deletion of Nkx2.1 inhibits PNEC differentiation, while late repression does not.
62 lung development, and following lung injury, PNECs can contribute to Clara cells and ciliated cells.
63 r, these studies provide unique insight into PNEC lineage and function and establish the foundation o
67 y-state immune cells and innervating nerves, PNECs, as prototype tissue-resident neuroendocrine cells
68 y of local cell targets, and we show the new PNEC signal angiotensin directly activates one subtype o
71 ficient mice after subcutaneous injection of PNEC-containing cultures in which expression of both RB
73 fectively attenuated by either prevention of PNEC formation, inactivation of CGRP gene, endothelium-s
76 rrent model, we observed that elimination of PNECs has no apparent consequence on Clara cell recovery
77 ion in mouse lung results in an inability of PNECs to cluster into sensory organoids and triggers inc
84 In particular, we prove that summing up PEC/PNEC ratios might serve as a justifiable CA-approximatio
86 dings identify a local circuit in which rare PNECs within submucosal glands sense an environmental cu
89 a corroborate this role and demonstrate that PNECs are important for lung response to signals, such a
91 s, and as xenografted tumors, indicated that PNECs express consistent features ex vivo and in vivo an
101 ogenesis and proinflammatory responses in WD-PNECs compared with WD-PBECs that reproduce many hallmar