ライフサイエンスコーパス: heteromer

1 se-type starch-debranching enzyme (ISA1/ISA2 heteromer).

2 sigma1R) also associates with the CRF1R-OX1R heteromer.

3 the series that bridges the protomers of the heteromer.

4 idging of protomers in a putative MOR-mGluR5 heteromer.

5 study the pharmacology and signaling by this heteromer.

6 ranching enzyme activity present is ISA1/ISA heteromer.

7 for the unique behavioral function of a GPCR heteromer.

8 actions between the protomers of the DOR-KOR heteromer.

9 rrestin recruitment at the alpha(1A)AR-CXCR2 heteromer.

10 till lagging behind for the majority of GPCR heteromers.

11 sensitive to loss-of-function mutations than heteromers.

12 ivation of the 5-HT2C protomer of MT2/5-HT2C heteromers.

13 so potentially assemble into functional GPCR heteromers.

14 nin MT2 and 5-HT2C receptors into functional heteromers.

15 , was consistent with the activation of both heteromers.

16 neurons due to the fast kinetics of GluA2A3 heteromers.

17 -V relation of EPSCs mediated by GluA1/GluA2 heteromers.

18 ng a small residual pool of synaptic GluA2A3 heteromers.

19 plasmic reticulum (ER) and to form homo- and heteromers.

20 recursors and mature receptors exist as homo/heteromers.

21 acted the reduction of striatal A(2A)R-D(2)R heteromers.

22 compared with other KCNQ channels or KCNQ2/3 heteromers.

23 iants have a similar propensity to form homo/heteromers.

24 in the plasma membrane to form homo- and/or heteromers.

25 it arrangement of six- to eight-subunit core heteromers.

26 ed with those of KCNQ4 homomers and KCNQ2/Q3 heteromers.

27 T7-containing hexamers to generate octameric heteromers.

28 2 cells contain both hexameric and octameric heteromers.

29 helial A549 cells, can form homo- as well as heteromers.

30 , we show that AT1R and CB(1)R form receptor heteromers.

31 udy showing that TPCs are capable of forming heteromers.

32 eloped to target previously undruggable GPCR heteromers.

33 abolishes the desensitization of GluK1/GluK5 heteromers.

34 pe dictated the ATP regulatory properties of heteromers.

35 stin1 recruitment through binding to CB1-D2L heteromers.

36 d interaction or the signaling properties of heteromers.

37 ed by the unique IP3 binding affinity of the heteromers.

38 mbrane signaling, but precisely how receptor heteromers affect receptor pharmacology remains largely

39 ermore, promoting degradation of the DOR/MOR heteromer after the right shift in the ED50 had occurred

40 tion showed de novo appearance of Sur1-Trpm4 heteromers after spinal cord injury in rats.

41 ive effect of DPDPE in vivo, and the DOR-KOR heteromer agonist 6'-GNTI inhibited adenylyl cyclase act

42 chanism showed that formation of GHSR1a:DRD2 heteromers allosterically modifies canonical DRD2 dopami

43 genetic evidence for the importance of Btnl heteromers also applied to the steady-state, since susta

44 MT2/5-HT2C heteromers amplified the 5-HT-mediated Gq/phospholipase

45 signaling through Galphaq or through a D1/D2 heteromer and challenge the existence of such a signalin

46 and CB1 receptors are capable of (i) forming heteromers and (ii) whether such heteromers could exhibi

47 nd a significant upregulation of AT1R-CB(1)R heteromers and enhancement of angiotensin II-mediated si

48 , reduces the desensitization of GluK1/GluK2 heteromers and fully abolishes the desensitization of Gl

49 ing (7TM) receptors/GPCRs can form homo- and heteromers and initiate distinct signaling pathways.

50 es of recombinant ASIC1a homomers, ASIC1a/2a heteromers and native ASICs from sensory neurons to 1 ms

51 Data from overexpressed Kv7.2/Kv7.3 heteromers and native M currents in dorsal root ganglion

52 ions bind to the dimer interface of GluK2/K5 heteromers and slow their desensitization.

53 existence of functionally unique MT2/5-HT2C heteromers and suggest that the antidepressant agomelati

54 enopus oocytes, we observed the formation of heteromers and their coexistence with homomers by electr

55 essed somatodendritic receptors (alpha1/beta heteromers) and showed similar clustering and pharmacolo

56 ot exhibit selective activation of D(1)-D(2) heteromers, and its significant cross-reactivity to othe

57 and D(3) receptors to form both homomers and heteromers, and show that in cells expressing each subty

58 e currently no ligands selective for DOR/MOR heteromers, and, consequently, their role in nociception

59 its activity is blocked by the muOR-deltaOR heteromer antibody.

60 s in the same cell type: LRRC8A/D-containing heteromers appear to dominate release of uncharged osmol

61 dition, when both ISA1 homomer and ISA1/ISA2 heteromer are present.

62 iometry and arrangement within this putative heteromer are so far unknown.

63 interactions, we now show that Kv7.4/Kv.7.5 heteromers are endogenously expressed in vascular smooth

64 A receptor (A2AR)-dopamine D2 receptor (D2R) heteromers are key modulators of striatal neuronal funct

65 Based on the observation that heteromers are less active than BAFF, we speculate that

66 ilin (BTN) and butyrophilin-like (BTNL/Btnl) heteromers are major regulators of human and mouse gamma

67 Heteromers are observed for MORF protein combinations af

68 CRF1R-OX1R heteromers are the conduits of a negative crosstalk betw

69 We conclude that ASIC1a, ASIC2a, and ASIC3 heteromers are the principle channels in skeletal muscle

70 CB1R-5-HT2AR heteromers are thus good targets to dissociate the cogni

71 uOR) and the delta opioid receptor (deltaOR) heteromer as a credible novel target in pain management

72 , using the GABA(B) receptor and Girk1/Girk2 heteromer as a model system.

73 rich cytoplasmic loops within the ZIP6/ZIP10 heteromer as a novel scaffold for GSK3 binding.

74 This study supports the MOR-CCR5 heteromer as a novel target for the treatment of chronic

75 explained by a model that considers A2AR-D2R heteromers as heterotetramers, constituted by A2AR and D

76 Together, these findings define HER2-CB(2)R heteromers as new potential targets for antitumor therap

77 xpressed TRPC5 homomers but also TRPC1:TRPC5 heteromers as well as native TRPC5-like currents in the

78 fied the quaternary structure of the D1R-D3R heteromer, as demonstrated by complementation of hemipro

79 gnificant reduction of striatal A(2A)R-D(2)R heteromers, as demonstrated by the AlphaLISA-based metho

80 ression of Sur1 and Trpm4 yielded Sur1-Trpm4 heteromers, as shown in experiments with Forster resonan

81 es recombinant ASIC1a homomers and ASIC1a/2a heteromers, as well as native ASICs of sensory neurons,

82 ral principles governing ligand recognition, heteromer assembly, ion permeation and desensitization i

83 ctively activates and stabilizes the DOR/MOR heteromer at the cell surface by blocking its endocytosi

84 of M2-M2 and M3-M3 homomers alongside M2-M3 heteromers at the surface of stably transfected Flp-In(T

85 aptic glycine receptors (GlyRs) as alphabeta heteromers attract considerable research attention, litt

86 f the JCI, Cai and collaborators reveal that heteromers between GalR1 and MOR in the rat ventral tegm

87 isassembled to allow the formation of enzyme heteromers between sequentially acting medial-Golgi enzy

88 affold for the development of a unique type (heteromer-biased) of drug that is more potent and withou

89 mation of functional MT2 and 5-HT2C receptor heteromers both in transfected cells and in human cortex

90 d surface expression of CXCR4 and PAR1:CXCR4 heteromers, but not of PAR1.

91 GPR55 and CB1 receptors can form heteromers, but the internalization of both receptors is

92 unsuspected allosteric mechanisms within the heteromer by which not only A2AR agonists, but also A2AR

93 an allosteric modulation within the A2AR-D2R heteromer, by which adenosine decreases the affinity and

94 The MOR-Gal1R heteromer can explain previous results showing antagonis

95 ing properties, and that modulation of these heteromers can modify the antitumoral activity of cannab

96 ctively, and furthermore that different Btnl heteromers can seemingly shape different intestinal gamm

97 ce expression of PAR1, CXCR4, and PAR1:CXCR4 heteromers, chemokine (CXC motif) ligand 12 stimulation

98 ch subtype a complex mixture of homomers and heteromers co-exists at steady state.

99 ne the intriguing possibility that different heteromer combinations comprise channels with different

100 agonist orexin A to regulate the CB(1)-OX(1) heteromer compared with the OX(1)-OX(1) homomer present

101 exhibits high G-protein activity at mu-delta heteromers compared to the homomeric deltaOR or muOR and

102 These findings support the concept of GPCR heteromer complexes exhibiting distinct pharmacology, th

103 A and kainate receptor complexes in vivo are heteromers composed of different subunits.

104 tudies defined the functional fingerprint of heteromers composed of G(i) -coupled melatonin MT(2) rec

105 with a number of subunits >/=6, and that the heteromer composition depends on the relative expression

106 nd CD experiments identified 4F-Abeta(M1-42) heteromers comprised of unstructured Abeta(M1-42) and he

107 and mu opioid receptors (MOR) can complex as heteromers, conferring functional properties in agonist

108 ) coupling, whereas a low ratio destabilizes heteromer conformation, restoring GHS-R1a-Galpha(q11) co

109 ng an established model system of a receptor heteromer consisting of mu and delta opioid receptors.

110 diphosphate synthase, mammalian cis-PT is a heteromer consisting of NgBR (Nus1) and hCIT (dehydrodol

111 Heteromers consisting of one APRIL and two BAFF (ABB) bi

112 Similar to APRIL, heteromers consisting of one BAFF and two APRILs (BAA) b

113 cific characteristic of CB(1)-CB(2) receptor heteromers consists of both the ability of CB(1) recepto

114 or a tetrameric stoichiometry of the D1R-D3R heteromer, constituted by two interacting D1R and D3R ho

115 These receptors are obligate heteromers containing glycine- and glutamate-binding sub

116 ncer cells, and that the expression of these heteromers correlates with poor patient prognosis.

117 as a heteromer, the possibility that such a heteromer could be a target in vivo was addressed by the

118 Previous studies suggested that this heteromer could be involved in the ability of D3R agonis

119 onclusion, antagonists selective for DOR/MOR heteromer could provide an avenue for alleviating reduce

120 (i) forming heteromers and (ii) whether such heteromers could exhibit novel signaling patterns.

121 DA neuron GIRK channel subtype (GIRK2/GIRK3 heteromer) could represent a promising therapeutic targe

122 nted biochemical properties of the MOR-Gal1R heteromer, could then be identified in situ in slices of

123 iously identified agonist targeting mu-delta heteromers, CYM51010.

124 de a molecular basis for the pivotal role of heteromer-dependent signal integration in pathology.

125 with a drug that promotes degradation of the heteromer did not.

126 ies, but the molecular mechanisms underlying heteromer-directed selectivity remain elusive.

127 so a potential target for the development of heteromer-directed therapies to treat allergic diseases.

128 The heteromer displayed specific pharmacological characteris

129 novel function of platelet-derived chemokine heteromers during ALI and demonstrate means for therapeu

130 iven transitions between enzyme homomers and heteromers during their trafficking within the early sec

131 itization and fast deactivation of ASIC1a/2a heteromers enables them to sustain postsynaptic response

132 In GluK2/GluK5 heteromers, enhanced permeation is due to a single proli

133 ting with Gq proteins, cell-surface D1-mGlu5 heteromers exacerbated PLC signaling and intracellular c

134 low potency for the mu-opioid-Gal1 receptor heteromer, exemplified by methadone.

135 However, R1aR2 heteromers exhibited increased cell surface stability co

136 We also showed that the heteromer exhibits restricted distribution in the brain

137 en together, these data suggest that DOR-KOR heteromers exist in rat primary sensory neurons and that

138 Within CB(1)-CB(2) receptor heteromers expressed in a neuronal cell model, agonist c

139 and motor learning deficits and the loss of heteromer expression.

140 ajor functional K(v)1.2 channel complexes: a heteromer, for which kappaM-RIIIJ has high affinity, and

141 A high ratio enhances heteromer formation and Galpha(i/o) coupling, whereas a

142 provides the first example of ligand-induced heteromer formation in GPCR class B.

143 ide antagonist disrupting platelet chemokine heteromer formation in mouse models of ALI.

144 The degree of A(2A)R-D(2)R heteromer formation in schizophrenia might constitute a

145 s signaling of the interacting receptor, and heteromer formation leads to a switch in G-protein coupl

146 to adiponectin was delayed in cells wherein heteromer formation was favored.

147 tics of wild-type prestin is not affected by heteromer formation with V499G/Y501H prestin.

148 Direct evidence for Kv7.4/7.5 heteromer formation, however, is lacking.

149 NMDA receptors are obligate heteromers formed by coassembly of two or three divergen

150 Using Sod1-KD cells we found that the WT-A4V heteromers formed higher molecular weight species compar

151 However, ASIC1a/2 heteromers gave robust responses when using a baseline p

152 These results indicate that the Kv7.2/Kv7.3 heteromer generated by cells expressing approximately eq

153 ized in the tetramerization domain prevented heteromer generation and resulted in the formation of ho

154 suggests that targeting of specific putative heteromers has the potential to identify leads for analg

155 GPCR homomers or heteromers have been explored widely for GPCR classes A

156 D1/D2 heteromers have been proposed as relevant to the pathoph

157 al and behavioral relevance for the proposed heteromers have not yet been established.

158 he specific location and properties of these heteromers have remained largely unknown.

159 acts by bridging the protomers of a MOR-CCR5 heteromer having a TM5,6 interface.

160 L compartments, with combinatorially diverse heteromers having differential impacts on different IEL

161 ifically, our data unveil that the A2AR-CB1R heteromer (i) is essentially absent from corticostriatal

162 lizing the G protein-coupled receptor (GPCR) heteromer identification technology on the live cell-bas

163 ggest an anti-analgesic role for the DOR/MOR heteromer in pain.

164 is to establish optimal levels of transducin heteromer in the outer segment, thereby indirectly contr

165 pled receptors (GPCRs) can form homomers and heteromers in addition to functioning as single monomers

166 work for understanding the role of PC-1/PC-2 heteromers in ADPKD and suggest new therapeutic strategi

167 Here we show that CB2R and GPR55 form heteromers in cancer cells, that these structures posses

168 native receptors are thought to assemble as heteromers in complex with auxiliary proteins, our data

169 on through targeting CB(1)-5-HT(2A) receptor heteromers in HEK293 cells and using an array of biochem

170 INTA) strongly activated KOR-DOR and KOR-MOR heteromers in HEK293 cells.

171 s to identify and functionally evaluate GPCR heteromers in heterologous cells, with recent approaches

172 The two chemokines were found to form heteromers in human and murine ALI samples, positively c

173 FRET established the presence of GHSR1a:DRD2 heteromers in hypothalamic neurons.

174 evidence that mGlu receptors can function as heteromers in intact brain circuits.

175 Disruption of CCL5-CXCL4 heteromers in LPS-, acid-, and sepsis-induced ALI abolis

176 a mechanism that required their assembly as heteromers in mammalian cells.

177 as implemented to detect native A(2A)R-D(2)R heteromers in mouse and human brain.

178 Evidence for DOR-KOR heteromers in peripheral sensory neurons included coimmu

179 that allowed a precise visualization of the heteromers in situ in combination with sophisticated gen

180 led functional characterization of A2AR-CB1R heteromers in the dorsal striatum.

181 itions between B4GALT1 and ST6GAL1 homo- and heteromers in the Golgi, and cooperative B4GALT1/ST6GAL1

182 that they function as enzyme homomers and/or heteromers in the living cell.

183 trate constitutive formation of GHS-R1a:SST5 heteromers in which ghrelin, but not SST, suppresses GSI

184 GluA1A2 heteromers in which the ATD of GluA1 is absent fail to t

185 nce that these mutants were expressed in the heteromers includes shifted TEA sensitivity compared wit

186 g the presence of cell surface D(2long)-D(3) heteromers, individual clones were assessed for levels o

187 Nonetheless, heteromer interactions of p75(NTR) with TrkA increase fu

188 -M2 homomer interactions but decreased M2-M3 heteromer interactions.

189 ficantly alter either M3-M3 homomer or M2-M3 heteromer interactions.

190 dues from two defective protomers across the heteromer interface.

191 e dopamine D1 receptor-D3 receptor (D1R-D3R) heteromer is being considered as a potential therapeutic

192 We demonstrate that the D(1)R-H(3)R heteromer is expressed in HD mice at early but not late

193 the basis of the possibility that a MOR-CCR5 heteromer is involved in such cross-talk, we have synthe

194 n coupling and the formation of GHS-R1a:SST5 heteromers is dependent on the ratio of ghrelin to SST.

195 demonstrate that the activity of TRPA1-TRPV1 heteromers is governed by Tmem100 and that disabling Tme

196 also suggest that the stoichiometry of LRRC8 heteromers is variable, with a number of subunits >/=6,

197 of surface GluA1-containing AMPARs (GluA1A2 heteromers), leaving a small residual pool of synaptic G

198 hin-1, demonstrating a key role of MOR-Gal1R heteromers localized in the VTA in the direct control of

199 hondria as well, suggesting that the NS1-NS2 heteromer localizes to the mitochondria.

200 ent control circuit for this regulon where a heteromer made up of the transcription regulators Ifh1 (

201 her these results suggest that the MOR-SSTR2 heteromer may constitute a novel therapeutic target for

202 The GPR55-CB1R heteromer may play an important physiological and/or pat

203 onociceptive, and that drugs that spare such heteromers may also induce reduced tolerance.

204 Because of these differences, DOR/MOR heteromers may be a novel therapeutic target in the trea

205 ORco, the common subunit of odorant receptor heteromers, may allosterically alter olfactory receptor

206 uced previous findings indicating that LRRC8 heteromers mediate anion and osmolyte flux with subunit-

207 Additionally, we found that LRRC8 heteromers mediate glutamate and ATP flux and that the i

208 results suggest that mu-opioid-Gal1 receptor heteromers mediate the dopaminergic effects of opioids t

209 The discovery of D1-mGlu5 functional heteromers mediating maladaptive molecular and motor res

210 Therefore the CRTH2/DP heteromer might not only represent a functional signalin

211 These heteromers might participate in the in vivo effects of a

212 ystem and have been reported to associate as heteromer (MOP-CB1) in cultured cells, the possibility o

213 e known structures, this rotor ring is a 9:1 heteromer of F- and V-type c-subunits and therefore feat

214 directly induces itch by signaling through a heteromer of opioid- and itch-mediating G protein-couple

215 However, heteromers of BAFF and APRIL that occur in patients with

216 ution of function approach both homomers and heteromers of D(2long) and D(3) receptors were shown to

217 or Galpha11 protein coupling to homomers or heteromers of D1 or D2 receptors using a variety of bios

218 In conclusion, BAFF-APRIL heteromers of different stoichiometries have distinct re

219 e synaptic response in cb3a/b cells and were heteromers of GluK1 and GluK5.

220 hat VRACs are formed by differently composed heteromers of LRRC8 proteins.

221 VRACs are formed by heteromers of LRRC8 proteins; LRRC8A (also called SWELL1

222 Recent work has shown that heteromers of LRRC8A with other LRRC8 members (B, C, D,

223 We also discuss preliminary evidence that heteromers of the delta opioid receptor and the MOR are

224 synaptic plasticity, predominantly exist as heteromers of the subunits GluA1 to GluA4.

225 her, our results indicate that D(1)R - H(3)R heteromers play a pivotal role in dopamine signaling and

226 fic properties that either facilitate septin heteromer polymerization along microtubules or modulate

227 lexibility' of the NTD not only explains why heteromers predominate but also how GluA2-lacking, Ca(2+

228 While the prevalent adult forms of GlyRs are heteromers, previous reports suggested functional alpha

229 Finally, MT2/5-HT2C heteromers provide a new strategy for the discovery of n

230 tified tissue-specific repertoires of septin heteromers provide insights into how higher-order septin

231 l subtype in VTA DA neurons, the GIRK2/GIRK3 heteromer, regulates the sensitivity of the mouse mesoli

232 c septin paralogue expression may shape core heteromer repertoires and thereby modulate properties of

233 Among the many heteromers reported in the opioid receptor family are mu

234 Thus, the muOR-deltaOR heteromer represents a potentially unique target for the

235 vestigated how ASIC1a homomers and ASIC1a/2a heteromers respond to brief stimuli, jumping from pH 8.0

236 These SMN protein heteromers restore snRNP assembly of Sm proteins onto sn

237 Relief of polyamine block in GluK2/GluK5 heteromers results from a key proline residue that produ

238 munoprecipitation of DOR with KOR, a DOR-KOR heteromer selective antibody augmented the antinocicepti

239 gy transfer assays, as well as receptor- and heteromer-selective antibodies, we show that AT1R and CB

240 ly, characterization of a putative D(1)-D(2) heteromer-selective ligand, 6-chloro-2,3,4,5-tetrahydro-

241 s dissociate in response to adiponectin, but heteromers separate faster than homomers.

242 nal transduction from the stabilized DOR/MOR heteromer, shifted the ED50 for analgesia back to the le

243 The results also indicate that MOR-Gal1R heteromers should be viewed as targets for the treatment

244 th SEPT2/6/7, the minimal subunits of septin heteromers, shows that SEPT2/6/7 has a biphasic concentr

245 R antagonist properties, was identified as a heteromer-specific-biased agonist exhibiting partial ago

246 ignaling pathways, and may not be completely heteromer-specific.

247 Although AMPARs act predominantly as heteromers, structural studies have focused on homomeric

248 Here we report the first AMPAR heteromer structures, which deviate substantially from e

249 igation experiments identified novel CB1-Smo heteromers, suggesting allosteric CB1-Smo interactions.

250 utants are more sensitive to DH-CBD than are heteromers, suggesting presynaptic GlyRs as a primary ta

251 der a physiological pH of 7.4 with ASIC1a/2a heteromers, suggesting that they may sustain postsynapti

252 In AMPA receptor heteromers, TARP stoichiometry further modifies these ac

253 Xenopus oocytes expressing the Kir3.1/Kir3.4 heteromer that underlies I(K,ACh).

254 studies, we show that CB1R and 5-HT2AR form heteromers that are expressed and functionally active in

255 cate that AdipoR1 and AdipoR2 form homo- and heteromers that present unique interaction behaviors and

256 EPOR and the ss-common receptor (CD131) form heteromers (the innate repair receptor; IRR), and exert

257 5 receptors in cultured cells associate as a heteromer, the possibility that such a heteromer could b

258 By forming both homomers and heteromers, the hdeltaOR-Cys-27 variant may thus regulat

259 ndicating the involvement of MT(2) /5-HT(2C) heteromers. The antidepressant agomelatine had a similar

260 are able to bind each other as homomers and heteromers, they are structurally plastic and can exert

261 fication of compounds targeting muOR-deltaOR heteromers through high-throughput screening of a small-

262 ntrast, in S. cerevisiae, the linkage of the heteromer to Rap1 occurs through Ifh1.

263 hen channels were effectively converted from heteromers to 1a homomers by expressing a fragment corre

264 ur results based on the resistance of LRP5-6 heteromers to a selective inhibitor of E1/2-binding Wnt-

265 auditory brainstem are more vulnerable than heteromers to hyperekplexia mutation-induced impairment.

266 we explored the kinetics of ASIC1a and 1a/2a heteromers to such brief pH transients over a wider [H(+

267 nits to yield both 2:1 and 1:2 ASIC1a:ASIC2a heteromers together with ASIC1a and ASIC2a homomers.

268 In all TRPC1-containing heteromers, TRPC1 subunits significantly decreased calci

269 During this relocation, heteromers undergo a reverse transition back to enzyme h

270 dance of evidence demonstrating that KCNQ2/3 heteromers underlie critical potassium conductances, it

271 We have documented an LRP5-6 heteromer using immiscible filtration assisted by surfac

272 e numbers, and localization of AIS Kv7.2/7.3 heteromers using live imaging.

273 The heteromer was inhibited by extracellular acidification a

274 The heteromer was isolated through binding of either tag to

275 The existence of homo/heteromers was confirmed in living cells by bioluminesce

276 nerate detectable cell surface D(2long)-D(3) heteromers was defined.

277 ant and pronounced reduction of A(2A)R-D(2)R heteromers was next demonstrated in postmortem caudate n

278 nces in inactivation between different LRRC8 heteromers, we now used chimeras assembled from isoforms

279 Such homomers and heteromers were found to co-exist and using a reconstitu

280 nnels, the KA1 and KA2 subunits are obligate heteromers which function only in combination with GluR5

281 of allosteric modulations within the D1R-D3R heteromer, which can be involved with the reported behav

282 as adaptors to transactivate the Gbetagamma heteromers, which then act responsible for cell activati

283 duces a protein isoform, P2X7L, that forms a heteromer with P2X7A.

284 2 (mGlu2) receptor to be assembled as a GPCR heteromer with the serotonin 5-hydroxytryptamine 2A (5-H

285 wn whether AdipoR2 may also form homomers or heteromers with AdipoR1 or if such interactions may be f

286 ovide the first evidence that GPR55 can form heteromers with another 7TM/GPCR and that this interacti

287 we discovered that CB(2) receptors can form heteromers with CB(1) receptors in transfected neuronal

288 Also, CXCR4 forms heteromers with CC chemokine receptor (CCR) 2, CCR5, the

289 We show that HCMV-encoded UL33 and UL78 form heteromers with CCR5 and CXCR4 chemokine receptors in tr

290 e devised protocols to analyze native septin heteromers with distinct numbers of subunits.

291 es contain functional HAS2 homomers and also heteromers with HAS3.

292 nmrASIC3 forms functional, proton-sensitive heteromers with other ASIC subunits.

293 ant population of these MORs form functional heteromers with the galanin receptor subtype Gal1 (Gal1R

294 There is evidence that DOR can form heteromers with the kappa-opioid receptor (KOR).

295 We also show that V499G/Y501H prestin forms heteromers with wild-type prestin and that the fast moto

296 been explained in terms of the formation of heteromers with, for example, distinct signaling propert

297 yloid (Abeta) peptides coexist as neurotoxic heteromers within the plaques.

298 her's signaling properties and form CRTH2/DP heteromers without altering their ligand-binding capacit

299 to selectively target putative kappa opioid heteromers without recruiting beta-arrestin upon activat

300 ents from NMDA receptors, which are obligate heteromers, yielded channels made up of A/C and B/D subu