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1 somes to both lysosomes and LROs such as the melanosome.
2  protein that forms physiological amyloid in melanosomes.
3  further evidence that these microbodies are melanosomes.
4 cin granules, melanolipofuscin granules, and melanosomes.
5 ative roles of AP-1 and AP-3 in transport to melanosomes.
6 adative lysosomal pathway toward early stage melanosomes.
7 showed that the melanocytes contained mature melanosomes.
8 anogenic enzymes and the formation of mature melanosomes.
9  their fur and irides and had more pigmented melanosomes.
10  stage I melanosomes but lacked stage III-IV melanosomes.
11 the likelihood of interaction with dispersed melanosomes.
12  Pmel17 and thus for establishing functional melanosomes.
13 which are abundant in early (stage I and II) melanosomes.
14 nocytes and dendritic melanocytes containing melanosomes.
15 of melanosome morphology, and loss of mature melanosomes.
16 to function in trafficking other proteins to melanosomes.
17 in but fails to associate with and transport melanosomes.
18 ccurs entirely in early endosomes or stage I melanosomes.
19  copper within specialized organelles called melanosomes.
20  movement of some, but not all, phagocytized melanosomes.
21 istinct layers of spheroidal and cylindrical melanosomes.
22 termed mPmel17), which is sorted directly to melanosomes.
23 cellular localization and transport of early melanosomes.
24 ance by directly patch-clamping skin and eye melanosomes.
25 and made fewer, more transient contacts with melanosomes.
26 from recycling endosomal domains to maturing melanosomes.
27 ome-related organelles, such as pigment cell melanosomes.
28 m fibrils upon which melanin is deposited in melanosomes.
29 but did not change the number of unpigmented melanosomes.
30 nin, in intimate association with fossilized melanosomes.
31 t production and delivery system and produce melanosomes.
32        One well studied cargo in vivo is the melanosome, a pigment organelle that is moved first by k
33        The proper peripheral distribution of melanosomes, a dense pigment-containing organelle, is de
34 ls lacking BLOC-3 have impaired formation of melanosomes, a type of lysosome-related organelle (LRO),
35                                              Melanosome accumulation in keratinocytes was accelerated
36 tion pH (4 --> 7) mimicking pH conditions of melanosomes, acidic organelles where Pmel17 fibrils are
37 cteristics and forms fibrillar structures in melanosomes after a complex sequence of post-translation
38 ocusing, kinetochore-microtubule attachment, melanosome aggregation and peroxisome motility in cultur
39 d MT plus ends could reduce the half-time of melanosome aggregation by ~50%.
40                                              Melanosome aggregation is triggered by melatonin, wherea
41  myosin-Va works as a transporter dispersing melanosomes along actin tracks whose +/barbed ends are o
42 ps6, known to impair the formation of mature melanosomes, also increased cDDP sensitivity.
43 a (myoVa), a protein known to be involved in melanosome and secretory granule trafficking to the plas
44  were detected in tissues containing remnant melanosomes and decayed keratin plates.
45  enzymes from recycling endosomes to nascent melanosomes and for organelle biogenesis.
46 d either AP-1 or AP-3 each trafficked toward melanosomes and functionally complemented OCA2 deficienc
47 s involved in the trafficking of proteins to melanosomes and in the transport of mature pigmented mel
48  roles of AP-1 and AP-3 in OCA2 transport to melanosomes and indicate that BLOC-1 can cooperate with
49 malities in retinal pigment epithelium (RPE) melanosomes and misrouting of optic axons.
50                                              Melanosomes and other lysosome-related organelles obtain
51  a Rab protein involved in the biogenesis of melanosomes and other lysosome-related organelles.
52 cialized lysosome-related organelles such as melanosomes and platelet delta granules.
53 f lysosome-related organelles (LROs) such as melanosomes and platelet dense bodies.
54 s are caused by defects in the biogenesis of melanosomes and platelet dense granules, often referred
55 as been implicated in protein trafficking to melanosomes and shown to function as an AKAP on mitochon
56  a gradual loss of RPE, an absence of mature melanosomes and the subsequent degradation of RPE/photor
57  tubular transport intermediates to maturing melanosomes and thereby promote cargo delivery and optim
58  defects in the formation and/or survival of melanosomes and with malformations in the retinal pigmen
59 morphology of melanin-containing organelles (melanosomes) and colour in extant bird feathers.
60 ed morphologically abnormal mitochondria and melanosomes, and exhibited marked functional defects in
61 analysis revealed that GPNMB is localized in melanosomes, and GPNMB is a membrane-bound glycoprotein
62 iogenesis, preserves the formation of mature melanosomes, and has no effect on cis-platin or vinblast
63 tionally transport intraflagellar particles, melanosomes, and neuronal vesicles.
64 restingly all bacteriochlorins accumulate in melanosomes, and subsequent illumination leads to melano
65  a gradual loss of RPE, an absence of mature melanosomes, and the subsequent degradation of RPE/photo
66 ytes, packaged in cellular organelles called melanosomes, and then dispersed to neighboring keratinoc
67 pressed OCA2 localizes within melanocytes to melanosomes, and, like other melanosomal proteins, local
68                            Results show that melanosomes are incorporated into the cytoplasm of both
69                This occurrence suggests that melanosomes are inefficient Ag-processing compartments.
70                                              Melanosomes are lysosome-related organelles that serve a
71                  These experiments show that melanosomes are more rapidly lost in KCs derived from LS
72 ons with other effectors during transport to melanosomes are not clear.
73                                              Melanosomes are organelles responsible for the synthesis
74                                              Melanosomes are organelles specialized for the productio
75                           Organelles such as melanosomes are transported by multiple motors including
76                                              Melanosomes are unique membrane-bound organelles special
77                       Pigment organelles, or melanosomes, are transported by kinesin, dynein, and myo
78 melanosomes, illuminate SNARE recycling from melanosomes as a critical BLOC-3-dependent step, and lik
79 c in melanosome biogenesis as an effector of melanosome-associated Rab GTPases.
80 ent sensitivity and influences the degree of melanosomes available for sequestration of therapeutic a
81 ations in three separate genes that regulate melanosome biogenesis (Dtnbp1, Pldn, Vps33a) also result
82 gnals in the same pathway as OA1 to regulate melanosome biogenesis and axonal growth through the opti
83            Mutations result in dysfunctional melanosome biogenesis and macromelanosome formation in p
84 ta demonstrate a novel role for Myosin Vc in melanosome biogenesis and secretion.
85             Like other trafficking pathways, melanosome biogenesis and transport of enzymes involved
86 the discovery of a function for Myosin Vc in melanosome biogenesis as an effector of melanosome-assoc
87 omponents required for melanin formation and melanosome biogenesis away from the degradative lysosoma
88 nosomes in melanocyte dendrites, even though melanosome biogenesis involves lysosomes rather than Gol
89                                              Melanosome biogenesis requires successive waves of cargo
90                      We conclude that during melanosome biogenesis the NTR controls the hierarchical
91  in autophagy did not cause major defects in melanosome biogenesis, nor did it produce visually strik
92 mal regulatory gene, Hps1, minimally affects melanosome biogenesis, preserves the formation of mature
93 tions that cannot be carried out by Rab38 in melanosome biogenesis.
94 pha i3, like Oa1, plays an important role in melanosome biogenesis.
95 more than doubled the abundance of pigmented melanosomes but did not change the number of unpigmented
96     WIPI1-depleted cells accumulated stage I melanosomes but lacked stage III-IV melanosomes.
97 ent resulted in the accumulation of stage IV melanosomes but not autophagosomes, whereas starvation r
98 is in OCA2-deficient cells when localized to melanosomes but not when specifically retained in the ER
99 hat OCA2 is targeted to and functions within melanosomes but that residence within melanosomes may be
100 n states that this processing step occurs in melanosomes, but in light of recent reports this issue h
101 ling impedes maturation of the key organelle melanosome by concerted regulation of several pigmentati
102 al contact may promote the biogenesis of the melanosome by providing it with ATP.
103                        Copper is supplied to melanosomes by ATP7A, a cohort of which localizes to mel
104 e loss of fluorescently labeled and isolated melanosomes by cultured human KCs.
105 erning, ecology and thermoregulation, fossil melanosomes can also carry a phylogenetic signal.
106 ular level, and unequivocally determine that melanosomes can be preserved in fossil feathers.
107 e-interacting 1 (WIPI1) in the biogenesis of melanosomes, cell type-specific lysosome-related organel
108  to high cytoplasmic cAMP, while at low cAMP melanosomes cluster at the cell center.
109  cells are irregularly shaped and have fewer melanosomes compared with pigmented RPE cells.
110 ecreased proportion of intracellular, mature melanosomes compared with undepleted cells.
111 n of melanosomes requires myosin Va, because melanosomes concentrate in the center of melanocytes fro
112 not dilute melanocytes, readily transfer the melanosomes concentrated in their center to surrounding
113 melanosome transfer that involves release of melanosome-containing globules, similar to shedding vesi
114 tion of hypothalamic pmch and pmchl mRNA and melanosome contraction in dermal melanocytes in response
115                         Cargo sorting toward melanosomes correlates with binding via cytoplasmically
116 of cargo delivery from endosomes to immature melanosomes, coupled with recycling of the trafficking m
117 le in skin color determination by regulating melanosome degradation in keratinocytes, and thereby con
118 hibition led to increased autophagy-mediated melanosome degradation in keratinocytes.
119 zed in melanocytes and modulating autophagic melanosome degradation in keratinocytes.
120 hagy in determining skin color by regulating melanosome degradation in keratinocytes.
121 s, melanosome transfer to keratinocytes, and melanosome degradation, is also critical for pigmentatio
122 n the cell body, galectin-3 colocalizes with melanosome-destined cargo, specifically tyrosinase and T
123 c glycoprotein that plays a critical role in melanosome development by forming a fibrillar amyloid ma
124  late endosomes, and accumulates in stage II melanosomes devoid of MHC-II molecules.
125 opteryx based on fossilized colour-imparting melanosomes discovered in this isolated feather specimen
126 brafish melanophilin (Mlpha) interferes with melanosome dispersion downstream of cAMP.
127 odel exemplifies this view and suggests that melanosome distribution in melanocyte dendrites is maint
128  dilute mice without restoring intracellular melanosome distribution, indicate that melanoregulin is
129  pigmented epithelium (RPE) that compromised melanosome distribution.
130 wild-type melanocytes to hyperdisperse their melanosomes, does not affect dispersion in mutant melano
131                            The processing of melanosomes during keratinocyte (KC) terminal differenti
132 me-related organelle biogenesis resulting in melanosome dysfunction and absent platelet dense bodies.
133 f the retina and the size and density of RPE melanosomes, electroretinograms to study retinal functio
134                                 Purified RPE melanosomes emitted the same signal.
135 el17 form a functional amyloid in vertebrate melanosomes essential for melanin synthesis and depositi
136 membrane trafficking, and a failure to reach melanosomes, explaining the boy's severe albinism and es
137 mbined with the known presence of RPT in the melanosome filaments and the requirement of this domain
138 nophilin (Mlph), which links myoVa to Rab27a-melanosomes for in vivo transport.
139  and maniraptoran dinosaurs including birds, melanosome form and colour are linked and colour reconst
140 arly, mammals show an increased diversity of melanosome form compared to all ectothermic amniotes.
141                 We conclude that early stage melanosome formation and Pmel17 trafficking are preserve
142  and without functional molecules regulating melanosome formation show that sensitivity to the chemot
143 al protein tyrosinase, resulting in aberrant melanosome formation, also causes increased cis-platin s
144 reases with the mutation of genes regulating melanosome formation, concomitant disruption of melanoso
145 esulted in an increased proportion of mature melanosomes formed and in decreased sensitivity (i.e., i
146 g protein decreased the proportion of mature melanosomes formed and increased cDDP sensitivity, where
147  Tullimonstrum of spheroidal and cylindrical melanosomes forming the remains of retinal pigment epith
148                               Here we sample melanosomes from the integument of 181 extant amniote ta
149 intercellular transfer of pigment-containing melanosomes from the tips of melanocyte dendrites to sur
150 specific and lysosome-related organelle, the melanosome, from melanocytes to keratinocytes is crucial
151                                   Defects in melanosome function cause albinism, characterized by vis
152 tion through two fundamental determinants of melanosome function: pH and size.
153 olecules, and proteins normally localized to melanosomes give rise to MHC-II-restricted epitopes in m
154                      In melanomas containing melanosomes, gp100 is underrepresented in late endosomes
155 re; however, the chemistry of these proposed melanosomes has remained unknown.
156  of BLOC-1-dependent transport carriers with melanosomes, illuminate SNARE recycling from melanosomes
157 mes by ATP7A, a cohort of which localizes to melanosomes in a biogenesis of lysosome-related organell
158 in filament cytoskeleton and accumulation of melanosomes in a disordered distribution in the keratino
159 melanin deposition 1 in mammals and found in melanosomes in a filamentous form.
160 pically in melanocytes, SLC35D3 localizes to melanosomes in a manner requiring a HPS-associated prote
161 and is enriched in mature (stage III and IV) melanosomes in contrast to MART-1 and Pmel17, which are
162                                 By contrast, melanosomes in lizard, turtle and crocodilian skin, as w
163 imilar, mechanistically, to the transport of melanosomes in melanocyte dendrites, even though melanos
164  lysosome-related organelles (LROs), such as melanosomes in melanocytes, populate nascent LROs with c
165 sosome-related organelles that also includes melanosomes in melanocytes.
166 d melanin photobleaching, and endogenous RPE melanosomes in primary cultures of porcine retinal pigme
167 onger-range fast movements characteristic of melanosomes in shaker1 RPE.
168                         These cells disperse melanosomes in the cytoplasm in response to high cytopla
169                       The data indicate that melanosomes in the RPE and choroid are the dominant sour
170 retinas, the NIR-AF source was traced to the melanosomes in the RPE and choroid.
171  synthesized in a specialized organelle, the melanosome, in melanocytes.
172 requent and prolonged contacts with maturing melanosomes; in contrast, tubules from BLOC-2-deficient
173 oth protein trafficking and the formation of melanosomes, intracellular organelles unique to melanocy
174 lanophores, the capture of pigment granules (melanosomes) involves the +TIP CLIP-170, which is enrich
175 fied as key regulators of melanin synthesis, melanosome ion transport and its contribution to pigment
176 Vc is not particularly abundant on pigmented melanosomes, its knockdown in MNT-1 melanocytes caused d
177                                    Moreover, melanosome-like microbodies preserved in association wit
178  sensitivity and that the presence of mature melanosomes likely contributes to melanoma resistance to
179 xpressed in melanocytes and localizes to the melanosome-limiting membrane and, to a lesser extent, to
180 cesses of the RPE, thus correlating with the melanosome localization defects described previously by
181  AP-3 binding was necessary for steady-state melanosome localization.
182 -II restricted epitopes from gp100 and other melanosome-localized proteins, leading to enhanced immun
183                                The extent of melanosome loss has been qualitatively assessed using tr
184           Ethnic differences exist regarding melanosome loss in keratinocytes, but the mechanisms und
185 images suggest that LKCs display accelerated melanosome loss.
186 geted to melanosomes, we determined that the melanosome lumen in TPC2-KO MNT-1 cells and primary mela
187 idic conditions typical of the lysosome-like melanosome lumen, and the filaments quickly become solub
188                                              Melanosomes make pigments and mitochondria make ATP.
189 f melanin biosynthesis, but is essential for melanosome maturation and healthy maintenance of the RPE
190 of melanin biosynthesis, but is required for melanosome maturation and healthy maintenance of the RPE
191 about those processes during early stages of melanosome maturation are not well understood.
192 the transcription of melanogenic enzymes and melanosome maturation, a process that is distinct from s
193 order for GPR143 to function as a monitor of melanosome maturation.
194 ils upon which melanins are deposited during melanosome maturation.
195 etic components, supplying directionality to melanosome maturation.
196 within melanosomes but that residence within melanosomes may be regulated by secondary or alternative
197 t that protein-lysolipid interactions within melanosomes may regulate amyloid formation in vivo.
198 ng membrane compartments via Rab11 or to the melanosome membrane via recognition of the melanophilin
199 mediated by Rab11b through remodeling of the melanosome membrane, followed by subsequent endocytosis
200              However, these putative ancient melanosomes might alternatively represent microorganisma
201 er a 48-hour time frame, LKCs appear to lose melanosomes more efficiently than DKCs.
202  formation of amyloid fibrils and downstream melanosome morphogenesis.
203 s, the observed increase in the diversity of melanosome morphologies appears abruptly, near the origi
204                           The solid rod-like melanosome morphology has evolved in a directional manne
205 xtant bird feathers, statistical analysis of melanosome morphology predicts that the original colour
206 anosome formation, concomitant disruption of melanosome morphology, and loss of mature melanosomes.
207 man and mouse RPE cells were used to measure melanosome motility and rod outer segment (ROS) phagocyt
208                                              Melanosome motility was also comparable, and, after RNAi
209 ls by RNAi to test for a mutant phenotype in melanosome motility.
210 t is also applied to an in vivo recording of melanosome motion, where strong evidence is found for re
211 n for the uncharacteristically slow speed of melanosome movement by myoVa in vivo.
212 lates proteins involved in melanogenesis and melanosome movement.
213   Instead, mutant melanocytes disperse their melanosomes much more slowly than normal and less than h
214 melanins ultimately are deposited within the melanosomes of pigment cells.
215 melanin in their eyes, but the possession of melanosomes of two distinct morphologies arranged in lay
216  that regulate the overall directionality of melanosomes on the actin/microtubule networks have not y
217 ar, no ion channel has been characterized in melanosomes, organelles that produce and store the major
218 ght regulate melanin synthesis by modulating melanosome pH.
219                        TPC2 likely regulates melanosomes pH and size by mediating Ca(2+) release from
220                                              Melanosome photobleaching, which makes granules more pho
221  initiation of transport of membrane-bounded melanosomes (pigment granules) to the cell center involv
222  might be important in the functions of late melanosomes, possibly their transport and/or transfer to
223                                           In melanosome precursor organelles, proteolytic fragments o
224 lum but forms amyloid only within post-Golgi melanosome precursors; thus, PMEL must traverse the secr
225 phagocytized black latex beads, phagocytized melanosomes pretreated to simulate age-related melanin p
226  feathers is generated by large, ellipsoidal melanosomes previously unknown for birds.
227      Post-transfer modification of pigmented melanosomes provides an attractive and distinct avenue o
228 tibodies that detect Pmel17 within fibrillar melanosomes recognize only the luminal products of propr
229 estoration of coat color, but, surprisingly, melanosomes remain concentrated in the center of their m
230                          Tip accumulation of melanosomes requires myosin Va, because melanosomes conc
231 ar larger than the largest 129Sv and B6/NCrl melanosomes, respectively.
232       Analyses of fossilized color-imparting melanosomes reveal that their dimensions were similar to
233 t involves the shedding by the melanocyte of melanosome-rich packages, which subsequently are phagocy
234 ion in vivo and is a component of fibrils in melanosomes, RPT is not necessary for fibril formation i
235  more melanosomes to the SC, suggesting that melanosome secretion could contribute to the more acidic
236 ions in oculocutaneous albinism II (OCA2), a melanosome-specific transmembrane protein with unknown f
237 the retina and RPE and is currently the only melanosome-specific, noninvasive technique for monitorin
238 locate several thousand of pigment granules (melanosomes), spherical organelles of a diameter of appr
239 ies have reconstructed color on the basis of melanosome structure; however, the chemistry of these pr
240  zoning patterns may be preserved long after melanosome structures have been destroyed.
241 PC2-KO MNT-1 cells have significantly larger melanosomes than control cells, but the number of organe
242 iosynthesis in specialized organelles termed melanosomes that are produced only by melanocytic cells.
243  identify a pathway for VAMP7 recycling from melanosomes that employs distinct tubular carriers.
244 ha i3(-/-) and Oa1(-/-) mice showed abnormal melanosomes that were far larger than the largest 129Sv
245 ale arrays of melanin-containing organelles (melanosomes) that play a central role in sexual selectio
246 y at the mildly acidic pH (4-5.5) typical of melanosomes, the repeat domain (RPT) of human Pmel17 can
247 mediates the early steps in the formation of melanosomes, the subcellular organelles of melanocytes i
248                           The progression of melanosomes through the different stages of their format
249 uting these ends to more efficiently capture melanosomes throughout the cytoplasm.
250 1-positive perinuclear organelles instead of melanosomes, thus preventing melanogenesis.
251 ay critical roles in the maturation of early melanosomes; thus, we speculate that GPNMB might be impo
252 tein that is essential for the maturation of melanosomes to form mature, fibrillar, and pigmented org
253 yloid derived from the protein Pmel17 within melanosomes to generate melanin pigment.
254 e we used direct patch-clamp of skin and eye melanosomes to identify a novel chloride-selective anion
255 t also enhance CLIP-170-dependent binding of melanosomes to MT tips.
256 ph) is the adapter protein that links Rab27a-melanosomes to myoVa.
257 a property likely to enhance the transfer of melanosomes to the adjacent keratinocyte.
258 mes and in the transport of mature pigmented melanosomes to the dendrites of melanocytic cells are be
259 aused the mislocalization of tyrosinase from melanosomes to the plasma membrane and also led to the i
260 m type I-II subjects, and they transfer more melanosomes to the SC, suggesting that melanosome secret
261 s distribution defect results in inefficient melanosome transfer and a dilution of coat color.
262               Although several mechanisms of melanosome transfer are likely to occur in the skin, And
263 onstrate here a requirement for filopodia in melanosome transfer from melanocytes to keratinocytes an
264                               The process of melanosome transfer has fascinated pigment cell biologis
265 el adds further complexity to the process of melanosome transfer in the skin.
266 different colors, we define an intercellular melanosome transfer pathway that involves the shedding b
267 n, Ando et al. focused on a new mechanism of melanosome transfer that involves release of melanosome-
268  melanin synthesis in epidermal melanocytes, melanosome transfer to keratinocytes, and melanosome deg
269 hat melanoregulin is a negative regulator of melanosome transfer, and provide insight into the mechan
270 podia were also necessary for UVR-stimulated melanosome transfer, as this was also inhibited by MyoX
271  insight into the mechanism of intercellular melanosome transfer.
272 ption or attenuation of melanogenesis and/or melanosome transfer.
273 y overlapping phenotypes including defective melanosome transport and disruption of the ciliated Kupf
274      Previously we reported an intracellular melanosome transport delay as a cardinal feature of redu
275 erminal FERM domain of MYO7A is critical for melanosome transport in RPE cells.
276 duction mechanism in the stereocilia and for melanosome transport in the retina, in line with the phe
277                                     As such, melanosome transport is an excellent model system to stu
278                     In Xenopus melanophores, melanosome transport is regulated by cAMP-dependent prot
279 reduced Kupffer's vesicle size and delays in melanosome transport, two phenotypes that are observed u
280  of melanocytes, where myoVa-Mlph engages in melanosome transport.
281         The role of cAMP is to regulate both melanosome travel along microtubules and their transfer
282 derived keratinocytes were more sensitive to melanosome treatment as shown by their enhanced autophag
283 ng control retinas, the density of their RPE melanosomes was significantly lower than in control RPEs
284 nthesized PMEL17 is ultimately routed to the melanosome, we find substantial amounts accessible to ou
285                              Focusing on the melanosome, we show that the ubiquitous machinery intera
286 ed genetically encoded pH sensor targeted to melanosomes, we determined that the melanosome lumen in
287    Myo7a-null mouse retinas and purified RPE melanosomes were analyzed by spectral deconvolution conf
288                             Isolated porcine melanosomes were phagocytized by ARPE-19 cells, then cul
289                                        Other melanosomes were preloaded with a photosensitizer before
290                              Melanin-bearing melanosomes were suggested to preserve as organic residu
291     Melanophores aggregate or disperse their melanosomes when the host needs to change its color in r
292 e/melanoma-specific protein that traffics to melanosomes where it forms a fibrillar matrix on which m
293 sis of gut granules as compared to mammalian melanosomes, where BLOC-1 has been most extensively stud
294 ific protein that subcellularly localizes to melanosomes, where it forms a fibrillar matrix that serv
295 arise, have intracellular organelles, called melanosomes, wherein the synthesis and storage of the pi
296 ng these are fibrils formed by Pmel17 within melanosomes, which act as a template for melanin deposit
297          Cells known as melanophores contain melanosomes, which are membrane organelles filled with m
298 tant and fossil amphibians generally exhibit melanosomes with a mixed eumelanin/phaeomelanin composit
299 trafficking of integral membrane proteins to melanosomes with substantially increased surface express
300 ow that the v-SNARE VAMP7 mediates fusion of melanosomes with tubular transport carriers that also ca
301 ds 3 and 4 corresponds to the RPE nuclei and melanosomes zone.

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