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1 anism involving NTR1 and NTR3 (also known as sortilin).
2 her ATZ levels and secretion are affected by sortilin.
3 nt mannose-6-phosphate receptor (CI-MPR) and sortilin.
4 ortilin that impair lysosomal degradation of sortilin.
5 ation of proNGF interactions with p75NTR and sortilin.
6 nsulin-responsive aminopeptidase (IRAP), and sortilin.
7 R) receptors and cell death via p75(NTR) and Sortilin.
8  and required both p75NTR and its coreceptor sortilin.
9 ng to p75 neurotrophin receptor (p75NTR) and sortilin.
10 ed neurons, and recombinant proBDNF binds to sortilin.
11 ed cells by double transfection of Glut4 and sortilin.
12 er receptors macrophage mannose receptor and sortilin.
13 rest, cluster of differentiation 4 (CD4) and sortilin.
14 that physically interact and colocalize with sortilin.
15 he common neurotrophin receptor (p75NTR) and sortilin.
16 se 2-dependent C-terminal phosphorylation of sortilin.
17 at was independent of the endocytic receptor sortilin.
18 on, indicating a primary role of SMC-derived sortilin.
19 found that the cellular trafficking receptor sortilin 1 (Sort1) inhibits hepatic apolipoprotein B sec
20                                              Sortilin 1 (SORT1) is a lysosomal trafficking receptor t
21            The cellular trafficking receptor sortilin 1 (Sort1) was recently identified to transport
22 tional TDP-43 was measured by monitoring the sortilin 1 mRNA splicing activity.
23                                              Sortilin 1 regulates the levels of brain progranulin (PG
24 nd markedly increased expression of the gene sortilin-1 (SORT1) in liver.
25 sclerotic cardiovascular disease is the 1p13 sortilin-1 (SORT1) locus.
26 ssociated with altered expression of hepatic sortilin-1 (SORT1), which encodes a protein thought to b
27  led to amelioration of ER stress, increased sortilin-1 expression, and reduced apoB and triglyceride
28 icamycin led to marked repression of hepatic sortilin-1 expression, while administration of the chemi
29 ray identified reduced protein expression of sortilin-1 in liver and increased plasma enzyme activity
30  mRNA in ob/ob mice led to increased hepatic sortilin-1 levels and decreased apoB and triglyceride se
31 et models of obesity; restoration of hepatic sortilin-1 levels resulted in reduced triglyceride and a
32 mice reduced ER stress and increased hepatic sortilin-1 levels.
33                     Furthermore, we identify sortilin-1(Sort1), a known regulator of circulating low-
34 orebrain-derived inhibitors, one of which is sortilin, a lysosomal sorting receptor.
35            This revealed that the protein is sortilin, a novel membrane protein that was cloned in an
36 n component of Glut4-containing vesicles, is sortilin, a novel type I receptor-like protein recently
37                 Here we investigated whether sortilin, a Vps10p domain-sorting receptor believed to p
38 on of either p115 or CHC22, but not GM130 or sortilin, abrogates insulin-responsive GLUT4 release.
39 essure homeostasis after 14 days of systemic sortilin administration.
40         Understanding the mechanism by which sortilin affects LDL cholesterol will increase our under
41                    Here we demonstrated that sortilin also directly affects atherogenesis, independen
42  bind beta-amyloid effector proteins such as sortilin and 14-3-3.
43 significantly reduces cell surface-expressed sortilin and abolishes proneurotrophin-induced neuronal
44                                         Both sortilin and BDNF are trafficked to and degraded by the
45 rotein consisting of the cytoplasmic tail of sortilin and EGFP is co-localized with ectopically expre
46 ilin and the cytoplasmic interaction between sortilin and GGA adaptors play an important role in recr
47 lin signaling but decreases the stability of sortilin and Glut4 and blocks their entry into the small
48                However, double expression of sortilin and Glut4 reconstitutes functional GSVs that in
49 Microglia express only the receptor 3 (NTR3)/sortilin and not the NTR1 or NTR2.
50  hypothesized that overexpression of proNGF, sortilin and p75(NTR) play a role in ts1-induced neurode
51      We found that complex formation between sortilin and p75(NTR) relies on contact points in the ex
52     To identify the interaction site between sortilin and p75(NTR), we analyzed binding between chime
53 l apoptosis using a dual receptor complex of sortilin and p75(NTR).
54  Here, we explore the expression of pro-NGF, sortilin and p75NTR in the mouse lumbar dorsal root gang
55  induce apoptosis of cells coexpressing both sortilin and p75NTR, suggesting that interaction of proB
56          In sympathetic neurons coexpressing sortilin and p75NTR, we found that proBDNF is an apoptot
57  that a subpopulation of neurons coexpresses sortilin and p75NTR.
58  strategies for brain-specific regulation of sortilin and possibly sortilin-driven pathologies.
59 , addition of preformed complexes of soluble sortilin and proBDNF failed to induce apoptosis of cells
60  levels of p75(NTR) and its interaction with sortilin and proNGF set the dependency on BDNF for survi
61 nd direct control of BDNF levels, while both sortilin and SorCS2 function as cell surface receptors t
62                                        Also, sortilin and SorLA both bind and mediate internalization
63  replicated the interaction between PGRN and sortilin and that between TNF and TNFRI/II, but not the
64 at the lumenal interaction between Glut4 and sortilin and the cytoplasmic interaction between sortili
65 mote apoptosis by engaging in a complex with sortilin and the p75 neurotrophin receptor (p75(NTR)).
66              The data provide a link between sortilin and the pathological findings of microglia and
67 a to disrupted interactions between PGRN and Sortilin and/or other binding partners yet to be identif
68 complexes with ERGIC tether p115, GLUT4, and sortilin, and downregulation of either p115 or CHC22, bu
69               SORT1 encodes a protein called sortilin, and hepatic sortilin modulates LDL metabolism
70 liver is independent of mannose 6-phosphate, sortilin, and Limp2.
71 ized storage vesicles containing IRAP, LRP1, sortilin, and VAMP2, which are sequestered by TUG, Ubc9,
72                              We suggest that sortilin- and retromer-mediated Glut4 retrieval from end
73                                 In addition, sortilins are required for delivery of a key protease in
74       Our studies suggest a new function for sortilin as a modulator of BACE1 retrograde trafficking
75                             We here identify sortilin as a novel APP interaction partner.
76            Together, our findings identified sortilin as an essential neuronal pathway for APOE-conta
77  we identified the pro-neurotrophin receptor sortilin as major endocytic pathway for clearance of APO
78 ether, these data reveal TrkA, p75(NTR), and sortilin as potential therapeutic targets in thyroid can
79 the non-neuronal isoforms, leaving SorLA and sortilin as the only receptors for sAPP generated by neu
80             Together, our findings establish sortilin, as a novel APP interaction partner that influe
81 etrograde transport of IRAP does not require sortilin, as retromer can directly bind to the cytoplasm
82  caused a 1.7-fold increase in the amount of sortilin at the plasma membranes of 3T3-L1 adipocytes, a
83 he life span of the Tg mice, suggesting that sortilin, at least in part, inhibits forebrain tau prion
84  on cellular coexpression of both p75NTR and sortilin, because neurons deficient in p75NTR are resist
85 as biosynthetic analysis, we discovered that sortilin binds and stabilizes APLP2, and hence could reg
86                                              Sortilin binds APOE with high affinity.
87 tent with a model in which increased hepatic sortilin binds intracellular APOB-containing particles i
88                                     However, sortilin binds to numerous ligands and plays a major rol
89 l loop of Glut4, and the cytoplasmic tail of sortilin binds to retromer.
90 ed apoptosis, and competitive antagonists of sortilin block sympathetic neuron death.
91 of the LDLR independently of either APLP2 or sortilin both ex vivo and in mice.
92 eriments reveal that the cytoplasmic tail of sortilin, but not those from other VPS10p domain recepto
93                                              Sortilin can impact the intracellular response to brain-
94                          A truncated form of sortilin causes BDNF missorting to the constitutive secr
95 ntrast, we demonstrate NSG2 has no effect on sortilin cell surface abundance or progranulin uptake, s
96 ce biotinylation, we found only NSG1 reduced sortilin cell surface expression, which caused significa
97 ng specificity for NSG1 in the regulation of sortilin cell surface expression.
98                                 Furthermore, sortilin co-localizes with, and enhances accumulation of
99 njury; however, the majority of small p75NTR-sortilin coexpressing neurons are lost 25 days after sci
100 for the p75 neurotrophin receptor (p75(NTR))-sortilin complex.
101 hat sortilin interacts with BACE1 and that a sortilin construct lacking its cytoplasmic domain, which
102               Together, these data show that sortilin contributes to pancreatic cancer invasion and c
103     Collectively, our findings indicate that sortilin controls adipose tissue fatty acid oxidation by
104 e in neurons, and this is dependent upon the sortilin cytoplasmic tail.
105 found that siRNA against TrkA, p75(NTR), and sortilin decreased cell survival and cell migration thro
106                                 Knockdown of sortilin decreases both formation of GSVs and insulin-re
107 duced atherosclerosis, we found no effect of sortilin deficiency on macrophage recruitment or lipopol
108                                   Macrophage sortilin deficiency protects against atherosclerosis by
109 etermine the mechanism by which hematopoetic sortilin deficiency reduced atherosclerosis, we found no
110 lve (AV) wire injury (AVWI) mouse model with sortilin deficiency was used to determine the effects of
111 ether this effect was a result of macrophage sortilin deficiency, we transplanted Sort1(-/-);LDLR(-/-
112 espite higher than normal brain APOE levels, sortilin-deficient animals display anomalies in brain li
113                    Additionally, transfer of sortilin-deficient BM cells to irradiated atheroscleroti
114                                  Transfer of sortilin-deficient BM into irradiated atherosclerotic mi
115                                 In contrast, sortilin-deficient macrophages had significantly reduced
116                                  Altogether, sortilin defines a pathway required for optimal intracel
117 ficking switch to impair lysosomal-dependant sortilin degradation and to redistribute sortilin to the
118 ontrast, the tagged luminal Vps10p domain of sortilin demonstrates partial co-localization with Glut4
119                                         Thus sortilin-dependent as well as sortilin-independent sorti
120 mpathetic neuron death that is p75(NTR)- and sortilin-dependent, with hallmark features of apoptosis
121  multiple cytokines including IFN-alpha, and sortilin depletion in plasmacytoid dendritic cells (pDCs
122      Furthermore, mice deficient in APLP2 or sortilin do not exhibit significant changes in liver LDL
123   Thus, although the intracellular domain of sortilin does not contribute to p75(NTR) binding, it doe
124 specific regulation of sortilin and possibly sortilin-driven pathologies.
125 ted the role of the proneurotrophin receptor sortilin during phagosome maturation and mycobacterial k
126  stalk region, to release the ligand binding sortilin ectodomain from the transmembrane and cytoplasm
127 ding and identify a novel mechanism by which sortilin ectodomain shedding acts as a regulatory switch
128                    Indeed, expression of the sortilin ectodomain, which corresponds to the domain rel
129                                              Sortilin ectopically expressed in undifferentiated cells
130  identify an endosomal trafficking component sortilin (encoded by Sort1) in adipose tissues that show
131 lesterol transport and metabolism, including sortilin, endoplasmic reticulum-Golgi intermediate compa
132                Also, primary neurons lacking sortilin exhibit significantly impaired uptake of APOE/A
133 er element that regulates the inclusion of a sortilin exon cassette (termed Ex17b) not normally prese
134 llular uptake and activity of gapmer ASOs in sortilin expressing cells (sixfold) and in spinal cord i
135 strong association between increased hepatic sortilin expression and reduced plasma LDL-C levels in h
136  evidence that genetically increased hepatic sortilin expression both reduces hepatic APOB secretion
137 n through the posttranscriptional control of sortilin expression by TLR signals.
138               Conversely, down-regulation of sortilin expression in HeLa cells leads to an up-regulat
139 e previously reported that increased hepatic sortilin expression in mice reduced plasma LDL-C levels.
140                            We also show that sortilin expression is higher in the forebrain than the
141                        This study found that sortilin expression was higher in pancreatic cell lines
142 and alterations of intracellular zinc affect sortilin expression.
143 n export, whereas other studies suggest that sortilin facilitates lipoprotein export.
144    SorCS1 and SorL1/SorLA/LR11 belong to the sortilin family of vacuolar protein sorting-10 (Vps10) d
145                             As hypothesized, sortilin function impacts the levels of secreted ATZ in
146                                         Yet, sortilin gene-targeted mice (Sort1(-/-)) and chimeras de
147                          In dendritic cells, sortilin had an impact on Ag processing.
148 te atherosclerotic plaque formation) lacking sortilin had reduced secretion of IL-6 and IFN-gamma, bu
149        The overexpression of both proNGF and sortilin has been associated with several neurodegenerat
150                 Previous characterization of sortilin has led to the suggestion that it functions to
151                                 Mice lacking Sortilin have elevations in brain and serum PGRN levels
152 corresponding to vertebrate Trk, p75(NTR) or Sortilin have not been identified in Drosophila, thus it
153                            The expression of sortilin in 3T3-L1 cells occurred only upon differentiat
154                                 Depletion of sortilin in adipocytes results in an increase of mitocho
155                   Given the emerging role of sortilin in Alzheimer's disease, these insights may help
156 r study was to elucidate the distribution of sortilin in different immune cell types in mice and huma
157  contrast, little is known about the role of sortilin in immune cells and inflammatory diseases.
158 uences cytokine secretion and that targeting sortilin in immune cells attenuates inflammation and red
159 Studies by several groups support a role for sortilin in inhibiting lipoprotein export, whereas other
160 several groups support an important role for sortilin in lipoprotein metabolism; however, the directi
161 emains controversial, as genetic deletion of sortilin in mice has resulted in variable and conflictin
162 initial studies revealed increased levels of sortilin in post-mortem brain tissue of AD patients and
163 ), neurotrophin receptor p75 (p75(NTR)), and sortilin in the areas showing spongiform changes.
164 lpha secretion, suggesting a pivotal role of sortilin in the exocytic trafficking of IFN-alpha in pDC
165 t ADAM10 is the preferred protease to cleave sortilin in the extracellular stalk region, to release t
166  mice (Sort1(-/-)) and chimeras deficient in sortilin in the immune system were as susceptible as wil
167                         Forced expression of sortilin in undifferentiated cells does not recruit IRAP
168 am of VPS35, suggesting a potential role for sortilins in PD.
169 n studies implicate the human Vps10 homolog, sortilin, in cardiovascular disease, and because hepatic
170  novel function for a Vps10p domain protein, sortilin, in controlling BDNF sorting to the regulated s
171                              Coexpression of sortilin increased targeting of myc7-Glut4 to the IRVs,
172 f the transporter, whereas overexpression of sortilin increases formation of GSVs and stimulates insu
173  the Golgi protein galactosyltransferase was sortilin independent and occurred even in the absence of
174           Thus sortilin-dependent as well as sortilin-independent sorting mechanisms target aggregate
175        Together, these data demonstrate that sortilin influences cytokine secretion and that targetin
176                                              Sortilin inhibition also decreased the phosphorylation o
177                                              Sortilin inhibition by siRNA and the pharmacologic inhib
178 ysosomes is mediated by the sorting receptor sortilin interacting with the lumenal stem domain of GPP
179                                              Sortilin interacts specifically with BDNF in a region en
180 rLA mainly colocalizes with APP in the soma, sortilin interacts with APP in neurites.
181                           We also found that sortilin interacts with BACE1 and that a sortilin constr
182 nd the yeast two-hybrid system, we show that sortilin interacts with Glut4 and IRAP in the vesicular
183 echanistically, the luminal Vps10p domain of sortilin interacts with the first luminal loop of Glut4,
184 aled an important regulatory function of the sortilin intracellular domain in p75(NTR)-regulated intr
185                           We determined that sortilin is a high-affinity receptor for the proinflamma
186              Here, we have demonstrated that sortilin is a key regulator of smooth muscle cell (SMC)
187                                              Sortilin is a lysosomal sorting protein that binds ligan
188                                              Sortilin is a multiligand sorting receptor responsible f
189                 The proneurotrophin receptor sortilin is a protein with dual functions, being involve
190                                              Sortilin is also expressed in macrophages, but its role
191                     Here we demonstrate that sortilin is also involved in retrograde protein traffic.
192                                              Sortilin is an intracellular chaperone that binds to the
193 Interestingly, the phagosomal association of sortilin is critical for the delivery of acid sphingomye
194                The neuronal membrane protein sortilin is emerging as a regulator of cancer cell devel
195                                  In the CNS, Sortilin is expressed by neurons and PGRN is most strong
196         Like the related APP receptor SorLA, sortilin is highly expressed in the CNS, but whereas Sor
197                                              Sortilin is modified by ectodomain shedding, although th
198                                        Thus, sortilin is not only essential, but also sufficient for
199 e and accessible to proneurotrophin ligands, sortilin is primarily localized to intracellular membran
200 ere, we show that IRAP, similar to Glut4 and sortilin, is retrieved from endosomes to the trans-Golgi
201        In Xenopus embryos, overexpression of sortilin leads to a decrease in phospho-Smad2 levels and
202 ue of AD patients and that overexpression of sortilin leads to increased BACE1-mediated cleavage of A
203 ed expression of Glut4 prior to induction of sortilin leads to rapid degradation of the transporter,
204                                The increased sortilin level in pancreatic cancer cells was confirmed
205         We hypothesized that variants in the sortilin-like receptor (SORL1) gene would affect multipl
206 ovel function of the endolysosomal T. gondii sortilin-like receptor (TgSORTLR), which mediates traffi
207                                              Sortilin localized to calcifying vessels in human and mo
208                               In conclusion, sortilin-mediated engagement of LIF signaling in BECs pr
209 hese results propose pro-NGF-induced, p75NTR-sortilin-mediated neuronal death as a critical aspect of
210                                              Sortilin-mediated PGRN endocytosis is likely to play a c
211                                              Sortilin-mediated uptake of native LDL into macrophages
212 codes a protein called sortilin, and hepatic sortilin modulates LDL metabolism by targeting apolipopr
213  contrast to mice, the inclusion of Ex17b in sortilin mRNA generates a truncated, nonfunctional, extr
214                                    Moreover, sortilin mRNA was degraded posttranscriptionally upon st
215 ed the C-rich element (CRE) in the 3' UTR of sortilin mRNA, and depletion of PCBP1 enhanced the degra
216 ed Ex17b) not normally present in the mature sortilin mRNA.
217 gulatory inhibitor, Ex17b is included in the sortilin mRNA.
218   We found that proNGF and p75(NTR), but not sortilin, mRNA and protein were significantly elevated i
219                     Our results suggest that sortilin negatively regulates TGF-beta signaling by dive
220 , a kinase-dead TrkA, and siRNA against TrkA sortilin, neurotensin, whereas siRNA against p75(NTR) an
221          Here we show that increased hepatic sortilin not only reduced hepatic apolipoprotein B (APOB
222 iciency was used to determine the effects of sortilin on AV stenosis, fibrosis, and calcification.
223 ntiating 3T3-L1 adipocytes upon induction of sortilin on day 2 of differentiation.
224 however, the directionality of the effect of sortilin on plasma cholesterol and its role in the secre
225  NRH2 critically regulates the expression of sortilin on the neuronal cell surface and promotes p75(N
226 his hypothesis, we have studied targeting of sortilin, one of the major IRV constituents.
227 Secreted PGRN is incorporated into cells via sortilin or cation-independent mannose 6-phosphate recep
228 n demonstrate that mRNA knockdowns of APLP2, sortilin, or both in the human hepatocyte cell lines Hep
229 reduced foam cell formation in vivo, whereas sortilin overexpression in macrophages resulted in incre
230  NT (10 nM) increases the gene expression of sortilin (P < 0.0001) and causes the receptor to be tran
231   Our findings also show increased levels of sortilin (P < 0.0001) in the serum from children with AS
232 mation of a stable ternary complex of proNGF-sortilin-p75NTR.
233 Together, the results of this study identify sortilin phosphorylation as a potential therapeutic targ
234     Here we report that the sorting receptor sortilin plays a key role in cytokine production.
235 e conclude that the proneurotrophin receptor sortilin plays a role in innate, rather than in adaptive
236  TRKB with the intracellular sorting protein sortilin, prevented TRKB degradation, and promoted its a
237                              The presence of sortilin promotes alpha-secretase cleavage of APP, unlik
238                              Expression of a sortilin protein rescues these defects, downstream of VP
239                                              Sortilin rapidly endocytoses and delivers PGRN to lysoso
240 ronal cell surface and promotes p75(NTR) and sortilin receptor complex formation, rendering cells res
241   Interestingly, gene expression of the NTR3/sortilin receptor is reduced in the amygdala and dorsola
242 be dependent upon membrane expression of the sortilin receptor, which interacts with p75NTR to promot
243 a the neurotrophin receptor p75(NTR) and the sortilin receptor.
244 ins, combined with prior work on the role of sortilin receptors in mucocyst biogenesis, suggests that
245 tes p75 neurotrophin receptor (p75(NTR)) and sortilin receptors to mediate proapoptotic responses.
246        However, expression of this truncated sortilin redistributes BACE1 from the trans-Golgi networ
247                   The use of siRNA to target sortilin reduces (P < 0.001) the NT-stimulated cytokine
248                                              Sortilin regulated the loading of the calcification prot
249 d as the causative gene within the locus, as sortilin regulates hepatic lipoprotein metabolism.
250 s have reported that genetic variants in the Sortilin-related receptor (SORL1) increased the risk of
251              In humans, genetic variation of sortilin-related receptor, L(DLR class) A repeats contai
252 xplored the role of one of its homologs, the sortilin-related VPS10 domain containing receptor 1 (SOR
253                 However, the role of hepatic sortilin remains controversial, as genetic deletion of s
254 along with glucose transporter 4 (Glut4) and sortilin, represents a major component protein of the in
255             In contrast, RNAi suppression of sortilin results in decreased BACE1-mediated cleavage of
256  enhancer element is consistently present in sortilin RNA of mice and other species but absent in pri
257 Mase activity and increased plasma levels of sortilin, S1P, and soluble NOX2-derived peptide (sNOX2-d
258                The current studies show that sortilin selectively co-immunoprecipitates with the clea
259   Loss-of-function studies demonstrated that sortilin serves as a bona fide receptor for LDL in vivo
260 hese findings characterize the regulation of sortilin shedding and identify a novel mechanism by whic
261                                  We identify sortilin shedding at the cell surface and in an intracel
262 al framework for NSG1-mediated regulation of sortilin shedding.
263 hermore, the inhibition of both p75(NTR) and sortilin signaling attenuated synapse elimination.
264                                 In addition, sortilin small interfering RNA introduced into primary n
265 x (Vps35, Vps26) and its putative receptors (sortilin, SorL1, SorCS1)] have been implicated in the mo
266 ng 10 (Vps10) family of receptors (including sortilin, SorL1, SorCS1, SorCS2, and SorCS3) play pleiot
267 the vesicular sorting of the retromer cargo, sortilin, SorLA and cation-independent mannose 6-phospha
268 , and unbiased expression cloning identifies Sortilin (Sort1) as a binding site.
269  issue of Neuron, Hu and colleagues identify Sortilin (SORT1) as a key neuronal receptor for PGRN tha
270                            The gene encoding sortilin (SORT1) has been implicated as the causative ge
271             Recent discoveries demonstrating sortilin (SORT1) is a neuronal receptor for PGRN endocyt
272                 SNP rs646776 is located near sortilin (SORT1), and the minor C allele of rs646776 was
273 potential mechanism linking misregulation of sortilin splicing with altered PGRN metabolism.
274  between the cytoplasmic domains of NRH2 and sortilin that impair lysosomal degradation of sortilin.
275  splicing events were detected (including in sortilin, the receptor for progranulin) following deplet
276 fied two potential binding interfaces on the sortilin TMD and demonstrated that the T770W mutation sh
277 ant sortilin degradation and to redistribute sortilin to the cell surface, rendering p75(NTR)-express
278               In cultured 3T3-L1 adipocytes, sortilin together with retromer rescues Glut4 from degra
279 PCBP1 may therefore control the stability of sortilin transcripts by sensing intracellular zinc level
280 pletion of PCBP1 enhanced the degradation of sortilin transcripts, suggesting that PCBP1 can act as a
281 an act as a trans-acting factor to stabilize sortilin transcripts.
282 ere, we probed for novel binding partners of sortilin using multiple and complementary approaches and
283 red the binding characteristics of proNGF to sortilin using surface plasmon resonance and cell-based
284 proteins requires classical receptors of the sortilin/VPS10 family, which indicates that dual mechani
285                                              Sortilin was expressed most profoundly in murine and hum
286                                 Accordingly, sortilin was highly expressed by infiltrated perivascula
287                                              Sortilin was overexpressed in thyroid cancers compared w
288 er with GLUT4 vesicle isolation, showed that sortilin was primarily located in the low density micros
289 is after binding to p75NTR and a coreceptor, sortilin, we asked whether the precursor of BDNF (proBDN
290 death after binding to co-receptors p75(NTR)/sortilin, we hypothesized that overexpression of proNGF,
291 r p75(NTR), and the proneurotrophin receptor sortilin were analyzed with immunohistochemistry in a co
292 ines that stably express wild-type or mutant sortilin were recently established, we examined whether
293 Amyloid precursor-like protein 2 (APLP2) and sortilin were reported to individually bind the proprote
294 when co-expressed with PCSK9, both APLP2 and sortilin were targeted for lysosomal degradation.
295 ds on the expression of the sorting receptor sortilin, which interacts with the unique amino acid res
296                                Another NTSR, sortilin, which is common to neurotensin and neurotrophi
297 AP-1 acted through the multi-ligand receptor sortilin while AP-4 sorted multi-transmembrane proteins.
298                  We observed interactions of sortilin with multiple cytokines including IFN-alpha, an
299                             Co-expression of sortilin with TGF-beta family members leads to decreased
300 timulated by proNGF and mediated by TrkA and sortilin, with the activation of Akt and Src, for the st
301 atherosclerosis in mice lacking hematopoetic sortilin without an effect on plasma LDL-C levels.

 
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