ライフサイエンスコーパス: surface expression

1 an understanding of the dynamics of Siglec-8 surface expression.

2 tein that binds PD-L1 and maintains its cell surface expression.

3 l migration by up-regulating mast cell CXCR4 surface expression.

4 aralleled by a reduction in transporter cell surface expression.

5 cellular mechanisms that acutely control DAT surface expression.

6 l tumor cells from blood independent of cell surface expression.

7 zed the polypeptides and enhanced their cell-surface expression.

8 r a general mechanism counteracting low MHCI surface expression.

9 es NF-kappaB activation and reduces CD4 cell surface expression.

10 G-proteins coupled to 5-HT2ARs and receptor surface expression.

11 dynein/dynactin, thereby facilitating GABAAR surface expression.

12 and phosphatidylserine and protein receptor surface expression.

13 via Proline-rich region and regulates TRPV1 surface expression.

14 leads to defects in protein folding and cell-surface expression.

15 important role in TPbeta maturation and cell-surface expression.

16 adhesion to MAdCAM-1 without affecting CCR9 surface expression.

17 migration and decreased beta1-integrin cell surface expression.

18 whether mRNA levels reliably represent cell surface expression.

19 olymerization is sufficient to enhance Kv2.1 surface expression.

20 Golgi complex and show markedly reduced cell-surface expression.

21 o the mechanism by which cocaine alters AMPA surface expression.

22 0 in LPS-mediated decrease in MC FcepsilonRI surface expression.

23 modulating its intracellular trafficking and surface expression.

24 y, whereas radioimmunolabeling measured cell-surface expression.

25 ulum seems to be the cause of the lower cell-surface expression.

26 was reduced, reflecting a reduction in ENaC surface expression.

27 tain recent interior activity and associated surface expressions.

28 of primary human monocytes increased MT1-MMP surface expression 31.7-fold and gene expression 24.5-fo

29 e in vascular endothelial (VE)-cadherin cell-surface expression above wild-type (WT) monolayers.

30 ampal neurons to limit their somatodendritic surface expression, although exerting little effect on V

31 gene products are characterized by low cell-surface expression and a highly conserved peptide-bindin

32 ins podocyte function by regulating podocyte surface expression and activity of TRPC6.

33 ous TCRs compete with the transgenic TCR for surface expression and allow mixed dimer formation.

34 cells reveal that deltaD140N attenuates cell surface expression and apparent channel gating, predicti

35 tism, human GluN2B S1415L, displayed reduced surface expression and binding to PSD-95.

36 ion in inflammatory chemokine receptor CXCR3 surface expression and cellular activation of lipid phos

37 addition of cyclic nucleotides enhanced AQP1 surface expression and concomitantly diminished its ubiq

38 s, along with other characteristics, such as surface expression and continuous intracellular traffick

39 rast, in the same cells, DEX increased CXCR4 surface expression and CXCL12-mediated signaling and dow

40 ted (HCN) ion channels, alters both the cell surface expression and cyclic nucleotide dependence of t

41 ecycling of AMPA receptors to increase their surface expression and elicits structural changes in spi

42 that an SNX3-retromer complex regulates the surface expression and function of PC1 and PC2.

43 e in DAT(+) neurons produced increased AMPAR surface expression and function that lead to impaired in

44 activation of Rho GTPases that dictates DAT surface expression and function.SIGNIFICANCE STATEMENT S

45 ous alphabeta chains reduces therapeutic TCR surface expression and generates self-reactive TCRs.

46 we show that this mutation also reduced cell-surface expression and glycine sensitivity.

47 lel with phosphorylation to promote Smo cell-surface expression and Hh signaling.

48 AB receptors (GABABRs) to control their cell surface expression and intracellular trafficking via a d

49 During this phase, CTLA4 surface expression and its complexation with CD80/CD86 c

50 membrane, while the R153Q mutation impaired surface expression and markedly reduced sensitivity to g

51 Blockade of ICOSL rescues T cell ICOS surface expression and rescues, at least in part, T foll

52 nt proteolytic processing but increased cell surface expression and secretion.

53 re involved in the regulation of immune cell surface expression and signaling, but their function in

54 Alterations in both cell-surface expression and single-channel properties account

55 to the plasma membrane, thereby enhancing IR surface expression and strengthening insulin signal rece

56 A-to-I-edited Gabra3 has reduced cell surface expression and suppresses the activation of AKT

57 The observed maintenance of PD-1 surface expression and the demethylated PD-1 promoter we

58 lity of NMDARs to regulate potassium channel surface expression and thus, beta-cell excitability prov

59 ression, modifying neurotransmitter receptor surface expression and trafficking, and modulating neuro

60 s the most efficacious compound in restoring surface expression and transport activity to the folding

61 hat the truncated subunits had no to minimal surface expression and unchanged or reduced surface expr

62 ndings indicate that the signal that affects surface expression and/or internalization of Env from th

63 compromised NHE3 activity by reducing basal surface expression and/or loss of basal transport functi

64 d eosinophil shape change, chemotaxis, CD11b surface expression, and adhesion as well as production o

65 egments, with consequences for the assembly, surface expression, and function of the polycystin compl

66 educes epithelial Na(+) channel function and surface expression, and impairs subunit maturation.

67 receptor (AMPAR)-mediated currents and cell-surface expression, and that these phenotypes result fro

68 neered and evaluated for GP1-GP2 processing, surface expression, and the ability to mediate cell-to-c

69 the ectodomain of HAP2 is essential for its surface expression, and the cytoplasmic region targets H

70 -term stress was sufficient to increase RAGE surface expression as well as anhedonic behavior, reflec

71 features of SAMs and indicate that increased surface expression, as observed for APLP1, is essential

72 ursor protein subcellular localization, cell-surface expression, as well as its metabolism.

73 teracts with NaV1.5 channel and controls its surface expression at the lateral membrane by regulating

74 ulated wild type NHE3 activity and increased surface expression but failed to stimulate NHE3 activity

75 u alteration does not affect protein or cell surface expression but rather significantly reduces, alt

76 d T cell subsets did not correlate with PD-1 surface expression but was inversely correlated with int

77 double-edged sword: increasing TAS2R14 cell surface expression, but when activated by beta-agonist,

78 , while antagonizing inhibition reduces KCC2 surface expression by increasing the lateral diffusion a

79 The increased Kv2.1 surface expression by leptin is dependent on actin depol

80 promoted MMP12 production and reduced CD200R surface expression by monocyte-derived cells.

81 beta or undergoing EMT upregulated CD73 cell-surface expression, confirming roles for these pathways.

82 dendritic development and glutamate receptor surface expression, core-glycosylated proteins are suffi

83 Crucially this reduced surface expression did not cause the reduced agonist res

84 In addition, we observed a deficit in surface expression for GluN2B S1413L.

85 e as well as promoter region that alter cell surface expression have been associated with disease pro

86 nt/beta-catenin pathway regulates BK channel surface expression in a protein synthesis-dependent mann

87 currents of DKO neurons and the GABAAR cell surface expression in DKO neurons and GODZ or SERZ-beta

88 transcript destabilization and reduced ULBP2 surface expression in several human cell lines.

89 ngth, active TMPRSS13 exhibits impaired cell-surface expression in the absence of the cognate Kunitz-

90 Thus, HDAC inhibition restored HLA class-I surface expression in vitro and in a mouse xenotransplan

91 ation and reduced nephrin signaling and cell surface expression in vitro In a rat model of reversible

92 enes: US18 and US20, to interfere with B7-H6 surface expression, in a mechanism involving endosomal d

93 Cu via regulatory endocytosis, lowering its surface expression, in response to elevated Cu loads.

94 -dependent mechanisms to interfere with CD1d surface expression, indirectly suggesting a role for iNK

95 This did not affect surface expression, inhibitor binding, and substrate inf

96 This reduced HLA class-I surface expression is caused by an impaired expression o

97 HLA class I cell surface expression is crucial for normal immune response

98 The effect of leptin on Kv2.1 surface expression is mediated by the AMP-activated prot

99 anchoring of CaValpha2delta1 averts its cell-surface expression, its interaction with CaValpha1, and

100 luding its subcellular localization and cell surface expression, its trafficking, and its metabolism.

101 We suggest that differences in cell surface expression level ensure the development of optim

102 ular B cells significantly down regulate the surface expression level of CD23 after undergoing isotyp

103 We found that the cell surface expression level of CD46 was markedly higher in

104 The cell surface expression level of MHC class I molecules varies

105 ar tonicity, despite equivalent constitutive surface expression levels and water permeability to wild

106 these results were correlated with gene and surface expression levels of alpha5 integrin and urokina

107 Notably, HRG treatment upregulates surface expression levels of CXCR4, a G protein-coupled

108 d Gly(239), as in HLA-A2, led to higher cell surface expression levels when compared with the presenc

109 ocalization microscopy at physiological cell surface expression levels, however, reveals efficient li

110 ygdala sensitivity to serotonin by promoting surface expression of 5-HT2CR without affecting tissue l

111 ng by the inhibitor combination and enhanced surface expression of A1-receptor-Y(288)A within 1 hour.

112 Surface expression of activation receptors NKp30, NKp46,

113 eceptive to Notch ligands via Taok3-mediated surface expression of ADAM10.

114 CCL11, CCL24, CCL5, MCP-3, and MCP-4), cell surface expression of adhesion molecules (such as VCAM-1

115 nusual Ag processing pathways, which reduces surface expression of Ag-derived peptides while selectiv

116 e Beta-2 Microglobulin (B2M) gene eliminates surface expression of all class I molecules, but leaves

117 CA10 promotes surface expression of alpha- and beta-neurexins, suggest

118 Stochastic cell-surface expression of alpha-, beta-, and gamma-clustered

119 d folding, yields an additive restoration of surface expression of alpha1(A322D) subunits in HEK293 c

120 is specifically involved in regulating cell surface expression of alpha2 subunit-containing GABAA re

121 ycosylation, proteolytic processing and cell-surface expression of alpha2delta-1, and also increase p

122 Irak1-deficient T cells failed to upregulate surface expression of alpha4beta7 integrin after transfe

123 a7 nAChR mRNA is detected by RT-PCR and cell surface expression of alpha7 nAChR is detected by confoc

124 o migrate was associated with decreased cell surface expression of alphaVbeta3 and alpha5beta1 integr

125 upregulating GLT-1 and resulted in increased surface expression of AMPA receptor subunits GluA1 and G

126 manipulation of xCT expression increases the surface expression of AMPA receptor subunits, providing

127 SHR, which was correlated with the decreased surface expression of AMPAR subunits.

128 nhibited the adverse effects of Abeta on the surface expression of AMPARs in neurons.

129 described that enhance the function and cell-surface expression of AMPARs.

130 f Syncrip by small interfering RNA increased surface expression of an HLA-A allotype that uses primar

131 We have shown that the surface expression of AOC3 is sensitive to digestion by

132 , Vgamma9Vdelta2 T cells presented increased surface expression of APC-associated markers HLA-DR and

133 CMA); inhibition of gamma-secretase enhanced surface expression of BCMA and reduced the release of sB

134 Human and mouse ILC2s were assessed for surface expression of beta1 and beta2 integrin adhesion

135 full-length and cleaved TLR3, demonstrating surface expression of both forms of TLR3.

136 small interfering RNA reduced total and cell-surface expression of both receptors and caused redistri

137 reticulin as a key anchor point for the cell surface expression of calreticulin on apoptotic cells.

138 ing in tsA201 cells that Stac3 could support surface expression of CaV1.1 (coexpressed with its auxil

139 RAP alone produced a small increase in cell-surface expression of CaV2.2, alpha2delta-1 and the asso

140 We observed preferential cell surface expression of CCR10 and CXCR3 by HSV-specific CD

141 infected with P. gingivalis and controls for surface expression of CD11b, Ly6G, and Ly6C.

142 Surface expression of CD138 increased heparan sulfate le

143 acid D(205) also regulates the turnover and surface expression of CD16A in the absence of FcepsilonR

144 Intracellularly labeled DAO(+) and surface expression of CD203c(bright), CD63(+), and CD107

145 ells by creating conditions that induce cell surface expression of CD39, an immunosuppressive molecul

146 The morphology, cell surface expression of CD4-1, and the presence of transcr

147 in clathrin-independent internalization and surface expression of CD44 and CD59.

148 e long 3' UTR of CD47 enables efficient cell surface expression of CD47 protein, whereas the short 3'

149 NK) cells as defined by accumulation of cell-surface expression of CD57 is associated with increased

150 Surface expression of CD63 and CD107a was greater at 6 h

151 uction in FcepsilonRI cross-linking-mediated surface expression of CD63 and CD203c was observed on ba

152 nto M2 macrophages as indicated by increased surface expression of CD68 (macrophage marker), M2 marke

153 ls and eosinophil activation, as assessed by surface expression of CD69 and serum levels of eosinophi

154 sistent with this, TFH maintained high-level surface expression of CD69, indicative of impaired migra

155 salt increased macrophage and dendritic cell surface expression of CD70 by 3- to 5-fold.

156 th of peptide presentation and level of cell surface expression of class I molecules are inversely co

157 ions 180 and 239 determine the level of cell surface expression of common HLA-A and -B allomorphs, pr

158 L lactis G121-induced cytokine release and surface expression of costimulatory molecules by untreat

159 We found that KLF2 deficiency enhanced surface expression of costimulatory molecules CD40 and C

160 insic apoptotic pathway along with increased surface expression of CRT.

161 rin and Ki67 expression levels and increased surface expression of CXCR3.

162 he transcriptional level, they increased the surface expression of CXCR4, an effect observed also in

163 -bet(lo)Eomes(hi) NK, distinguished by their surface expression of CXCR6, adapted for hepatic toleran

164 Large igneous provinces, as the surface expression of deep mantle processes, play a key

165 key role for ALK2 in the BMP9/BMP10-induced surface expression of E-selectin, and both ALK1 and ALK2

166 Here, we demonstrate that cell-surface expression of endogenous Notch1 in HEK293T cells

167 he core retromer protein VPS35 increased the surface expression of endogenous PC1 and PC2 in vitro an

168 er, TNF-alpha stimulation downregulates cell surface expression of endomucin concurrent with increase

169 This increases permeability, surface expression of endothelial adhesion molecules and

170 nd interleukin-27 (IL-27) also increases the surface expression of Env and thus boosts the ability of

171 h increased systemic IL-10 levels, decreased surface expression of FcepsilonRI on MCs and loss of sen

172 ingly, we found that these mutations reduced surface expression of full-length G1 but not G1-DeltaNT

173 s, the molecular composition of Dex includes surface expression of functional MHC-peptide complexes,

174 during development by the modulation of cell surface expression of Fz receptor.

175 However, the factors regulating cell surface expression of GABAB receptors are poorly charact

176 o surrounding amino acids, ensuring the cell surface expression of gH/gL.

177 ecrease in AMPAR function was due to reduced surface expression of GluA1 subunits through dynamin-dep

178 show that morphine dependence increases cell surface expression of GluA1, suggesting that neurons in

179 Surface expression of GluA3 was improved by co-assembly

180 nkyrin-B, and we propose that increased cell surface expression of GLUT4 in skeletal muscle and fatty

181 rapidly and specifically downregulates cell-surface expression of glycoprotein 130, which is require

182 These symptoms are caused by the decreased surface expression of GPI-APs or by structural abnormali

183 Here, we report that surface expression of GRP78 is increased in endothelial

184 tress signals induced Golgi-independent cell-surface expression of H723R-pendrin and restored its cel

185 n was able to induce the unconventional cell-surface expression of H723R-pendrin.

186 ve TKIs, and also caused a reduction in cell surface expression of hENT1 protein.

187 he second approach exploits the massive cell surface expression of HER2 and delivers of a variety of

188 Surface expression of highly glycosylated GP causes mark

189 fused to B2M and a peptide antigen), without surface expression of HLA-A, B or C.

190 HLA-DR and HLA-DQ RNA; we observed elevated surface expression of HLA-DR (P = 0.008) and HLA-DQ (P =

191 ner, resulting in a 2.5-fold increase in the surface expression of HLA-DR and DQ molecules on dendrit

192 in vitro, Vgamma9Vdelta2 T cells upregulated surface expression of HLA-DR, HLA-ABC, CD40, CD80, CD83,

193 a manner that confers inducible, regulated, surface expression of HLA-E single-chain dimers (fused t

194 4(+) T cells triggered the transcription and surface expression of HLA-F mRNA and HLA-F protein, resp

195 We conclude that the impaired surface expression of homomeric GluA3 receptors is cause

196 ration induces MR1 refolding and upregulates surface expression of human MR1, forms MR1 tetramers tha

197 However, we detected a decrease in surface expression of IFN-gamma receptor alpha-chain eve

198 ption 1 (STAT1), release of type 1 IFNs, and surface expression of IFNAR1 in microglia.

199 In the absence of FcmuR, the surface expression of IgM-BCR was increased, which resul

200 ology by constraining the transport and cell-surface expression of IgM-BCR.

201 We identified reduced surface expression of IL-7R and concomitant limited resp

202 Macrophage subpopulation cell-surface expression of immunological markers and phagocyt

203 RNA and siRNA significantly reduced the cell surface expression of inducibly expressed alpha2B-AR and

204 , the deletion ofDicer1resulted in increased surface expression of integrins alphaIIband beta3, and e

205 euronal properties including the feature and surface expression of ionotropic receptors.

206 Infection with HHV-8 did not alter the cell surface expression of langerin on LC but downregulated t

207 There was increased surface expression of Le(x) on PMN after TEM, and blocka

208 used a licensing defect in NK cells, but the surface expression of Ly49A was unaltered.

209 The B2M truncating mutation led to loss of surface expression of major histocompatibility complex c

210 filtration rate but alter the total and cell-surface expression of major Na(+) transporters all along

211 chymal stem cells are positively selected by surface expression of markers CD90 and CD105.

212 e functional changes were not accompanied by surface expression of markers specific for alternatively

213 maturation characterized by heightened cell surface expression of MHC and costimulatory molecules as

214 on decreases PD-L1 without compromising cell surface expression of MHC class I.

215 by inhibiting Grp94 enhances the functional surface expression of misfolding-prone alpha1(A322D) sub

216 Coculture of live NTHi increased macrophage surface expression of MR1 and induced IFN-gamma from CD4

217 tergic transmission, we quantitated the cell surface expression of N-methyl-D-aspartate (NMDA)-type a

218 ays showed that CASK silencing increased the surface expression of NaV1.5 without changing mRNA level

219 3 knockdown significantly inhibited the cell surface expression of newly synthesized alpha2B-AR witho

220 inent homeostatic-like reduction in the cell surface expression of NMDA-type and AMPA-type glutamate

221 STEP reduces the surface expression of NMDARs by promoting dephosphorylat

222 c density protein 95 (PSD-95) stabilizes the surface expression of NMDARs.

223 We demonstrate that N9 recognizes surface expression of Notch1 on the plasma membrane and

224 e may enhance this resistance by diminishing surface expression of pathogen-associated molecular patt

225 m chronically infected mice maintained their surface expression of PD-1 even after transfer into acut

226 and showed that 1,25D treatment induces cell-surface expression of PD-L1 in epithelial and myeloid ce

227 demonstrated that the epithelial cells with surface expression of PD-L1, E-cadherin, CD24, and VEGFR

228 dition, psoriatic Mo-MDSCs expressed reduced surface expression of programmed cell death protein 1 co

229 onal anti-HLA class I Abs, the level of cell-surface expression of proteins correlates with the level

230 CUS also increased surface expression of RAGE protein on hippocampal microg

231 Increased recycling and elevated cell surface expression of receptors serve as a mechanism for

232 s are composed of cells that differ in their surface expression of receptors such as Ly49C/I and NKG2

233 In addition, Vpu reduces cell surface expression of several cellular molecules such as

234 ysis enabled the identification of increased surface expression of several sialylated cell adhesion m

235 metry analyses indicated significantly lower surface expression of T66M TREM2 variant than wild type

236 FAT, and MAPK activities owing to attenuated surface expression of TCR, which were rescued on reconst

237 roportion of human neutrophils that mediates surface expression of the antineutrophil cytoplasmic ant

238 plex N-linked glycans, which facilitate cell surface expression of the channels.

239 a3-deficient mice displayed a marked loss of surface expression of the chemokine CCR7.

240 However, cell surface expression of the CIPs, CD46, CD55, and CD59, wa

241 Additionally, cell surface expression of the CML stem cell markers CD25, CD

242 18 and US20 work in concert to suppress cell surface expression of the critical NKp30 ligand B7-H6 th

243 uptake and glycolytic flux by promoting cell surface expression of the glucose transporter GLUT1/Slc2

244 tion of wild-type OPCs caused decreased cell-surface expression of the GluR2 AMPA receptor subunit an

245 a and colleagues reported that the defective surface expression of the glycosylphosphatidylinositol-a

246 s in the lytic phase and was associated with surface expression of the gp350/220 envelope Ag.

247 hanistically, S1PR4 activation preserves the surface expression of the human pDC-specific inhibitory

248 P conjugate delivery to APCs results in high surface expression of the immuno-modulatory molecule pro

249 mice an HCD resulted in upregulated MZB cell surface expression of the immunoregulatory ligand PDL1 i

250 hat SARA knockdown neurons exhibit increased surface expression of the L1 cell adhesion molecule.

251 quencies of Valpha7.2(+)CD161(+) MAIT cells, surface expression of the major histocompatibility compl

252 endogenous or exogenous ligands induced the surface expression of the metalloproteinase ADAM10 on T1

253 ly raised palmitoylation levels restored the surface expression of the p.G257R variant gamma2 subunit

254 s can arise via feedback loops that increase surface expression of the receptor tyrosine kinases (RTK

255 d plays an important part in regulating cell surface expression of the receptor tyrosine kinases MET

256 lls is accompanied by the down-regulation of surface expression of the short form of membrane IgE (mI

257 generates a late response by increasing the surface expression of the TNFalpha receptor, without aff

258 l extracellular trap generation and elevated surface expression of toll-like receptor 2 and CD11b on

259 Increased surface expression of transferrin receptor (TfR) is a do

260 ment strategy resulted in markedly increased surface expression of transgenic alphabeta and gammadelt

261 port is not sufficient to enable normal cell-surface expression of TREM2.

262 eversed the LPS-induced increase in podocyte surface expression of TRPC6 in wild-type mice.

263 synaptopodin also caused increased podocyte surface expression of TRPC6.

264 not conduct Ca(2+) ions, it reduced the cell-surface expression of wild-type CaV1.2 channels and cons

265 surface expression and unchanged or reduced surface expression of wild-type partnering subunits.

266 ressions in the age of volcanism are typical surface expressions of plate tectonic movement on top of

267 onnection between lithospheric evolution and surface expressions of plateau uplift and volcanism.

268 Here, surface-expression of a pre-T cell receptor (pre-TCR) in

269 EM localized the cell surface-expression of EphA7 essentially in postsynaptic

270 artment upon immunization, had reduced MHCII surface expression on GC cells, and developed accelerate

271 lass-I binding peptides restored HLA class-I surface expression on MCC cells.

272 anti-Clr-g mAb detected only residual Clr-g surface expression on splenic monocytes, whereas many he

273 CIN85/RukL deficiency preserved nephrin surface expression on the slit diaphragm and reduced pro

274 ect was not due to changes in beta1 integrin surface expression or activation.

275 CD70 in these patients abolished either CD70 surface expression or binding to its cognate receptor CD

276 nd, in some cases, have been shown to affect surface expression or ligand specificity of G-protein-co

277 These mutants did not alter DAT surface expression or surface DAT binding sites.

278 ion in PAS usage, which modulates their cell surface expression posttranscriptionally.

279 for UL20 membrane targeting and thus gK cell surface expression, providing new mechanistic insights i

280 echanistically, synaptopodin-dependent TRPC6 surface expression required functional actin and microtu

281 CH activation also enabled persistent NOTCH2 surface expression, suggesting a positive feedback loop.

282 icited enhanced beta2 but not beta1 integrin surface expression, suggesting increased adhesive capaci

283 tained SERT loss of function reduces 5-HT2AR surface expression that is critical for the synergistic

284 of Blimp1 transcription and decreased MHC-II surface expression that point to trout IL-6 as a differe

285 vitro fluticasone and budesonide reduced MR1 surface expression twofold and decreased NTHi-induced IF

286 gs indicate that FIP3 modulates TCR-CD3 cell surface expression via the regulation of steady-state Lc

287 Surface expression was measured with (125)I-mAb 295 bind

288 be the principal HC expressed, and its cell surface expression was prevented by siRNA inhibition of

289 Upon brefeldin A treatment, cell surface expression was rapidly lost, even for mutants la

290 PrP(C) cell-surface expression was reduced by down-regulation of RAB

291 Integrin alphaVbeta3 surface expression was specifically upregulated in stimu

292 Clr-g surface expression was strongly upregulated on splenic C

293 AT ligands for their ability to increase DAT surface expression, we found that bupropion and ibogaine

294 tions of immunoproteasome activity and MHC I surface expression were analyzed in human blood-derived

295 ailed to stimulate NHE3 activity or increase surface expression when NHE3 was mutated to either S663A

296 protein stability and decrease folded TREM2 surface expression, whereas Alzheimer's risk variants im

297 nd that bupropion and ibogaine increased DAT surface expression, whereas others, including cocaine an

298 -nAChR function principally by lowering cell-surface expression, whereas single-channel effects were

299 ing a mutant gamma2 subunit had reduced cell surface expression with altered subunit stoichiometry or

300 cific blocking of the proximal 3'UTR reduced surface expression without decreasing mRNA expression.