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1 erentiated phenotype of the adult pancreatic acinar cell.
2 or-like state before re-differentiation into acinar cells.
3 r potential vanilloid subfamily 4 (TRPV4) in acinar cells.
4 ccelerates disorders of the ER in pancreatic acinar cells.
5 xygen species generation in mouse pancreatic acinar cells.
6 r acinar cells are terminally differentiated acinar cells.
7  pathological Ca(2+) signals and necrosis in acinar cells.
8 e pathogenesis of pancreatitis in pancreatic acinar cells.
9 cholate-induced necrosis in mouse pancreatic acinar cells.
10  elicited simultaneously in the neighbouring acinar cells.
11 2R protein was expressed in mouse pancreatic acinar cells.
12 flammatory cells, compared to UEA-I purified acinar cells.
13 lithocholic acid 3-sulfate primarily affects acinar cells.
14 ed the regenerative potential of pre-labeled acinar cells.
15 trypsin activation were analyzed in isolated acinar cells.
16 SI rapidly accumulates in lumen formed by LG acinar cells.
17 a (PanIN), arise via reprogramming of mature acinar cells.
18 than 2-fold larger in PG and SMG than in SLG acinar cells.
19 normal acinar cells and 5% of dacryoadenotic acinar cells.
20 16A or TMEM16B as well as from mouse parotid acinar cells.
21 imary basolateral Cl(-) uptake mechanisms in acinar cells.
22 a regeneration of digestive enzyme-producing acinar cells.
23 secretion from primary rabbit lacrimal gland acinar cells.
24 old number of Neurogenin 3 (Ngn3)-expressing acinar cells.
25  a conditional knockout of Atg5, in salivary acinar cells.
26 KDM6A to genomic binding sites in pancreatic acinar cells.
27 L, for different downstream responses of the acinar cells.
28 model that involves apoptosis of the central acinar cells.
29 lumen formation via apoptosis of the central acinar cells.
30 a(2+)]i) overload and necrosis of pancreatic acinar cells.
31 and for the formation and differentiation of acinar cells.
32 c duct and subsequent exposure to pancreatic acinar cells.
33 ibrosis-associated genes in adult pancreatic acinar cells.
34 initiated by cerulein and GTL was studied in acinar cells.
35 fic D1-like dopamine receptor (InvD1L), with acinar cells.
36 ial neoplasia (PanINs) when induced in mouse acinar cells.
37 ve Orai1 inhibitor, prevents Ca(2+) entry in acinar cells.
38 ntumor pancreatic tissues, such as islet and acinar cells.
39 CCK cellular actions directly affected human acinar cells.
40 ive intestinal peptide and secretin on intra-acinar cell adenosine 3',5'-cyclic monophosphate are exp
41 llular Ca(2+) signals may protect pancreatic acinar cells against Ca(2+) overload, intracellular prot
42 s constituted approximately 2% of the normal acinar cells and 5% of dacryoadenotic acinar cells.
43 ymogen-containing subcellular compartment of acinar cells and activation of CTSD, CTSB, and trypsinog
44 cell (MPC) population that gives rise to pre-acinar cells and bipotent cells with ductal and islet en
45      A possible link between progenitor-like acinar cells and cancer initiators is proposed.
46 x transcription factor complex of pancreatic acinar cells and critical to acinar cell fate specificat
47           Ectopic pancreatic tissue included acinar cells and cystically dilated secretory ducts with
48 nisms involved in regulating the function of acinar cells and in the loss of salivary gland function
49 , leading to activation of EGFR signaling in acinar cells and increased ADM.
50 tin cytoskeleton and autophagy in pancreatic acinar cells and is potently protective against cerulein
51      Moreover, Arg-II is mainly expressed in acinar cells and is upregulated with aging, which enhanc
52 scribed in considerable detail in pancreatic acinar cells and oocytes.
53 ression, repressed renewal of Mist1-positive acinar cells and prevented recovery of salivary secretio
54 ing E-cadherin in adherens junctions between acinar cells and reduced the activity of neutrophil seri
55 n cytoskeleton controls the reprogramming of acinar cells and regulates cell morphology in vivo and i
56 re to cigarette smoke increased ER stress in acinar cells and sensitized the pancreas to LPS-induced
57 ) that induce saliva secretion from residual acinar cells and the use of saliva substitutes.
58 sed to reflect the proliferative activity of acinar cells and their role in salivary gland homeostasi
59 causes progressive destruction of pancreatic acinar cells and, ultimately, loss of pancreatic functio
60 stablishment of a generic endocrine state in acinar cells, and also promotes delta-specification in t
61 y reduced CTSB and trypsinogen activation in acinar cells, and CTSD directly activated CTSB but not t
62 ted in activation of stellate cells, loss of acinar cells, and fibrosis, which are characteristics of
63 tabolism were measured in pancreatic tissue, acinar cells, and isolated mitochondria.
64 ules, expansion of ductal epithelia, loss of acinar cells, and the induction of pancreatic inflammati
65 omplexes expressed in adipocytes, pancreatic acinar cells, and the nervous system in mice.
66         Its deletion or inhibition regulates acinar cell apoptosis but not necrosis in two models of
67                 As a result, Ptf1a-deficient acinar cells are dramatically sensitized to KRAS transfo
68                Despite this requirement, how acinar cells are generated during organogenesis is uncle
69 ophagy, and mitochondrial dysfunction in the acinar cells are now recognized to be important in drivi
70 tion, a loss and abnormal differentiation of acinar cells are observed.
71                                   Pancreatic acinar cells are reprogrammed to a "ductal-like" state d
72        We further demonstrate that binuclear acinar cells are terminally differentiated acinar cells.
73 ) that induce saliva secretion from residual acinar cells as well as artificial salivary substitutes.
74 n regulating protein secretion by pancreatic acinar cells, as does Rab3D.
75 ere inflammation in the salivary glands with acinar cell atrophy, fibrosis, and dilation of the ducts
76 zymes, packaged into the zymogen granules of acinar cells, become activated and cause autodigestion.
77      IER3 expression was discrete in healthy acinar cells, becoming highly prominent in peritumoral a
78         This involves not only signalling in acinar cells but also in stellate cells.
79 ally give rise to all endocrine, ductal, and acinar cells but become bipotent by embryonic day 13.5,
80  signals and necrosis in isolated pancreatic acinar cells but the effects of bile acids on stellate c
81 ates and enhanced oxidative and ER stress in acinar cells, but none of these effects is related to NF
82                Incubation of mouse and human acinar cells, but not HEK293 or COS7 cells, with iohexol
83  bone marrow chimeras, expression of BCL3 by acinar cells, but not myeloid cells, was required for re
84        Nicotine induced dedifferentiation of acinar cells by activating AKT-ERK-MYC signaling; this l
85  and CK 7-positive tonofilaments in the pale acinar cells by myriad mucus granules.
86  features of pancreatitis in EtOH-sensitized acinar cells by suppressing the adaptive unfolded protei
87 r TP53(f/f) specifically in adult pancreatic acinar cells by using a full-length pancreatic elastase
88              In summary, we demonstrate that acinar cell calcineurin is activated in response to Ca(2
89                             We now show that acinar cells can be converted to delta-like and alpha-li
90 terations in calcium signaling in pancreatic acinar cells can result in pancreatitis.
91                                   Pancreatic acinar cell carcinoma (ACC) is an aggressive exocrine tu
92  developed various subtypes of PC, including acinar cell carcinoma, ductal adenocarcinoma, sarcomatoi
93 Lesions with histological features mimicking Acinar Cell Carcinomas are also observed in some tumors.
94 pancreatic ductal adenocarcinomas and 40% of acinar cell carcinomas.
95 nstrate that Piezo1 activation in pancreatic acinar cells caused a prolonged elevation in intracellul
96 ng proximity of PTF1 and MIST1 in pancreatic acinar cell chromatin implies extensive collaboration, a
97 a was also suppressed in ex vivo cultures of acinar cell clusters isolated from mouse pancreas bearin
98 and thus transforms our understanding of the acinar cell compartment as a pool of equipotent secretor
99                                           In acinar cells, cooling decreased the lipolysis induced by
100                                              Acinar cell damage and dysfunction cause malnutrition an
101  risk factors, such as chronic pancreatitis, acinar cell damage, and/or defective autophagy increase
102 s of CM4620 on SOCE, trypsinogen activation, acinar cell death, activation of NFAT and NF-kappaB, and
103 1, die perinatally due to massive pancreatic acinar cell death, precluding investigation of the effec
104  of CTSB affected apoptotic but not necrotic acinar cell death.
105 ownstream of trypsin activation that lead to acinar cell death.
106  trypsin activity, cell death signalling and acinar cell death.
107 e of cathepsin B into the cytosol leading to acinar cell death.
108 so activates ER stress pathways that promote acinar cell death.
109 s expressed in response to caerulein-induced acinar cell dedifferentiation, early neoplasia, and thro
110 pment via down-regulation of Gata6 to induce acinar cell dedifferentiation.
111  is associated with chronic pancreatitis and acinar cell dedifferentiation.
112    Immunohistochemical stains demonstrate an acinar cell defect but normal islet cells.
113           Atg7(Deltapan) mice exhibit severe acinar cell degeneration, leading to pancreatic inflamma
114               In vitro studies using Par-C10 acinar cells demonstrated that when compared with L(1p)M
115  is only minimal and transient in the early, acinar cell-dependent phase of pancreatitis and much gre
116                        At the final stage of acinar cell development, the absence of NR5A2 affects th
117 iduals >2 years of age contained clusters of acinar cells devoid of amylase (AMY(-)).
118 te and expand at 72 hours, the Mist1-positve acinar cells did not re-appear until 96 hours post poly
119                                      Loss of acinar cell differentiation also drives pancreatic cance
120 s to form but are accelerated by deletion of acinar cell differentiation factors such as Ptf1a, sugge
121  cell line to study underlying mechanisms of acinar cell differentiation in culture has not been desc
122 ression of transcription factors that affect acinar cell differentiation suggested that acinar cells
123 tis, with pathways involved in inflammation, acinar cell differentiation, and cell junctions being sp
124 ption of acinar morphogenesis and incomplete acinar cell differentiation.
125                             However, whether acinar cells directly contribute to PSC activation is un
126 ith controls, Ddr1(-/-) models had increased acinar cell dropout and reduced proliferation with no di
127 d to regulate multiple signaling pathways in acinar cells during cerulein-induced pancreatitis.
128 cells in the pancreas, yet the source of new acinar cells during homeostasis remains unknown.
129  initially cause injury to organelles of the acinar cell (endoplasmic reticulum, mitochondria, and en
130 e with beta1 syntrophin deletion in exocrine acinar cells exhibit increased severity of cerulein-indu
131     Zymogen secretory granules in pancreatic acinar cells express two vesicle-associated membrane pro
132 -regulation of genes that promote the mature acinar cell fate is required to reduce injury associated
133 x of pancreatic acinar cells and critical to acinar cell fate specification and differentiation.
134 ature activation of digestive enzymes within acinar cells, followed by necrosis and inflammation.
135 EM16A is a significant pathway in pancreatic acinar cells for HCO3 (-) secretion into the lumen.
136 ce KLF5 activity might reduce progression of acinar cells from ADM to PanIN and pancreatic tumorigene
137 ells treated with a Piezo1 antagonist and in acinar cells from mice with genetic deletion of Piezo1.
138  Accordingly, conditioned medium of isolated acinar cells from old WT (not Arg-II(-/-)) mice contains
139 I) lectin has been used to label and isolate acinar cells from the pancreas.
140 lular and molecular mechanisms that maintain acinar cell function and whose dysregulation can lead to
141 pression of proteins critically relevant for acinar cell function.
142 cinar-to-ductal metaplasia (ADM), pancreatic acinar cells give rise to pancreatic intraepithelial neo
143 ense variants in genes related to pancreatic acinar cells (GP2) and insulin secretion (GLP1R).
144 C-S), known to induce Ca(2+) oscillations in acinar cells, had only minor effects on stellate cells i
145 generation and maintenance of exocrine gland acinar cells have not yet been established.
146 orm crucial functions in food digestion, and acinar cell homeostasis required for secretion of digest
147                                  The loss of acinar cell homeostasis, differentiation, and identity i
148 se in the number of acini without individual acinar cell hyperplasia.
149 , necrosis, acinar-to-ductal metaplasia, and acinar-cell hypertrophy; this led to tissue atrophy and
150 works that control pancreatic MPC expansion, acinar cell identity, duct morphogenesis and generation
151 tify a critical role for PDX1 in maintaining acinar cell identity, thus resisting the formation of pa
152 pecialized phenotype of the adult pancreatic acinar cell in vivo Transcriptome sequencing and chromat
153 s required for normal function of pancreatic acinar cells in adult mice.
154 lonal expansion of terminally differentiated acinar cells in all major salivary glands.
155 ovel strategy for generating and maintaining acinar cells in culture.
156             Granular, zymogen-rich pyramidal acinar cells in normal glands predominated over a previo
157 s in stellate cells compared to the adjacent acinar cells in pancreatic lobules; whereas taurolithoch
158 arate lineages of myoepithelial, ductal, and acinar cells in postnatal glands.
159                 SHP expression is induced in acinar cells in response to ER stress and regulates the
160 genesis, and a lack of differentiated mucous acinar cells in submandibular and sublingual glands.
161 at Lfng is uniquely expressed in a subset of acinar cells in the adult pancreas.
162 gglutinin (PNA) have a specific affinity for acinar cells in the mouse pancreas, with minimal affinit
163                  Maintaining the identity of acinar cells in the pancreas could help to prevent the d
164  activation of KRAS in normal, untransformed acinar cells in the pancreatic tissues of mice resulted
165 established PanINs reverts them to quiescent acinar cells in vivo.
166             The addition of IL22 to cultured acinar cells increased their expression of markers of du
167             Addition of NETs and histones to acinar cells induced formation of trypsin and activation
168                        Hippo inactivation in acinar cells induced yes-associated protein 1 (YAP1)/tra
169 ce that insulin directly protects pancreatic acinar cell injury induced by bona fide pancreatitis-ind
170 eatitis (AP) suggest a strong association of acinar cell injury with cathepsin B-dependent intracellu
171  FK506 prevented activation of NF-kappaB and acinar cell injury.
172 re selected based on those found to decrease acinar cell injury.
173      In conclusion, Hes1 plays a key role in acinar cell integrity and plasticity on cellular insults
174 n of PanINs by enabling dedifferentiation of acinar cells into duct-like cells that are susceptible t
175 cked the irreversible transition of exocrine acinar cells into pancreatic preneoplastic ductal lesion
176 rmeable ion channel Piezo1 in the pancreatic acinar cell is the initial step in pressure-induced panc
177  substrate p62/SQSTM1 in stressed Kras(G12D) acinar cells is associated with PDAC development and mai
178 e intracellular Ca(2+) signals in pancreatic acinar cells is largely unknown.
179  the fibroinflammatory program in pancreatic acinar cells is suppressed under normal physiological co
180 ne were also evaluated in primary pancreatic acinar cells isolated from wild-type, nAChR7a(-/-), Trp5
181 t acinar cell differentiation suggested that acinar cells lacking ATF3 maintain a mature cell phenoty
182           Our data demonstrate that lacrimal acinar cells lacking Orai1 do not exhibit SOCE following
183                          In cytokine-treated acinar cells, lacritin stimulated protein secretion as m
184 on, driven by cell-cell interactions between acinar cells, leukocytes, and resident fibroblasts.
185 old in tears (p = 0.0116) and 1.4-fold in LG acinar cells (LGAC)(p = 0.0026) from male NOD mice, a mo
186 ses in mouse and human primary acini and the acinar cell line AR42J.
187                          To date, a pure pro-acinar cell line to study underlying mechanisms of acina
188      Thus, SOX2 is a master regulator of the acinar cell lineage essential to the establishment of a
189     We confirmed PTF1a/TRIP12 interaction in acinar cell lines and in co-transfected HEK-293T cells.
190                                              Acinar cells make up the majority of all cells in the pa
191 1R signaling in mice reflects an increase in acinar cell mass, without changes in ductal compartments
192 ng with exocrine defects, including impaired acinar cell maturation, the mutant mice exhibited substa
193 te that FGF2 regulates specific steps during acinar cell maturation.
194 The proliferative capacity of differentiated acinar cells may prove critical in the implementation of
195  addition, Slug attenuated TGF-alpha-induced acinar cell metaplasia to ductal structures and TGF-alph
196                              However, in the acinar cell, Munc18c's functions in exocytosis and homeo
197 At study end, Ki-67-positive (proliferating) acinar cell number did not change, compared with baselin
198 in produced not only a dramatic reduction in acinar cell numbers, but also a significant reduction in
199 tion of Sec23b exclusively in the pancreatic acinar cells of adult mice results in decreased overall
200 in the developing ductal, serous, and mucous acinar cells of salivary glands.
201 netic recombination predominantly within the acinar cells of the glands.
202 secretion of bicarbonate-rich fluid from the acinar cells of the pancreas that accumulates within the
203 ease-activated Ca(2+) currents in pancreatic acinar cells offers remarkable protection against Ca(2+)
204  directly via G protein-coupled receptors on acinar cells or through inflammatory cells.
205                                           In acinar cells, our study demonstrates an age-associated A
206 n PSCs and their better studied neighbouring acinar cells (PACs) and found complete separation of Ca(
207 tested in freshly isolated murine pancreatic acinar cells (PACs) to determine inhibition of toxin-ind
208 bipotent progenitors (BPs) and unipotent pro-acinar cells (PACs).
209 nnabinoid receptor subtype 2 (CB2R) prevents acinar cell pathogenesis in animal models of acute pancr
210 olecule 1 (STIM1)/Orai complexes, attenuates acinar cell pathology and acute pancreatitis in mouse ex
211                        Epithelial pancreatic acinar cells perform crucial functions in food digestion
212 ying this Ca(2+)-dependent generation of the acinar cell phenotype.
213 f the pancreas and in the maintenance of the acinar cell phenotype.
214 s model, we studied the role of Hes1 in both acinar cell plasticity and pancreatic regeneration after
215                                      Damaged acinar cells play a passive role in activating pancreati
216                                              Acinar cells play an essential role in the secretory fun
217 ction of cellular plasticity in multiple non-acinar cell populations.
218                                   Pancreatic acinar cells possess very high protein synthetic rates a
219                                              Acinar cells prepared from the pancreas of rats or mice
220 approaches with acute dissociated pancreatic acinar cells prepared from wild type, CB1R-knockout (KO)
221 ATA6 and promoting differentiation toward an acinar cell program.
222 enhancer landscape, activates differentiated acinar cell programs, and indirectly suppresses oncogeni
223   Furthermore, oncogenic KRAS did not induce acinar cell proliferation, but did sustain the prolifera
224 delayed recovery of the pancreas and reduced acinar cell proliferation.
225 ppear to be excellent lectins for pancreatic acinar cell purification.
226 cal samples from 1795 volunteers, pancreatic acinar cell, rather than duct cell, function is presentl
227 s based predominantly on self-duplication of acinar cells, rather than on differentiation of stem cel
228 xpression, and ectopic expression of KLF4 in acinar cells reduces acinar lineage- and induces ductal
229                              We investigated acinar cell replacement during homeostasis, growth, and
230 ing, followed by a chase period, showed that acinar cell replacement is not driven by the differentia
231 oses to PDAC because it induces a process of acinar cell reprogramming known as acinar-to-ductal meta
232                                              Acinar cell responses to the muscarinic agonist carbacho
233            Kras activation in Mist1(+) adult acinar cells resulted in brisk PanIN formation, whereas
234 transcriptional program in normal pancreatic acinar cells, resulting in acinar-ductal metaplasia, a d
235             Transcriptome analysis of single acinar cells revealed the existence of a minor populatio
236  not been studied in CP, although pancreatic acinar cells seem to be especially vulnerable to ER dysf
237 dies of this disorder focus on the damage to acinar cells since they are assumed to be the primary ta
238                                    Mice with acinar cell-specific expression of Kras(G12D) were cross
239 )) via Cre(ERTM) recombinase regulated by an acinar cell-specific promoter (Ptf1a).
240 ed mice with tamoxifen-inducible, pancreatic acinar cell-specific Sec23b deletion.
241                   Perturbation of pancreatic acinar cell state can lead to acinar-to-ductal metaplasi
242 in rats and in vitro in rat pancreatic AR42J acinar cells stimulated with taurocholate or TNF-alpha.
243 educed caspase-3 activation and apoptosis in acinar cells stimulated with the intestinal hormone chol
244 last several months, the convergent roles of acinar cell stress, autophagy and proinflammatory signal
245 identified the presence of a progenitor-like acinar cell subpopulation.
246  (saliva-facing) membranes of salivary gland acinar cells, suggesting a dual role of this transporter
247 xes contributes to the disease in pancreatic acinar cells, supporting a role for endoplasmic reticulu
248 more extensive necrosis in both stellate and acinar cells than TLC-S alone.
249  the pancreas primarily comprises long-lived acinar cells that are not considered a bona fide source
250  pathway; this could be a mechanism by which acinar cells that express activated KRAS become suscepti
251 inar specific partner Rbpjl, so that the few acinar cells that form do not complete differentiation.
252 operties of the ion-transporting pathways in acinar cells that might account for the differences amon
253  salivary glands is due to the impairment of acinar cells, the major glandular cells of protein, salt
254       The transdifferentiation of pancreatic acinar cells to a ductal phenotype (acinar-to-ductal met
255 fa, and Pdx1, directly reprograms pancreatic acinar cells to beta-cells.
256 ous work demonstrating in vivo conversion of acinar cells to beta-like cells by viral delivery of exo
257  the conversion of terminally differentiated acinar cells to beta-like cells.
258 -22 acts directly at the level of pancreatic acinar cells to decrease expression of the pancreas asso
259 actors whose combinatorial actions reprogram acinar cells to distinct islet endocrine subtypes in viv
260 trast, TGF-beta1 efficiently converted human acinar cells to duct-like cells (AD) in a SMAD-dependent
261 tor Snail (Snai1) can cooperate with Kras in acinar cells to enhance ADM development, the contributio
262 uce cell-autonomous proliferation but primed acinar cells to exogenous pro-proliferative stimuli, imp
263       We investigated the ability of injured acinar cells to generate pancreatic fibrosis in acute pa
264 ound shifts in PDX1 chromatin occupancy from acinar cells to PDA.
265 ts that prevent conversion of differentiated acinar cells to proliferative ductal progenitors.
266                    Hippo disruption promotes acinar cells to secrete fibroinflammatory factors and in
267 lls connect liver hepatocytes and pancreatic acinar cells to the intestine, but the mechanism for the
268                   We exposed mouse and human acinar cells to the radiocontrast agent iohexol (Omnipaq
269 in the ductal cell layer and/or in surviving acinar cells, to drive transcellular flux of interstitia
270 y antagonizing the metaplastic conversion of acinar cells toward a ductal fate capable of responding
271 in vivo conversion of adult mouse pancreatic acinar cells toward beta cells, we show that induced bet
272 ical role for ATF3 as a key regulator of the acinar cell transcriptional response during injury and m
273                             An adipocyte and acinar cell Transwell coculture system, with or without
274 Notably, these effects were recapitulated in acinar cells treated with a pharmacological inhibitor of
275 of these pathological events were rescued in acinar cells treated with a Piezo1 antagonist and in aci
276 lder model) without directly affecting intra-acinar cell trypsin activation in vitro The absence of C
277 elial constituents, and uncovered 3 distinct acinar cell types, with possible implications for homeos
278 hat GRP78 could exert a protective effect on acinar cells under stress, as during PDAC development.
279 st-induced Ca(2+) oscillations in pancreatic acinar cells using multiple experimental approaches with
280 eltapan)) caused spontaneous and progressive acinar cell vacuolization and death, interstitial fibros
281 atitis features including pancreatic oedema, acinar cell vacuolization, intrapancreatic trypsin activ
282  Since CEL is expressed mainly in pancreatic acinar cells, we asked whether we could find structural
283 ing 3D explant culture of primary pancreatic acinar cells, we show that PKD1 acts downstream of TGFal
284              While amylase-positive (AMY(+)) acinar cells were detectable in pancreata from all study
285  transgenic mice expressing Slug and Kras in acinar cells were generated.
286 eata and primary acinar cells were isolated; acinar cells were incubated with an inhibitor of p110alp
287                               Rat pancreatic acinar cells were isolated by collagenase digestion and
288                                              Acinar cells were isolated from the tissues and the effe
289                        Pancreata and primary acinar cells were isolated; acinar cells were incubated
290                       Moreover, PNA-purified acinar cells were less contaminated with mesenchymal and
291 ajor apical Cl(-) efflux pathway in salivary acinar cells, were significantly greater in PG compared
292 naliculi, a specialized apical domain of the acinar cells, where protein and fluid secretion occur.
293 ment of Ca(2+) signaling in mouse pancreatic acinar cells, which suggests a potential cellular mechan
294 ocess involves activation of YAP1 and TAZ in acinar cells, which up-regulate JAK-STAT3 signaling to p
295 lasia (ADM), a process that replaces damaged acinar cells with duct-like structures.
296 ncubation of AR42J or primary mouse or human acinar cells with MKC-3946 reduced expression of XBP1s,
297  Better methods for purifying human or mouse acinar cells without the need for genetic modification a
298 mbination strategy in adult mouse pancreatic acinar cells (Yap1fl/fl;Tazfl/fl;Ela1-CreERT2).
299 verity of pancreatitis not by reducing intra-acinar cell zymogen activation but by reducing infiltrat
300                                              Acinar cell zymogen granules (ZG) express 2 isoforms of

 
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