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1 type I (SAI) neurons innervate skin-derived Merkel cells.
2 regions where Bdnf was deleted in embryonic Merkel cells.
3 seen during postnatal development of normal Merkel cells.
4 ratinocytes in juxtaposition with innervated Merkel cells.
5 er Atoh1 was sufficient to create additional Merkel cells.
6 ly activated cation channel, is expressed in Merkel cells.
7 e- or pre-B cell rather than the postmitotic Merkel cells.
8 rhans cells, while CK20 did not identify any Merkel cells.
9 cerebellum, hair cells of the inner ear, and Merkel cells.
10 (+) CD200(-) epidermis does not give rise to Merkel cells.
11 e rise to the epidermis, hair follicles, and Merkel cells.
12 s express several markers detected in normal Merkel cells, a nonproliferative population of neuroendo
13 increase in the number of lineage-committed Merkel cells, a specialized subtype of skin cells involv
18 nd signaling pathways required for targeting Merkel-cell afferents to discrete mechanosensory compart
20 ed stem cell niches and that might relate to Merkel cell and melanocyte ontogeny and tumorigenesis.
21 l discs are tactile end organs consisting of Merkel cells and Abeta-afferent nerve endings and are lo
22 Synapse-like junctions are observed between Merkel cells and associated afferents, and yet it is unc
23 for a two-receptor-site model, in which both Merkel cells and innervating afferents act together as m
25 .5 (E16.5), touch domes emerge as patches of Merkel cells and keratinocytes clustered with a previous
26 cent parallel studies clearly indicated that Merkel cells and the mechanosensitive piezo2 ion channel
27 anding controversy regarding the function of Merkel cells and their afferent nerve fiber partners.
28 onal epidermal barrier, formation of ectopic Merkel cells, and defective postnatal development of hai
29 onal epidermal barrier, formation of ectopic Merkel cells, and defective postnatal hair follicle deve
32 ogenetic approaches in intact skin show that Merkel cells are both necessary and sufficient for susta
35 ted afferents, and yet it is unclear whether Merkel cells are inherently mechanosensitive or whether
37 that Piezo2 and Ca(2+)-action potentials in Merkel cells are required for behavioral tactile respons
43 via K14Cre resulted in a decreased number of Merkel cells but had no effect on other epithelial compa
48 nts), squamous cell carcinoma (26 patients), Merkel cell carcinoma (6 patients), pigmented epithelioi
49 therapy-refractory, histologically confirmed Merkel cell carcinoma (aged >/=18 years) were enrolled f
50 cinoma (SCC) and rare skin tumors, including Merkel cell carcinoma (MCC) and dermatofibrosarcoma prot
51 ator of Merkel cell development, its role in Merkel cell carcinoma (MCC) carcinogenesis remains contr
52 le has been done to characterize how closely Merkel cell carcinoma (MCC) cell lines model native tumo
53 ous cell carcinoma (SCC), melanoma (MM), and Merkel cell carcinoma (MCC) in a cohort of US OTRs recei
82 targeted therapeutic intervention.IMPORTANCE Merkel cell carcinoma (MCC) is the most aggressive cutan
87 avirus (MCPyV) is frequently associated with Merkel cell carcinoma (MCC), a highly aggressive neuroen
88 Merkel cell polyomavirus (MCPyV) can lead to Merkel cell carcinoma (MCC), a lethal form of skin cance
89 n polyomavirus etiologically associated with Merkel cell carcinoma (MCC), a rare and aggressive form
91 to be clonally integrated in 80% of cases of Merkel cell carcinoma (MCC), a rare but aggressive form
92 or clinical applications of such pathways in Merkel cell carcinoma (MCC), a rare but lethal cutaneous
93 irus (MCPyV) causes the majority of cases of Merkel cell carcinoma (MCC), an aggressive skin cancer w
94 ed to support the etiologic role of MCPyV in Merkel cell carcinoma (MCC), an extremely lethal form of
95 l polyomavirus (MCPyV) in the development of Merkel cell carcinoma (MCC), making MCPyV the first poly
96 skin tumors, basal cell carcinoma (BCC) and Merkel cell carcinoma (MCC), with overlapping histologic
97 he biophysical properties of piezo2 in human Merkel cell carcinoma (MCC)-13 cells; piezo2 is a low-th
110 We conclude that MCV sT is required for Merkel cell carcinoma growth, but its in vitro transform
111 es of melanoma, squamous cell carcinoma, and Merkel cell carcinoma in this high-risk population.
118 e recently been discovered: MCV was found in Merkel cell carcinoma samples, while Karolinska Institut
119 noclonal antibody, in patients with stage IV Merkel cell carcinoma that had progressed after cytotoxi
120 that the 81% of patients with virus-positive Merkel cell carcinoma tumors had earlier stage disease a
122 ons; however, the spicules were positive for Merkel cell carcinoma virus, which is also a polyomaviru
123 yV-induced cellular proliferation.IMPORTANCE Merkel cell carcinoma was first described in 1972 as a n
125 avirus Merkel cell polyomavirus (MCV) causes Merkel cell carcinoma, an aggressive but rare human skin
127 d in the USA for the treatment of metastatic Merkel cell carcinoma, has shown antitumour activity and
128 progressive multifocal leukoencephalopathy, Merkel cell carcinoma, pruritic rash or trichodysplasia
129 MCV) causes an aggressive human skin cancer, Merkel cell carcinoma, through expression of small T (sT
130 made in the study of human papillomaviruses, Merkel cell carcinoma-associated polyomavirus, Epstein-B
131 -associated T cells correlates with improved Merkel cell carcinoma-specific survival, but the prognos
141 with pembrolizumab in patients with advanced Merkel-cell carcinoma was associated with an objective r
142 lled study, we assigned adults with advanced Merkel-cell carcinoma who had received no previous syste
146 ting conclusions regarding the proportion of Merkel cell carcinomas (MCCs) that contain the Merkel ce
148 ered in 2008, drives the development of most Merkel cell carcinomas (MCCs) through several canonical
149 MCV) contributes to approximately 80% of all Merkel cell carcinomas (MCCs), a highly aggressive neuro
150 CV) is the recently discovered cause of most Merkel cell carcinomas (MCCs), an aggressive form of non
151 ceptor repertoire associated with 72 primary Merkel cell carcinomas and correlated metrics of the T-c
153 viral T antigens is a common feature of most Merkel cell carcinomas, a primary neuroendocrine skin tu
157 erents lacking Merkel cells demonstrate that Merkel cells confer high-frequency responses to dynamic
159 Recordings from touch-dome afferents lacking Merkel cells demonstrate that Merkel cells confer high-f
160 iption factor ATOH1 is a master regulator of Merkel cell development, its role in Merkel cell carcino
170 ing Piezo2 in both adult sensory neurons and Merkel cells exhibit a profound loss of touch sensation.
173 rnover of large T (LT) proteins from BK, JC, Merkel cell, HPyV7 and trichodysplasia spinulosa polyoma
174 s acquired several characteristics of mature Merkel cells in a time frame similar to that seen during
175 nn cells form nerve-like bundles that target Merkel cells in organoid hair follicles, mimicking the n
176 toh1 expression is sufficient to produce new Merkel cells in the epidermis, that epidermal cell compe
178 lation of Sox2 results in a dramatic loss of Merkel cells, indicating that Sox2 is a critical regulat
179 r of differentiated cells in the case of the Merkel cell lineage and hair follicle type in the case o
180 ene expression and reduced expression of key Merkel cell lineage/MCC marker genes, including HES6, SO
181 d that NDRG1 exerts its biological effect in Merkel cell lines by regulating the expression of the cy
182 1 expression drove ectopic expression of the Merkel cell marker keratin 8 (K8) throughout the epiderm
183 main type of tactile end organ consisting of Merkel cells (MCs) and Abeta-afferent endings, are highl
186 n, but not in sensory neurons, and show that Merkel-cell mechanosensitivity completely depends on Pie
191 y adapting responses in vivo mediated by the Merkel cell-neurite complex show reduced static firing r
194 results indicate a division of labour in the Merkel cell-neurite complex: Merkel cells signal static
195 se touch domes, which contain mechanosensory Merkel cell-neurite complexes and abut primary hair foll
197 hanoreceptors that form Meissner corpuscles, Merkel cell-neurite complexes, and circumferential hair
201 implicate one of these mechanoreceptors, the Merkel cell/neurite complex, in two-point discrimination
203 l cells to directly test the hypothesis that Merkel cell/neurite complexes are necessary to perform t
204 ry afferents can functionally substitute for Merkel cell/neurite complexes in this sensory organ.
211 led 3 (Fz3) can rescue the hair follicle and Merkel cell polarity defects in frizzled 6-null (Fz6(-/-
214 hat we believe to be the first case in which Merkel cell polyomavirus (MCPyV) and human papillomaviru
215 rkel cell carcinomas (MCCs) that contain the Merkel cell polyomavirus (MCPyV) and the clinical signif
219 ex Virus (HSV), Influenza A Virus (IAV), and Merkel Cell Polyomavirus (MCPyV) could be targeted.
224 Accumulating evidence indicates a role for Merkel cell polyomavirus (MCPyV) in the development of M
235 d with clonal integration of a polyomavirus, Merkel cell polyomavirus (MCPyV), and MCC tumor cells ex
238 reading frame (ALTO) in the early region of Merkel cell polyomavirus (MCPyV), the causative agent of
239 reported in 2008 to be caused by a PyV named Merkel cell polyomavirus (MCPyV), the first PyV linked t
240 Notably, ectopic expression of different Merkel cell polyomavirus (MCPyV)-derived truncated large
248 mas (MCCs) that harbor a clonally integrated Merkel cell polyomavirus (MCV) genome have low mutation
252 Recently, it was demonstrated that human Merkel cell polyomavirus (MCV) is clonally integrated in
259 of the skin-is caused by the integration of Merkel cell polyomavirus and persistent expression of la
266 verses rodent cell transformation induced by Merkel cell polyomavirus small T antigen viral oncoprote
270 an option to interfere with proliferation of Merkel cell polyomavirus(+) Merkel cell carcinoma cell l
274 awi polyomavirus are shed from the skin, and Merkel cell polyomavirus, trichodysplasia spinulosa poly
285 ding simian virus 40 (SV40), murine PyV, and Merkel cell PyV, are found integrated in the host genome
286 ing rat whisker hair follicles, we show that Merkel cells rather than Abeta-afferent nerve endings ar
289 f labour in the Merkel cell-neurite complex: Merkel cells signal static stimuli, such as pressure, wh
294 ional network required to produce functional Merkel cells that are required for tactile discriminatio
295 We genetically engineered mice that lack Merkel cells to directly test the hypothesis that Merkel
297 aviruses (KI virus (KIV), WU virus (WUV) and Merkel cell virus (MCV)) to a class that previously had
298 Keratin-17-expressing keratinocytes but not Merkel cells were necessary to establish innervation pat
299 ile stimuli into Ca(2+)-action potentials in Merkel cells, which drive Abeta-afferent nerve endings t