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1 ared membrane targeting of newly synthesized canalicular ABC (ATP-binding cassette) transporters MDR1
2 ecretion, eyelid malposition, and punctal or canalicular abnormalities.
3 more, SLC30A10 and SLC39A14 localized to the canalicular and basolateral domains of polarized hepatic
4 ce suggests that AQPs are likely involved in canalicular and ductal bile secretion, gluconeogenesis a
5                          The pathway between canalicular and intracellular membranes that BSEP consti
6                    These differences in both canalicular and lamellar structure are probably linked t
7 station, period of maximal fetal growth, and canalicular and saccular stages of fetal lung developmen
8 canaliculi in KO livers along with decreased canalicular and sinusoidal microvilli.
9 tion and for normal development of secretory canalicular and tubulovesicular membranes in mouse parie
10 ifferentiation, and development of secretory canalicular and tubulovesicular membranes.
11 ges, including prebud, bud, pseudoglandular, canalicular, and terminal.
12 onally distinct sinusoidal (basolateral) and canalicular (apical) plasma membrane domains.
13 traffics from the trans-Golgi network to the canalicular area of hepatocytes, where it facilitates ex
14  copper into the bile, ATP7B traffics toward canalicular area of hepatocytes.
15                                         As a canalicular bile acid effluxer, the bile salt export pum
16 ial function of the liver, and impairment of canalicular bile acid secretion leads to cholestatic liv
17 to decreased expression of the major hepatic canalicular bile acid transport protein.
18 ies could demonstrate that deficiency of the canalicular bile acid transporter bile salt export pump
19 rget gene that functions as an ATP-dependent canalicular bile acid transporter.
20                           Insulin stimulates canalicular bile flow by interaction with hepatocytes.
21                                              Canalicular bile flow, as measured by [14C]erythritol cl
22 sport provides the osmotic driving force for canalicular bile formation.
23 nate-rich hypercholeresis when secreted into canalicular bile in unconjugated form; the mechanism is
24                                              Canalicular bile is formed by the osmotic filtration of
25 1 encoding bile salt export pump (BSEP), the canalicular bile salt export pump of hepatocyte.
26 olism enzymes CYP27A1 and CYP3A11 as well as canalicular bile salt pump ABCB11.
27 nd Fyn-dependent retrieval of sinusoidal and canalicular bile salt transport systems from the corresp
28 "flux proteins", including AQPs, involved in canalicular bile secretion.
29 quaporins are involved in agonist-stimulated canalicular bile secretion.
30  bile salt homeostasis without impairment of canalicular bile secretion; in humans this process is li
31 d its downstream targets, leading to loss of canalicular bile transport and altered bile acid pool.
32 e canaliculi, which was secondary to loss of canalicular bile transport and bile acid metabolism, lea
33 senger RNA (mRNA) expression of the two main canalicular bile transporters, bile salt export pump (BS
34 y also because of the absence of micelles in canalicular bile.
35 pose that polarization of hepatocytes (i.e., canalicular biogenesis) requires recruitment of rab11a a
36 ts (BS) and the functional expression of the canalicular BS export pump (BSEP; ABCB11).
37                                              Canalicular BSEP, mostly present in raft (high cholester
38  of membrane fractions localized Fic1 to the canalicular, but not basolateral, plasma membrane domain
39 tructural findings included coarse, granular canalicular Byler bile, effaced canalicular microvilli,
40 selectively transported to the apical (i.e., canalicular) cell membrane, revealed two polarization ph
41 most common complications of stents included canalicular cheese-wiring and tube prolapse in approxima
42 ytes and eosinophils, rosette formation, and canalicular cholestasis yielded an area under the receiv
43                       Liver histology showed canalicular cholestasis, mild-to-moderate fibrosis, and
44 type1 in humans, which is characterized by a canalicular cholestasis.
45 f the nuclear bile salt receptor FXR and the canalicular cholesterol transporter ABCG5/ABCG8 in the g
46 th the genes Abcg5 and Abcg8 that encode the canalicular cholesterol transporter.
47 intubation for PANDO, there were no cases of canalicular closure or stenosis at 12 months.
48 ation of highly purified Golgi membranes and canalicular (CMVs) and sinusoidal/basolateral (SMVs) mem
49 ns were intact, KO/KD livers had significant canalicular defects, which resulted from loss of hepatoc
50                                              Canalicular DHE could completely redistribute to the bas
51 p = 0.022), perimeter (+14%, p = 0.008), and canalicular diameter (+6%, p = 0.037).
52 efined donor hepatocyte colonies with strong canalicular dipeptidyl peptidase IV activity.
53                                     Cases of canalicular disease were excluded.
54 ocalized by immunohistochemistry to the bile canalicular domain of hepatocytes and to the luminal sid
55  membrane from where they transcytose to the canalicular domain.
56 om where they transcytose to the apical bile canalicular domain.
57 t liver revealed P2X4 in the basolateral and canalicular domains.
58                            Newly synthesized canalicular ectoenzymes and a cell adhesion molecule (cC
59          An improved awareness of the normal canalicular epithelial structure and its immunohistochem
60 ns in normal conjunctival epithelium, normal canalicular epithelium, and canaliculops epithelium.
61                              Basolateral and canalicular excretion of APAP was also assessed in the i
62  role in lipid homeostasis by regulating the canalicular excretion of bile acids.
63  can restore the polarity of hepatocytes and canalicular export of bile acids or act as bile alkalini
64                        De novo or retargeted canalicular expression of BSEP occurred in four of these
65                        De novo or retargeted canalicular expression of BSEP occurs in treatment respo
66                                          The canalicular expression of CD10 was identified in 9 of 15
67                                   Hepatocyte canalicular expression of hAQP1 through adenoviral gene
68 ds to Mrp2, and plays a critical role in the canalicular expression of Mrp2 and its function as a det
69    In vitro, integrin beta1 is essential for canalicular formation and is needed to prevent stellate
70 sion of the rab11a-GDP locked form prevented canalicular formation as did overexpression of the myosi
71 es a unique function of taurocholate in bile canalicular formation involving signaling through a cAMP
72 y, specification of cell-cell junctions, and canalicular formation.
73 ine, we observed that rab11a is required for canalicular formation.
74 ed apical ABCB11 (Bsep) trafficking and bile canalicular formation.
75 ats improves bile flow, in part by enhancing canalicular hAQP1-mediated osmotic water secretion.
76 e role of InsP(3)R2 and of Ca(2+) signals in canalicular insertion and function of Mrp2 is not known.
77  with radiologically confirmed PANDO without canalicular involvement underwent endonasal DCR without
78                 By contrast, no new ductular-canalicular junctions were observed in mouse models of b
79 etermine whether delayed repair of traumatic canalicular laceration affects the final outcome.
80 hod in 33 cases of acute and late presenting canalicular laceration for canalicular reconstruction wi
81 334 patients who underwent primary traumatic canalicular laceration repair were retrospectively revie
82 r, especially in patients with complex acute canalicular lacerations and late presenting canalicular
83 ports of monocanalicular stenting to address canalicular lacerations.
84 ious and well tolerated in the management of canalicular lacerations.
85  canalicular lacerations and late presenting canalicular lacerations.
86 ent an improvement in the surgical repair of canalicular lacerations.
87 f drugs with MDR3 and the effect of drugs on canalicular lipid secretion in a newly established polar
88 d cell line system that serves as a model of canalicular lipid secretion.
89 atocyte couplets confirmed the intracellular/canalicular localization of aquaporins 0 and 8 and the b
90      Active secretion of bile salts into the canalicular lumen drives bile formation and promotes bil
91 ion of fluorescent cholephiles into the bile canalicular lumina.
92 e cells show polarization defects as well as canalicular malformations.
93 othelial cell marker, RECA-1, but lacked the canalicular marker leucine aminopeptidase.
94 ntrast to organic anions, substrates for the canalicular mdr1a and b are usually organic cations and
95                      Transport of DHE to the canalicular membrane after photobleaching was very rapid
96 tate distribution after 20 h of SPGP between canalicular membrane and a combined endosomal fraction.
97 ransport of bile acids across the hepatocyte canalicular membrane and for generation of bile acid-dep
98  revealed that BSEP-YFP was localized at the canalicular membrane and in tubulo-vesicular structures
99 suggests cycling of ABC transporters between canalicular membrane and intrahepatic sites before degra
100 ated the exocytic insertion of Mrp2 into the canalicular membrane and the recovery of bile flow and b
101                  Transporters at the hepatic canalicular membrane are essential for the formation of
102 ved, and BSEP, which was not detected at the canalicular membrane before treatment, appeared at the c
103  by favoring bile acid-induced injury in the canalicular membrane but does not directly affect FXR ex
104  amounts of SPGP, MDR1, and MDR2 in the bile canalicular membrane by 3-fold; these effects abated aft
105 ut during stimulation, it is shuttled to the canalicular membrane by a poorly understood mechanism th
106 rter pools, one of which is mobilized to the canalicular membrane by cAMP and the other, by taurochol
107 ering that BSEP activity directly depends on canalicular membrane cholesterol content, decreased BSEP
108 ic bile acid CDCA resulted in focal areas of canalicular membrane disruption by electron microscopy a
109                    With both basolateral and canalicular membrane fractions, sulindac inhibited choly
110 ne proteins to their site of function at the canalicular membrane front.
111 nslocator specifically expressed at the bile canalicular membrane in hepatocytes, highly homologous t
112 thelial cells in the kidney, intestine, bile-canalicular membrane in the liver, blood-brain barrier,
113 strated endocytic retrieval of Mrp2 from the canalicular membrane into pericanalicular and intracellu
114 ny cell systems, and Ca(2+) release near the canalicular membrane is mediated by the type II inositol
115               Its localization in the apical canalicular membrane is physiologically regulated by the
116 istance-associated protein 2 (Mrp2) from the canalicular membrane leading to cholestasis.
117 es phosphatidylcholine (PC) secretion at the canalicular membrane of hepatocytes and its genetic defe
118    The secretion of phospholipids across the canalicular membrane of hepatocytes occurs via the multi
119 inding cassette transporter localized at the canalicular membrane of hepatocytes that plays an import
120 wo sites (apical membrane of enterocytes and canalicular membrane of hepatocytes) to mediate choleste
121  cassette (ABC) transporter expressed at the canalicular membrane of hepatocytes, where it mediates p
122  pump, which is exclusively expressed at the canalicular membrane of hepatocytes.
123 t the apical membrane of enterocytes and the canalicular membrane of hepatocytes.
124  the major bile salt transport system at the canalicular membrane of hepatocytes.
125 tte (ABC) transporters and is located in the canalicular membrane of hepatocytes.
126        Mrp2 remained localized at the apical/canalicular membrane of NHERF-1(-/-) mouse hepatocytes,
127 ntly discovered that NPC1L1 localizes to the canalicular membrane of primate hepatocytes and that NPC
128 alt export pump (Bsep), a transporter on the canalicular membrane of the hepatocyte.
129 ctivity and abundance of transporters in the canalicular membrane regulate bile flow; however, little
130 as associated with a marked reduction in the canalicular membrane structure as observed by differenti
131 atocytes, thereby increasing exposure of the canalicular membrane to bile salts linking to increased
132            As a consequence, exposure of the canalicular membrane to bile salts was increased, allowi
133  the polarized targeting and/or retaining of canalicular membrane transporters and is a critical dete
134 e and dinitrophenyl-glutathione transport in canalicular membrane vesicles above maximal ATP-dependen
135   HAX-1 was bound to BSEP, MDR1, and MDR2 in canalicular membrane vesicles and co-localized with BSEP
136  macrophages doubled PI 3-kinase activity in canalicular membrane vesicles and enhanced taurocholate
137 ate and PI 3-kinase activity were reduced in canalicular membrane vesicles isolated from rat liver th
138 ncrease in the amount of ABC transporters in canalicular membrane vesicles was observed, whereas the
139 a rat liver subcellular fraction enriched in canalicular membrane vesicles, and MLC2 colocalized with
140 rat liver subcellular fractions enriched for canalicular membrane vesicles, microsomes, and clathrin-
141                                           In canalicular membrane vesicles, translocase activity had
142 hosphate-dependent taurocholate transport in canalicular membrane vesicles, was induced by 90% (P < 0
143                      Release of DHE from the canalicular membrane was also ATP-independent but slower
144 ocytes, (2) altered targeting of BSEP to the canalicular membrane, and (3) increased ileal BA absorpt
145 8 expression was localized to the hepatocyte canalicular membrane, and bile Mn levels were increased
146 omol/L E(2)17G, respectively, whereas in rat canalicular membrane, both E(2)17G and the choleretic es
147 bstrates by inducing Mrp2 retrieval from the canalicular membrane, whereas cyclic adenosine monophosp
148 molecules and the ectoplasmic leaflet of the canalicular membrane, which result in biliary secretion
149 secretion into bile by targeting Mrp2 to the canalicular membrane.
150 es, and maintained an abnormal intracellular canalicular membrane.
151 ated Ca(2+) signals in targeting Mrp2 to the canalicular membrane.
152 tes, although Bsep remained localized to the canalicular membrane.
153 r (FXR) or by impairing the structure of the canalicular membrane.
154 esistance-associated protein 2 to the apical canalicular membrane.
155 traffic directly from Golgi membranes to the canalicular membrane.
156 solateral membranes, but only fused with the canalicular membrane.
157 compared with the amount present in the bile canalicular membrane.
158 d and nonbile acid organic anions across the canalicular membrane.
159 r membrane before treatment, appeared at the canalicular membrane.
160  retrieval of bile salt export pump from the canalicular membrane.
161  the endoplasmic reticulum instead of at the canalicular membrane.
162 ABC transporters are targeted to the apical (canalicular) membrane of hepatocytes where they execute
163 tte transporters are targeted to the apical (canalicular) membrane of hepatocytes, where they mediate
164 , recombinant ABCG5 localized to the apical (canalicular) membrane when coexpressed with ABCG8, but n
165 of DHE but not its enrichment in the apical (canalicular) membrane.
166 ietal cells exhibited limited development of canalicular membranes and a virtual absence of tubuloves
167 Electron microscopy revealed abnormal apical canalicular membranes and loss of tubulovesicles in muta
168                                          Rat canalicular membranes contain microdomains enriched in c
169                        Slc30a10 localized to canalicular membranes of hepatocytes, but mice with live
170 tical trans-locator for phospholipids across canalicular membranes of hepatocytes, evidenced by the f
171 ed that single BSEP-YFP molecules resided in canalicular membranes only transiently before exchanging
172 cid transporters on both the basolateral and canalicular membranes, resulting in intrahepatic cholest
173 2 and 4, which localize to granules and open canalicular membranes, together with the general target
174 ll, predominantly localizing with F-actin to canalicular membranes.
175 ile acid transporters on both sinusoidal and canalicular membranes.
176 a protein, which is highly enriched in mouse canalicular membranes.
177 d along basolateral (sinusoidal) and apical (canalicular) membranes of hepatocytes, are integral dete
178 1-transduced cholestatic rats, BSEP showed a canalicular microdomain distribution similar to that of
179 ls had dilated canaliculi and lacked typical canalicular microvilli and tubulovesicles, and subsets o
180 se, granular canalicular Byler bile, effaced canalicular microvilli, and proliferative pericanalicula
181    The codistribution of parallel cisternae, canalicular-mitochondrial complexes, and synaptic-like v
182                             KO mice had bile canalicular morphologic abnormalities as evidenced by st
183 loss of beta-catenin leads to defective bile canalicular morphology, bile secretory defect, and intra
184                                              Canalicular multidrug resistance-associated protein 2 (M
185  the endocytic retrieval and function of the canalicular multidrug resistance-associated protein 2 (M
186 sistance-associated protein 1 (MRP1) and the canalicular multispecific organic anion transporter (cMO
187 rug resistance-associated protein (MRP)1 and canalicular multispecific organic anion transporter (cMO
188 ic expression of Mrp2 (Abcc2), the principal canalicular multispecific organic anion transporter.
189  on probing and irrigation suggested further canalicular narrowing, silicone intubation was offered.
190                              Abnormal lacuno-canalicular network and negative correlation between ser
191 s between the bile duct and the lobular bile canalicular network by the canals of Hering decreases pr
192       In control cultures, an extensive bile canalicular network developed with properly localized ap
193                     Taurocholate accelerated canalicular network formation and concomitantly increase
194  another cAMP downstream kinase, accelerated canalicular network formation similar to the effect of t
195  that activated-LKB1 and AMPK participate in canalicular network formation.
196       Investigation reveals a complex lacuno-canalicular network in highly mineralized tendon regions
197  potential link of abnormal osteocyte lacuno-canalicular network structure and function to the observ
198 ciliary region and outflow through a ventral canalicular network that connects with an aqueous plexus
199 drites, as well as the characteristic lacuno-canalicular network, and do not express SOST.
200      These concentrations are present in the canalicular network, bile ducts, and gallbladder.
201                                    The vital canalicular networks required for osteocyte nourishment
202 hnique showed a significant reduction in the canalicular number and length as well as an increase in
203 adiologically confirmed nasolacrimal duct or canalicular obstruction.
204 ceived chemotherapy or radiation, and common canalicular obstructions.
205 displayed oscillatory movement toward either canalicular or basolateral membranes, but only fused wit
206 ate pseudoglandular stage but not during the canalicular or saccular stage surprisingly delayed dista
207 ve measured the effects of substrates of the canalicular organic ion transporter multidrug resistance
208 njugated form and induced hypercholeresis of canalicular origin.
209 patic shunting, a pathway that amplifies the canalicular osmotic effects of bile acids.
210        These studies indicate that FIC1 is a canalicular P-type ATPase that participates in maintaini
211 ne intubation for the purpose of maintaining canalicular patency is not necessary when performing end
212 nd endoscopic evidence of ostium patency and canalicular patency.
213 d consent and who had no lid malpositions or canalicular pathology.
214 p cells during either the pseudoglandular or canalicular phases of development.
215  resistance 3 gene (MDR3), which encodes the canalicular phospholipid flippase, cause a wide spectrum
216 ficiency of multidrug resistance 2 (mdr2), a canalicular phospholipid floppase, leads to excretion of
217 ult transgenic livers lack expression of the canalicular phospholipid transporter, mdr2, which is con
218 rectional (i.e., from the outer to the inner canalicular plasma membrane leaflet).
219 phosphatidylcholines across the hepatocyte's canalicular plasma membrane provides the driving force f
220 yryl cAMP), aquaporin 8 redistributed to the canalicular plasma membrane; the subcellular distributio
221 ment of aquaporins 0 and 8 in microsomes and canalicular plasma membranes; aquaporin 9 was enriched o
222 hat allows lysosome translocation toward the canalicular pole of hepatocytes.
223 rough the pericellular matrix in the lacunar-canalicular porosity due to mechanical loading can induc
224  apex of infrequent, previously unrecognized canalicular projections.
225                It has been proposed that all canalicular proteins are targeted via this indirect rout
226     We studied the membrane targeting of rat canalicular proteins by in vivo [(35)S]methionine metabo
227 al vein radicles that failed to exhibit bile canalicular reconstitution.
228 d late presenting canalicular laceration for canalicular reconstruction without any complications.
229  (InsP(3)R2) regulates Ca(2+) release in the canalicular region of hepatocytes.
230            InsP(3)R2 was concentrated in the canalicular region of WT mice but absent in InsP(3)R2 KO
231 docytic recycling compartment and the apical canalicular region paralleling the movement of SR-BI.
232 sP3R2 and Bsep are in close proximity in the canalicular region, both in rat liver and in hepatocytes
233 lcium-to-phosphorus ratio at the perilacunar/canalicular region.
234                                      Delayed canalicular repair in unstable patients did not lead to
235 llowing trauma is the most difficult part of canalicular repair, especially in patients with complex
236 s Golgi bodies intermingled with this apical canalicular reticulum (CR).
237  was equal in WT versus Hrn, indicating that canalicular secretion capacity was normal.
238 pendent bile acid transporter and diminished canalicular secretion of bile salts secondary to down-re
239                                              Canalicular secretion of the organic anion 5-chloromethy
240  mice, 6-CF remained largely in hepatocytes, canalicular secretion was delayed, and 6-CF appeared in
241 ermore, when sodium dehydrocholate augmented canalicular secretion, biliary glucose excretion increas
242 of hepatocellular secretion of bile salts is canalicular secretion.
243 ype and distribution of terminals across the canalicular sensory neuroepithelium with morphophysiolog
244 tocytes actively secrete bile acids into the canalicular space and cholangiocytes then transport bile
245                                       At the canalicular stage of E16.5, the lungs of TACE mutant mic
246 ansgenic lungs retained many features of the canalicular stage of lung development, including undilat
247                By contrast, during the later canalicular stage, the distal epithelial tip cells only
248 n a cluster expressed in pseudoglandular and canalicular stages whereas adenocarcinoma homologues wer
249                             A characteristic canalicular-staining pattern was observed in normal hepa
250                           Moderate or severe canalicular stenosis was seen in about one-third of pati
251              During each visit, epiphora and canalicular stenosis were graded.
252                   Nine patients had worsened canalicular stenosis; six underwent surgery.
253           The definitive treatment of severe canalicular stricture remains conjunctivodacryocystorhin
254 ion of BA transporters, hepatocyte polarity, canalicular structure, and the regenerative response.
255                                           In canalicular structure, and to some extent in fibre bundl
256 ed that loss of LKB1 led to longer and wider canalicular structures correlating with mislocalization
257 lular polarity by delimiting functional bile-canalicular structures, forming the blood-biliary barrie
258 urred in cells that resemble PHH, exhibiting canalicular structures.
259 e architectural complexity of the hepatocyte canalicular surface has prevented examination of apical
260  located in very narrow portions of the open canalicular system (OCS) to antibodies, the same methods
261 that both cells share an identical dendritic canalicular system and express extensive processes formi
262 d the fusion of alpha-granules with the open canalicular system and plasma membrane.
263 hese studies provide a link between the open canalicular system and platelet adhesive function that h
264                       All cases had a patent canalicular system as demonstrated by syringing and prob
265    Solute transport through the bone lacunar-canalicular system is believed to be essential for osteo
266         The osteocyte and cementocyte lacuno-canalicular system of both alveolar bone and cementum is
267 at cardiac ventricular myocytes and the open canalicular system of human platelets.
268                    Osteocytes in the lacunar-canalicular system of the bone are thought to be the cel
269       Interstitial fluid flow in the lacunar canalicular system produces focal strains at localized a
270  on external (surface) versus internal (open canalicular system) membranes in resting discoid platele
271 rcation membrane system) and platelets (open canalicular system) that results in dysregulated platele
272  among membranes of alpha-granules, the open canalicular system, and plasma membrane.
273 abnormal lipid inclusions, abnormal platelet canalicular system, and reduced number of microtubules)
274 gins, differentiation, morphology and lacuno-canalicular system, selective markers, and potential fun
275 failed to empty their contents into the open canalicular system.
276 cteristic anatomical features of the lacunar-canalicular system.
277 h one another and with membranes of the open canalicular system.
278 s been measured directly in the bone lacunar-canalicular system.
279 embrane network resembling the platelet open canalicular system.
280  to ABCB11 missense mutations affecting BSEP canalicular targeting.
281 estation is required for transition from the canalicular to the saccular stage of lung development.
282  normally in Tr(-) rats, indicating that its canalicular transport did not require mrp2.
283 f proteins for storage, glucuronidation, and canalicular transport of bilirubin.
284 ntification of the mechanisms directing bile canalicular transport of these agents will provide insig
285                                  ABCB11 is a canalicular transport protein that controls the rate-lim
286 er PEBD, perhaps by induction of alternative canalicular transport proteins.
287  expression profiles, phase I/II metabolism, canalicular transport, secretion of liver-specific produ
288 rized using Tr(-) rats (deficient in mrp2, a canalicular transporter for organic anions), the isolate
289 -AC-PKA is a key factor in the alteration of canalicular transporter function and localization induce
290 trongly prevented E17G-induced impairment of canalicular transporter function and localization.
291  tranferases, and TR- rats, deficient in the canalicular transporter Mrp2 (Abcc2).
292  resistance associated protein 2 (Mrp2) is a canalicular transporter responsible for organic anion se
293  rapid decline in the expression of the bile canalicular transporters Abcb4, Abcb11, and Abcc2.
294            Changes in the expression of bile canalicular transporters were analyzed by real-time poly
295 olestasis in rat liver with retrieval of the canalicular transporters, bile salt export pump (Abcb11)
296 te and dinitrophenyl-glutathione in isolated canalicular vesicles from rat liver was reduced 50-70% b
297 ring elements that attach the process to the canalicular wall and their finite flexural rigidity EI.
298  between the osteocyte cell membrane and its canalicular wall are sites where pN-level fluid-flow ind
299 hed directly at discrete locations along the canalicular wall by beta(3) integrins at the apex of inf
300 lets to dibutyryl cAMP caused an increase in canalicular water transport in the presence and absence

 
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