ライフサイエンスコーパス: TSPO

1 gulation of the 18-kDa translocator protein (TSPO).

2 tory protein (StAR) or translocator protein (TSPO).

3 gands that bind to the translocator protein (TSPO).

4 and targets the 18-kDa translocator protein (TSPO).

5 considered a conserved endogenous ligand for TSPO.

6 eric-like interaction at the wild type human TSPO.

7 to induce complex binding to wild type human TSPO.

8 specially because of the basal expression of TSPO.

9 an aquaporin regulatory mechanism involving TSPO.

10 d by the binding of this class of ligands to TSPO.

11 the regional variation of Kb and endothelial TSPO.

12 ives displayed subnanomolar affinity for the TSPO (0.37 to 0.86 nM), comparable to that of 2 (0.91 nM

13 ease the expression of translocator protein (TSPO) 18 kDa, thereby making the TSPO expression a marke

14 tecting alterations in translocator protein (TSPO) (18 kDa), a biomarker of microglial activation, in

15 (18)F-FDG (n = 43) and translocator protein (TSPO) ((18)F-GE180; n = 58) small-animal PET, with volum

16 nvolvement and role of translocator protein (TSPO), a biomarker of microglial and astrocyte gliosis i

17 Translocator protein 18 kDa (TSPO), a biomarker of neuroinflammation, is overexpresse

18 PET imaging of 18-kDa translocator protein (TSPO), a biomarker of neuroinflammation, most second-gen

19 Ligands of the 18 kDa translocator protein (TSPO), a marker for activated microglia, have been used

20 d radioligands for the translocator protein (TSPO), a marker for glial activation, have yielded incon

21 )C]PBR28 to the 18 kDa translocator protein (TSPO), a marker for microglial activation in a group of

22 To measure translocator protein 18 kDa (TSPO), a marker of activated glial cell response, in a c

23 xpression of the 18kDa translocator protein (TSPO), a marker of activated microglia/macrophages, in c

24 ed brain levels of the translocator protein (TSPO), a marker of glial activation, in patients with ch

25 Brain levels of 18-kDa translocator protein (TSPO), a marker of microglial activation and neuroinflam

26 imaging of the 18-kDa translocator protein (TSPO), a marker of neuroinflammation.

27 ial to bind the translocator protein 18 kDa (TSPO), a protein today recognized as an early biomarker

28 blood draws during PET scanning to determine TSPO affinity genotype and plasma nicotine levels.

29 Probes with relevant TSPO affinity, favorable spectroscopic properties, and i

30 Consistent with previous reports, the TSPO Ala147Thr genotype predicted the in vivo binding of

31 e crossed with Tspo-floxed mice to obtain F1 Tspo Amhr2 cKO mice (Tspo(fl/fl);Amhr2-Cre(/+)).

32 The correlation between TSPO and endothelial cell mRNA supports the relationship

33 ficant correlation was seen between mRNA for TSPO and genes specific to endothelial cells.

34 into the controversial physiological role of TSPO and how the mutation affects cholesterol binding.

35 ves 4-10 with improved potencies toward both TSPO and MDM2.

36 croglia/macrophages (GAM) were identified as TSPO and MMP sources.

37 tion and quantification of the expression of TSPO and MMP.

38 Coexpression of TSPO and PIP2;7 resulted in decreased levels of PIP2;7 i

39 [(18)F]DPA-714 (TSPO) and [(18)F]BR-351 (MMP) matched with histology.

40 invasive imaging by PET with [(18)F]DPA-714 (TSPO) and [(18)F]BR-351 (MMP) was used for the assessmen

41 invasion, such as the translocator protein (TSPO) and matrix metalloproteinases (MMP), may serve as

42 toma multiforme (GBM), translocator protein (TSPO) and murine double minute (MDM)2/p53 complex repres

43 the radiotracer [(11)C]DAA1106 (a ligand for TSPO) and positron emission tomography (PET) to determin

44 icroglia (18-kD translocator protein ligand [TSPO]) and static 30- to 60-min recordings with (18)F-FD

45 Immunohistochemical analyses with TSPO antisera, methoxy-X04 staining for fibrillary beta-

46 ia with caution, especially when measures of TSPO are not complemented with other markers of inflamma

47 Therefore, we evaluated the validity of TSPO as a disease-relevant marker of inflammation using

48 PO in CNS disease, and our results implicate TSPO as a potential therapeutic target in MS.

49 d that these probes specifically labeled the TSPO at the mitochondrial level in the U343 cell line.

50 In a post hoc analysis, we also compared TSPO availability between patients with and without suic

51 have used [(11)C](R)-PK11195 PET to compare TSPO availability in a predominantly antipsychotic-naive

52 We found no evidence for increased TSPO availability in antipsychotic-free patients compare

53 1195 positron emission tomography to compare TSPO availability in the anterior cingulate cortex (ACC)

54 In the patients, TSPO availability was also strongly correlated with nega

55 Regional TSPO availability was measured as a distribution volume

56 However, TSPO availability was significantly elevated in medicate

57 We confirm evidence for increased TSPO availability, suggestive of predominantly microglia

58 eport crystal structures for Bacillus cereus TSPO (BcTSPO) down to 1.7 A resolution, including a comp

59 all correlation between (18)F-FDG uptake and TSPO binding (R = 0.69, P < 0.005).

60 e been explored further by the synthesis and TSPO binding affinity evaluation of N-benzyl-N-ethyl/met

61 We demonstrated that all TSPO binding groups (HAB, MAB, and LAB) have same level

62 e similar in AD and MCI subjects among the 3 TSPO binding groups.

63 er underscores the need to interpret altered TSPO binding in schizophrenia with caution, especially w

64 -713 revealed a strong trend towards reduced TSPO binding in the middle frontal gyrus of patients wit

65 Similarly, cortical TSPO binding increased to a maximum at 14.5 mo (+15%, P

66 that accounts for the effect of endothelial TSPO binding on the quantification of (18)F-DPA-714 PET

67 ly that the pathological meanings of altered TSPO binding or expression are disease-specific, and the

68 While altered TSPO binding or expression may indeed mirror ongoing neu

69 these ligands are still easily lodged in the TSPO binding site.

70 ligands and the lipophilic L1 pocket of the TSPO binding site.

71 The observed decrease in TSPO binding suggests reduced numbers or altered functio

72 Participants with homozygous low-affinity TSPO binding were excluded.

73 blems, including a polymorphism that affects TSPO binding.

74 tically stratified for translocator protein (TSPO) binding status, underwent PET scanning with TSPO r

75 sive quantification of translocator protein (TSPO) binding using SPECT and 6-chloro-2-(4'-(123)I-iodo

76 d in vivo using 18-kDa translocator protein (TSPO)-binding radioligands and PET.

77 It is a high-quality second-generation TSPO-binding PET radiotracer.

78 3 HABs underwent a repeated brain scan after TSPO blockade with XBD173 (N-benzyl-N-ethyl-2-(7-methyl-

79 ting the recently available 3D structures of TSPO bound to its standard ligand (PK11195).

80 Our preliminary results suggest that TSPO brain imaging in GBM may be a useful tool for predi

81 We suggest that TSPO can be a good marker for early pathogenesis detecti

82 Ex vivo autoradiography and TSPO/CD68 immunostaining were also performed using brain

83 Nr5a1-driven Tspo cKO mice exhibited highly reduced Tspo levels in ad

84 In contrast, Nr5a1-driven Tspo cKO mice lost their ability to form corticosterone

85 ublication, we examined Leydig cell-specific TSPO conditional knock-out mice that suggested TSPO was

86 TSPO, we generated two lines of Cre-mediated Tspo conditional knockout (cKO) mice.

87 udies, for the first time, demonstrated that TSPO could serve as a potential imaging biomarker for BA

88 In fibroblasts, we observed that TSPO deficiency decreased the oxygen consumption rate an

89 o expectations, our results demonstrate that TSPO deficiency does not adversely affect erythropoiesis

90 ion in brain and peripheral organs with high TSPO densities such as lung and spleen were greater in H

91 TSPO distribution volume (VT) is an index of TSPO density.

92 e activated during neuroinflammation and the TSPO distribution volume (VT) is an index of TSPO densit

93 n these findings, we conclude that mammalian TSPO does not have a critical physiological function rel

94 rch has mostly accepted these denotations of TSPO, even if they may be inadequate and misleading unde

95 or protein (TSPO) 18 kDa, thereby making the TSPO expression a marker for neuroinflammation.

96 tumor tissue was quantitatively assessed for TSPO expression and infiltration of GAMs using immunohis

97 tory citokine interleukin-6, suggesting that TSPO expression exerts pain-protective/anti-inflammatory

98 Positive correlation between high TSPO expression in cancer cells and susceptibility to ph

99 erall TSPO expression within the tumors, and TSPO expression in GAMs did not correlate with tumor BPN

100 TSPO expression in the adrenal medulla and increased epi

101 1195 in human gliomas predominantly reflects TSPO expression in tumor cells.

102 g in human gliomas and its relationship with TSPO expression in tumor tissue and glioma-associated mi

103 TSPO expression levels in cancer cells do not correlate

104 on in schizophrenia is mirrored by increased TSPO expression or ligand binding.

105 Finally, in aged RPE cells, TSPO expression was reduced and cholesterol efflux impai

106 ith the exception of cortical lesions, where TSPO expression was similar, (11) C-PBR28 uptake across

107 Ms only partially contributed to the overall TSPO expression within the tumors, and TSPO expression i

108 loxed mice to obtain F1 Tspo Amhr2 cKO mice (Tspo(fl/fl);Amhr2-Cre(/+)).

109 The resulting Tspo(fl/fl);Nr5a1-Cre(/+) mice were born at a normal Men

110 We generated a TSPO floxed mouse, and then crossed this mouse with a Cr

111 l-targeting Amhr2-Cre mice were crossed with Tspo-floxed mice to obtain F1 Tspo Amhr2 cKO mice (Tspo(

112 l-targeting Nr5a1-Cre mice were crossed with Tspo-floxed mice.

113 ed to search for a new translocator protein (TSPO) fluorescent probe endowed with improved affinity a

114 at 1.8, 2.4, and 2.5 angstrom resolution) of TSPO from Rhodobacter sphaeroides and a mutant that mimi

115 of the A139T mutant of translocator protein TSPO from Rhodobacter sphaeroides should be used to 1.65

116 rystal structure for a translocator protein (TSPO) from Rhodobacter sphaeroides in which some of the

117 n the presence of light, and in vertebrates, TSPO function has been linked to porphyrin transport and

118 and synthetic ligands to assess the role of TSPO function in a number of natural and pathological ci

119 As the Ala147Thr polymorphism in the TSPO gene affects binding affinity for (11)C-PBR28, nine

120 All subjects were screened for TSPO genotype and underwent detailed clinical and neurop

121 econd-generation TSPO tracers depends on the TSPO genotype coded by the rs6971 single-nucleotide poly

122 Scale (>3 points of the scale), but age and TSPO genotype did not.

123 analyses were performed controlling for both TSPO genotype, which is known to affect [(11)C]PBR28 bin

124 ied the (18)F-DPA-714 radioligand in healthy TSPO-genotyped volunteers and developed a method to elim

125 Here, we investigated whether different TSPO genotypes influence cognitive function, amyloid loa

126 it is crucial to establish the influence of TSPO genotypes on AD.

127 However, the existence of three human TSPO genotypes that show differential affinity to almost

128 hese compounds and biochemical associations, TSPO has been proposed to play a role in the mitochondri

129 used to detect discrete neurotoxic damages, TSPO has generally turned into a biomarker of 'neuroinfl

130 ers that target translocator protein 18 kDa (TSPO) has become a popular approach to assess putative n

131 lective for the 18 kDa translocator protein (TSPO) has become the most widely used technique to asses

132 The mitochondrial translocator protein (TSPO) has been implicated in CNS diseases.

133 imaging of the 18 kDa translocator protein (TSPO) has been used to investigate whether microglial ac

134 s targeting the translocator protein 18 kDa (TSPO) have been limited by high nonspecific binding of t

135 s targeting the 18-kDa translocator protein (TSPO) have been used as in vivo markers of neuroinflamma

136 Ten healthy controls, 6 TSPO high-affinity binders, and 4 mixed-affinity binders

137 e, we evaluated various ratio approaches for TSPO imaging and compared them with standard kinetic mod

138 In this review, the developments in TSPO imaging are discussed, and current limitations and

139 It remains unclear, however, whether TSPO imaging can accurately capture low-grade inflammato

140 Although TSPO imaging demonstrates great promise, its signal exhi

141 warranted to test the clinical potential of TSPO imaging in GBM, including presurgical planning and

142 as to evaluate whether translocator protein (TSPO) imaging could be used to visualize the diffuse inf

143 Here we compare translocator protein (TSPO) imaging using 6-chloro-2-(4'-(123)I-iodophenyl)-3-

144 utively expressed yellow fluorescent protein-TSPO in Arabidopsis.

145 (11)C-PBR28 images showed overexpression of TSPO in brain regions known to be affected in the HSE ra

146 Here, we investigate the function of TSPO in cholesterol efflux from the RPE cells.

147 ful tool in better understanding the role of TSPO in CNS disease, and our results implicate TSPO as a

148 vated embryonic lethality and involvement of TSPO in embryonic development.

149 rent tumor cell lines to examine the role of TSPO in erythropoiesis, heme levels, PPIX biosynthesis,

150 we sought to determine the specific role of TSPO in experimental autoimmune encephalomyelitis (EAE),

151 TSPO in gliomas was expressed predominantly by neoplasti

152 unctions and cellular expression patterns of TSPO in health and disease.

153 as consistent with the known distribution of TSPO in humans, with the thalamus displaying the highest

154 Radioligands with PET accurately quantify TSPO in neuroinflammatory conditions.

155 s of variance indicated significantly higher TSPO in patients compared with control subjects (p = .00

156 these data support a physiological role for TSPO in regulating the cell-surface expression of PIP2;7

157 SPO specific ligands or by overexpression of TSPO in RPE cells.

158 g, indicating an in vivo functional role for TSPO in suppressing EAE.

159 The loss of TSPO in the CNS did not result in overt developmental de

160 Accounting for endothelial TSPO in the kinetic model improved the fit of PET data.

161 Full quantitation of TSPO in vivo is needed to detect widespread inflammation

162 MS WM lesions showed relatively modest TSPO increases.

163 A split-ubiquitin screen for potential TSPO interacting partners uncovered a plasma membrane aq

164 temporal lobe epilepsy (TLE) found increased TSPO ipsilateral to seizure foci.

165 Our results indicate that TSPO is a promising molecular marker for imaging inflamm

166 its accumulation is strictly regulated, and TSPO is downregulated through a selective autophagic pat

167 Binding of TSPO is increased both ipsilateral and contralateral to

168 e the downstream p53 signaling is intact and TSPO is overexpressed.

169 Arabidopsis thaliana multi-stress regulator TSPO is transiently induced by abiotic stresses.

170 TSPO is upregulated in glial cells and used as a measure

171 The translocator protein (TSPO) is a commonly used imaging target to investigate n

172 Translocator protein of 18 kDa (TSPO) is a highly conserved, ubiquitous protein localize

173 Translocator protein (TSPO) is a key member of the mitochondrial cholesterol t

174 Translocator protein (TSPO) is expressed at a low level in healthy brain and i

175 In AD, the translocator protein 18 kDa (TSPO) is overexpressed in the activated microglia that s

176 e 18-kDa mitochondrial translocator protein (TSPO) is upregulated in high-grade astrocytomas and can

177 The 18 kDa translocator protein, TSPO, is a cholesterol-binding protein implicated in mit

178 Translocator protein (18 kDa), known as TSPO, is a recognized biomarker of neuroinflammation.

179 In this study, we used TSPO knock-out (Tspo(-/-)) mice, primary cells, and diff

180 A conditional TSPO knockout mouse was generated by utilizing the Cre-L

181 nctions of TSPO, we first developed a viable TSPO knockout mouse.

182 tant mouse was a neural linage line specific TSPO knockout.

183 riven Tspo cKO mice exhibited highly reduced Tspo levels in adrenal cortex and gonads.

184 ndence (P=0.034), corresponding to 10% lower TSPO levels in alcohol-dependent subjects.

185 Quantification of TSPO levels in MS could prove to be a sensitive tool for

186 ory analyses found a negative association of TSPO levels in the hippocampus and striatum with alcohol

187 In both models, the changes in TSPO levels were not restricted to microglia but emerged

188 ssion are associated with reduced prefrontal TSPO levels.

189 thinning correlated with increased thalamic TSPO levels.

190 to assess the potential of the radiolabeled TSPO ligand (123)I-DPA-713 for early detection of brain

191 this need, we varied the known high-affinity TSPO ligand (l)-N,N-diethyl-2-methyl-3-(2-phenylquinolin

192 A TSPO ligand attenuates brain injury after intracerebral

193 These results indicate that the TSPO ligand etifoxine attenuates brain injury and inflam

194 In this study, we determined the impact of a TSPO ligand, etifoxine, on brain injury and inflammation

195 80) is a recently developed third-generation TSPO ligand.

196 the antiproliferative effects of a synthetic TSPO ligand.

197 TSPO ligands have shown anti-inflammatory and neuroprote

198 ve, high-affinity, and moderately lipophilic TSPO ligands that may serve as leads for PET radioligand

199 hemistry, we also explore the ability of the TSPO ligands to detect activated microglial cells and as

200 TSPO ligands, including benzodiazepine drugs, are implic

201 better address SAR data presented by the new TSPO ligands.

202 -carboxamide series of translocator protein (TSPO) ligands have been explored further by the synthesi

203 unclear how different translocator protein (TSPO) ligands reflect the spatial extent of astrocyte or

204 s potent and selective translocator protein (TSPO) ligands, two subsets of novel derivatives, featuri

205 Thus, TSPO may be a suitable in vivo indicator of neurodegener

206 TSPO may be a viable therapeutic target that requires fu

207 Contrary to the early report, Tspo(-/-) mice survived with no apparent phenotypic abno

208 gonadal steroidogenesis showed no defects in Tspo(-/-) mice.

209 Star, Cyp11a1, and Hsd3b1) were unchanged in Tspo(-/-) mice.

210 In this study, we used TSPO knock-out (Tspo(-/-)) mice, primary cells, and different tumor cell

211 ws great potential as a tool for visualizing TSPO/microglia in the progression and treatment of AD.

212 ron emission tomography (PET) imaging of the TSPO microglial marker and found increased neuroinflamma

213 The TSPO-/- mouse could be a useful tool in better understan

214 The TSPO-/- mouse showed a decrease in GFAP expression, corr

215 y correlated with all 3 probes extracted for TSPO mRNA expression (r = 0.80, r = 0.79, and r = 0.90),

216 othelial cells were correlated with regional TSPO mRNA expression.

217 en the volume of distribution and one of the TSPO mRNA probes (r = 0.65).

218 The high correlation between Kb and TSPO mRNA suggests that the 2TC-1K model reveals more bi

219 mage expression of the translocator protein (TSPO) on activated microglia in the brain, has been used

220 expression of fluorescently tagged PIP2;7 in TSPO-overexpressing transgenic lines resulted in patchy

221 e than (R)-(11)C-PK11195 in the detection of TSPO overexpression in the HSE rat model, because more b

222 Analysis and interpretation of TSPO PET are challenging, especially because of the basa

223 Hence, the increasing popularity of TSPO PET imaging has paradoxically introduced substantia

224 s unlikely to be achieved by the sole use of TSPO PET imaging.

225 tic properties of the novel third-generation TSPO PET ligand (18)F-GE180 in humans: 2TCM4k is the opt

226 esent study uses the novel second-generation TSPO PET radioligand [(18)F]FEPPA to evaluate whether mi

227 w differential affinity to almost all useful TSPO PET radioligands hampers such studies.

228 imer disease (AD), and translocator protein (TSPO) PET imaging allows us to quantify this process.

229 ro-m-tyrosine, and the translocator protein (TSPO) PET ligand [(18)F]DAA1106.

230 sign, in which each patient was matched to a TSPO polymorphism-, age- and sex-matched control subject

231 ction of the mammalian translocator protein (TSPO; previously known as the peripheral benzodiazepine

232 The 18-kilodalton translocator protein (TSPO), proposed to be a key player in cholesterol transp

233 remitting MS patients were studied using the TSPO radioligand (11)C-(R)-PK11195.

234 ts and 16 healthy controls using PET and the TSPO radioligand [(11)C]PBR28.

235 TSPO radioligand uptake was increased in the brains of M

236 Using in vivo microPET imaging with a novel TSPO radioligand, (18)F-GE180, we detected significantly

237 binding status, underwent PET scanning with TSPO radioligands ((11)C-PBR28 or (18)F-PBR111).

238 uman PET imaging using the second-generation TSPO radiotracer [(11)C]DPA-713 revealed a strong trend

239 By autoradiography, the TSPO radiotracer binding potential in the injected hemis

240 , the application of these second-generation TSPO radiotracers has revealed additional problems, incl

241 patients relative to healthy controls with 2 TSPO radiotracers.

242 Because of the absence of a region devoid of TSPO, reference tissue models should be used with cautio

243 o)lipoprotein and human serum, while loss of TSPO resulted in impaired cholesterol efflux.

244 TSPO-/- RPE cells also had significantly increased produ

245 and accumulation were markedly increased in TSPO-/- RPE cells.

246 All analyses were corrected for TSPO rs6971 polymorphism (which is implicated in differe

247 development of any improved radioligand for TSPO should consider the possibility that in vitro prope

248 firm these findings and to determine whether TSPO signal and white matter changes in young NFL athlet

249 brain injury and repair, indicated by higher TSPO signal and white matter changes, may be associated

250 l activation in the retina and highlight DBI-TSPO signaling as a potential target for immodulatory th

251 The inducibility and effects of DBI-TSPO signaling in the retina reveal a mechanism of coord

252 - and eight-cell zygotes, suggesting ectopic Tspo silencing before the morula stage and demonstrating

253 The ambiguity of conceiving TSPO simply as a biomarker of 'neuroinflammation' or 'mi

254 d immunohistochemical analyses confirmed the TSPO small-animal PET findings.

255 timulating cellular cholesterol removal with TSPO specific ligands or by overexpression of TSPO in RP

256 We demonstrate in RPE cells that TSPO specific ligands promoted cholesterol efflux to acc

257 eat deal of work into the development of new TSPO-specific PET radiotracers.

258 arker for BAT imaging using [(18)F]-F-DPA, a TSPO-specific PET tracer.

259 vivo using positron emission tomography and TSPO-specific radioligands.

260 n brain regions containing elevated CD68 and TSPO staining in APP(L/S) mice, compared with wts).

261 Here, we used the novel TSPO-targeted PET tracer (18)F-GE180 (flutriciclamide) t

262 ively stratify patients who are suitable for TSPO-targeted treatment.

263 ic information about the regional density of TSPO than the 2TC.

264 The analyses also reveal the role of TSPO, TP53, and many other immune or cell cycle related

265 For the novel TSPO tracer (18)F-GE180, we then calculated distribution

266 with Pittsburgh compound B ((11)C-PIB) and a TSPO tracer, flutriciclamide ((18)F-GE-180), in the APP2

267 is a second-generation translocator protein (TSPO) tracer with characteristics supposedly superior to

268 of AD or MCI subject using second-generation TSPO tracers can be translated to the entire AD and MCI

269 However, the binding of second-generation TSPO tracers depends on the TSPO genotype coded by the r

270 ter than that reported for commonly used PET TSPO tracers.

271 ter than that reported for commonly used PET TSPO tracers.

272 o reduce the complexity of blood analyses of TSPO tracers.

273 ission tomography-based regional measures of TSPO using [11C]DPA-713, diffusion tensor imaging measur

274 issue (BAT) and translocator protein 18 kDa (TSPO) via a combination of disulfiram, an FDA approved d

275 Slightly lower elevations in TSPO VT (22%-29%) were present in other gray matter regi

276 The correlation between higher ACC TSPO VT and the severity of MDE is consistent with the c

277 The regional distribution of elevated TSPO VT argues that the autoimmune/neuroinflammatory the

278 The magnitude of TSPO VT elevation was 26% in the prefrontal cortex (mean

279 In MDE, greater TSPO VT in the ACC correlated with greater depression se

280 sive behaviors significantly correlated with TSPO VT in the orbitofrontal cortex (uncorrected Pearson

281 Values of TSPO VT in the prefrontal cortex, ACC, and insula.

282 To determine whether TSPO VT is elevated in the dorsal caudate, orbitofrontal

283 The TSPO VT was measured in the dorsal caudate, orbitofronta

284 In MDE, TSPO VT was significantly elevated in all brain regions

285 In OCD, TSPO VT was significantly elevated in these brain region

286 ein density measured by distribution volume (TSPO VT) is increased in activated microglia, an importa

287 2.4] in controls), 32% in the ACC (mean [SD] TSPO VT, 12.3 [3.5] in patients with MDE and 9.3 [2.2] i

288 was 26% in the prefrontal cortex (mean [SD] TSPO VT, 12.5 [3.6] in patients with MDE and 10.0 [2.4]

289 controls), and 33% in the insula (mean [SD] TSPO VT, 12.9 [3.7] in patients with MDE and 9.7 [2.3] i

290 In conclusion, TSPO was found necessary for preimplantation embryo deve

291 In bacteria, TSPO was identified to regulate tetrapyrrole metabolism

292 On the other hand, TSPO was markedly upregulated in a mouse model of acute

293 TSPO was not elevated in patients without suicidal think

294 PO conditional knock-out mice that suggested TSPO was not required for testosterone production in viv

295 TSPO was up-regulated in Iba1(+) cells from brains of pa

296 To fundamentally elucidate the functions of TSPO, we first developed a viable TSPO knockout mouse.

297 To assess the function of TSPO, we generated two lines of Cre-mediated Tspo condit

298 The thalamic levels of TSPO were negatively correlated with clinical pain and c

299 Translocator protein (TSPO), which is upregulated in activated glia (predomina

300 AT contrast was due to (64)Cu-Dis binding to TSPO, which was further confirmed as a specific biomarke