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1 se-type starch-debranching enzyme (ISA1/ISA2 heteromer).
2 the series that bridges the protomers of the heteromer.
3 idging of protomers in a putative MOR-mGluR5 heteromer.
4 study the pharmacology and signaling by this heteromer.
5 ranching enzyme activity present is ISA1/ISA heteromer.
6 for the unique behavioral function of a GPCR heteromer.
7 actions between the protomers of the DOR-KOR heteromer.
8 rrestin recruitment at the alpha(1A)AR-CXCR2 heteromer.
9 he A(2A) receptor in the A(2A)-D(2) receptor heteromer.
10 ternary structure and function of a receptor heteromer.
11 respect to the individual components of the heteromer.
12 sigma1R) also associates with the CRF1R-OX1R heteromer.
13 , was consistent with the activation of both heteromers.
14 neurons due to the fast kinetics of GluA2A3 heteromers.
15 -V relation of EPSCs mediated by GluA1/GluA2 heteromers.
16 ng a small residual pool of synaptic GluA2A3 heteromers.
17 plasmic reticulum (ER) and to form homo- and heteromers.
18 pe dictated the ATP regulatory properties of heteromers.
19 stin1 recruitment through binding to CB1-D2L heteromers.
20 recursors and mature receptors exist as homo/heteromers.
21 compared with other KCNQ channels or KCNQ2/3 heteromers.
22 iants have a similar propensity to form homo/heteromers.
23 in the plasma membrane to form homo- and/or heteromers.
24 it arrangement of six- to eight-subunit core heteromers.
25 ed with those of KCNQ4 homomers and KCNQ2/Q3 heteromers.
26 T7-containing hexamers to generate octameric heteromers.
27 2 cells contain both hexameric and octameric heteromers.
28 helial A549 cells, can form homo- as well as heteromers.
29 , we show that AT1R and CB(1)R form receptor heteromers.
30 udy showing that TPCs are capable of forming heteromers.
31 rved in cells expressing A(2A)-D(2) receptor heteromers.
32 eteromer is one of the most studied receptor heteromers.
33 sembly conformations are KCNQ3/4 and KCNQ4/5 heteromers.
34 This is similar to that of recombinant heteromers.
35 t ([K68A] or [K299A]) produced no functional heteromers.
36 d interaction or the signaling properties of heteromers.
37 ed by the unique IP3 binding affinity of the heteromers.
38 till lagging behind for the majority of GPCR heteromers.
39 ivation of the 5-HT2C protomer of MT2/5-HT2C heteromers.
40 nin MT2 and 5-HT2C receptors into functional heteromers.
41 mbrane signaling, but precisely how receptor heteromers affect receptor pharmacology remains largely
42 ermore, promoting degradation of the DOR/MOR heteromer after the right shift in the ED50 had occurred
44 ive effect of DPDPE in vivo, and the DOR-KOR heteromer agonist 6'-GNTI inhibited adenylyl cyclase act
45 chanism showed that formation of GHSR1a:DRD2 heteromers allosterically modifies canonical DRD2 dopami
47 signaling through Galphaq or through a D1/D2 heteromer and challenge the existence of such a signalin
48 and CB1 receptors are capable of (i) forming heteromers and (ii) whether such heteromers could exhibi
49 nd a significant upregulation of AT1R-CB(1)R heteromers and enhancement of angiotensin II-mediated si
50 entral horn neurones in the juvenile rat are heteromers and have fast gating, similar to that of reco
51 ing (7TM) receptors/GPCRs can form homo- and heteromers and initiate distinct signaling pathways.
52 ransfection of AKAP79 to "sensitize" KCNQ2/3 heteromers and KCNQ2-5, but not KCNQ1, homomers to musca
53 es of recombinant ASIC1a homomers, ASIC1a/2a heteromers and native ASICs from sensory neurons to 1 ms
56 existence of functionally unique MT2/5-HT2C heteromers and suggest that the antidepressant agomelati
57 enopus oocytes, we observed the formation of heteromers and their coexistence with homomers by electr
58 essed somatodendritic receptors (alpha1/beta heteromers) and showed similar clustering and pharmacolo
59 ot exhibit selective activation of D(1)-D(2) heteromers, and its significant cross-reactivity to othe
60 and D(3) receptors to form both homomers and heteromers, and show that in cells expressing each subty
61 e currently no ligands selective for DOR/MOR heteromers, and, consequently, their role in nociception
63 s in the same cell type: LRRC8A/D-containing heteromers appear to dominate release of uncharged osmol
65 any of the individual receptor units in the heteromer are different from those obtained during coact
68 interactions, we now show that Kv7.4/Kv.7.5 heteromers are endogenously expressed in vascular smooth
69 A receptor (A2AR)-dopamine D2 receptor (D2R) heteromers are key modulators of striatal neuronal funct
73 st to prevailing views, we find that GluA1A2 heteromers are the dominant AMPARs at CA1 cell synapses
74 We conclude that ASIC1a, ASIC2a, and ASIC3 heteromers are the principle channels in skeletal muscle
79 explained by a model that considers A2AR-D2R heteromers as heterotetramers, constituted by A2AR and D
80 xpressed TRPC5 homomers but also TRPC1:TRPC5 heteromers as well as native TRPC5-like currents in the
81 fied the quaternary structure of the D1R-D3R heteromer, as demonstrated by complementation of hemipro
82 ression of Sur1 and Trpm4 yielded Sur1-Trpm4 heteromers, as shown in experiments with Forster resonan
83 es recombinant ASIC1a homomers and ASIC1a/2a heteromers, as well as native ASICs of sensory neurons,
84 e portion of receptors engaging in homo- and heteromers, as well as the effect of persistent receptor
85 ral principles governing ligand recognition, heteromer assembly, ion permeation and desensitization i
86 ctively activates and stabilizes the DOR/MOR heteromer at the cell surface by blocking its endocytosi
87 of M2-M2 and M3-M3 homomers alongside M2-M3 heteromers at the surface of stably transfected Flp-In(T
88 aptic glycine receptors (GlyRs) as alphabeta heteromers attract considerable research attention, litt
89 isassembled to allow the formation of enzyme heteromers between sequentially acting medial-Golgi enzy
90 affold for the development of a unique type (heteromer-biased) of drug that is more potent and withou
91 mation of functional MT2 and 5-HT2C receptor heteromers both in transfected cells and in human cortex
94 unsuspected allosteric mechanisms within the heteromer by which not only A2AR agonists, but also A2AR
95 an allosteric modulation within the A2AR-D2R heteromer, by which adenosine decreases the affinity and
97 onstrate that some neurotransmitter receptor heteromers can exert an effect as processors of computat
99 ing properties, and that modulation of these heteromers can modify the antitumoral activity of cannab
101 ne the intriguing possibility that different heteromer combinations comprise channels with different
102 agonist orexin A to regulate the CB(1)-OX(1) heteromer compared with the OX(1)-OX(1) homomer present
103 ce in receptor trafficking properties of the heteromers compared with their homomeric counterparts.
104 These findings support the concept of GPCR heteromer complexes exhibiting distinct pharmacology, th
106 ies have demonstrated that I Kr channels are heteromers composed of both hERG 1a and 1b subunits, yet
108 with a number of subunits >/=6, and that the heteromer composition depends on the relative expression
109 and mu opioid receptors (MOR) can complex as heteromers, conferring functional properties in agonist
110 ) coupling, whereas a low ratio destabilizes heteromer conformation, restoring GHS-R1a-Galpha(q11) co
111 ng an established model system of a receptor heteromer consisting of mu and delta opioid receptors.
112 diphosphate synthase, mammalian cis-PT is a heteromer consisting of NgBR (Nus1) and hCIT (dehydrodol
115 cific characteristic of CB(1)-CB(2) receptor heteromers consists of both the ability of CB(1) recepto
116 or a tetrameric stoichiometry of the D1R-D3R heteromer, constituted by two interacting D1R and D3R ho
118 as a heteromer, the possibility that such a heteromer could be a target in vivo was addressed by the
120 onclusion, antagonists selective for DOR/MOR heteromer could provide an avenue for alleviating reduce
122 nted biochemical properties of the MOR-Gal1R heteromer, could then be identified in situ in slices of
123 de a molecular basis for the pivotal role of heteromer-dependent signal integration in pathology.
126 so a potential target for the development of heteromer-directed therapies to treat allergic diseases.
128 novel function of platelet-derived chemokine heteromers during ALI and demonstrate means for therapeu
129 iven transitions between enzyme homomers and heteromers during their trafficking within the early sec
130 itization and fast deactivation of ASIC1a/2a heteromers enables them to sustain postsynaptic response
134 en together, these data suggest that DOR-KOR heteromers exist in rat primary sensory neurons and that
139 s signaling of the interacting receptor, and heteromer formation leads to a switch in G-protein coupl
146 These results indicate that the Kv7.2/Kv7.3 heteromer generated by cells expressing approximately eq
147 ized in the tetramerization domain prevented heteromer generation and resulted in the formation of ho
148 momers or 1a/3 heteromers), whereas ASIC2a/3 heteromers give much larger currents than ASIC3 homomers
149 suggests that targeting of specific putative heteromers has the potential to identify leads for analg
155 ifically, our data unveil that the A2AR-CB1R heteromer (i) is essentially absent from corticostriatal
156 lizing the G protein-coupled receptor (GPCR) heteromer identification technology on the live cell-bas
159 is to establish optimal levels of transducin heteromer in the outer segment, thereby indirectly contr
160 pled receptors (GPCRs) can form homomers and heteromers in addition to functioning as single monomers
162 native receptors are thought to assemble as heteromers in complex with auxiliary proteins, our data
164 s to identify and functionally evaluate GPCR heteromers in heterologous cells, with recent approaches
169 taneously visualize A(2A) and D(2) homo- and heteromers in living cells and to examine drug-induced c
172 that allowed a precise visualization of the heteromers in situ in combination with sophisticated gen
175 tSUN1 and AtSUN2 are present as homomers and heteromers in vivo, and that the coiled-coil domains are
176 trate constitutive formation of GHS-R1a:SST5 heteromers in which ghrelin, but not SST, suppresses GSI
178 nce that these mutants were expressed in the heteromers includes shifted TEA sensitivity compared wit
179 g the presence of cell surface D(2long)-D(3) heteromers, individual clones were assessed for levels o
180 rated that immunization with the native MSP1 heteromer induced strong immunoglobulin G (IgG) response
185 e dopamine D1 receptor-D3 receptor (D1R-D3R) heteromer is being considered as a potential therapeutic
186 the basis of the possibility that a MOR-CCR5 heteromer is involved in such cross-talk, we have synthe
187 The adenosine A(2A)-dopamine D(2) receptor heteromer is one of the most studied receptor heteromers
188 The existence of neurotransmitter receptor heteromers is becoming broadly accepted and their functi
189 n coupling and the formation of GHS-R1a:SST5 heteromers is dependent on the ratio of ghrelin to SST.
190 demonstrate that the activity of TRPA1-TRPV1 heteromers is governed by Tmem100 and that disabling Tme
191 also suggest that the stoichiometry of LRRC8 heteromers is variable, with a number of subunits >/=6,
192 of surface GluA1-containing AMPARs (GluA1A2 heteromers), leaving a small residual pool of synaptic G
193 hin-1, demonstrating a key role of MOR-Gal1R heteromers localized in the VTA in the direct control of
195 ent control circuit for this regulon where a heteromer made up of the transcription regulators Ifh1 (
196 cific physiological response produced by the heteromer may be directly attributed to a difference in
197 her these results suggest that the MOR-SSTR2 heteromer may constitute a novel therapeutic target for
202 uced previous findings indicating that LRRC8 heteromers mediate anion and osmolyte flux with subunit-
205 ystem and have been reported to associate as heteromer (MOP-CB1) in cultured cells, the possibility o
208 e known structures, this rotor ring is a 9:1 heteromer of F- and V-type c-subunits and therefore feat
209 directly induces itch by signaling through a heteromer of opioid- and itch-mediating G protein-couple
210 Multiple lines of evidence indicate that a heteromer of PS-derived N- and C-terminal fragments func
212 ution of function approach both homomers and heteromers of D(2long) and D(3) receptors were shown to
213 or Galpha11 protein coupling to homomers or heteromers of D1 or D2 receptors using a variety of bios
218 We also discuss preliminary evidence that heteromers of the delta opioid receptor and the MOR are
219 en identified that selectively target opioid heteromers of the delta-opioid receptor with the kappa a
220 s associated with antibodies against NR1-NR2 heteromers of the NMDA receptor was recently identified.
221 Antibodies to NR2B- and NR2A-containing heteromers of the NMDAR associate with a severe but trea
223 fic properties that either facilitate septin heteromer polymerization along microtubules or modulate
224 lexibility' of the NTD not only explains why heteromers predominate but also how GluA2-lacking, Ca(2+
225 While the prevalent adult forms of GlyRs are heteromers, previous reports suggested functional alpha
227 tified tissue-specific repertoires of septin heteromers provide insights into how higher-order septin
228 in isolated CB cells, and that the TASK-1/3 heteromer provides the major part of the oxygen-sensitiv
229 he potential role of the human TAS1R1-TAS1R3 heteromer receptor in umami taste by recording responses
230 l subtype in VTA DA neurons, the GIRK2/GIRK3 heteromer, regulates the sensitivity of the mouse mesoli
231 c septin paralogue expression may shape core heteromer repertoires and thereby modulate properties of
234 vestigated how ASIC1a homomers and ASIC1a/2a heteromers respond to brief stimuli, jumping from pH 8.0
235 Relief of polyamine block in GluK2/GluK5 heteromers results from a key proline residue that produ
236 munoprecipitation of DOR with KOR, a DOR-KOR heteromer selective antibody augmented the antinocicepti
237 gy transfer assays, as well as receptor- and heteromer-selective antibodies, we show that AT1R and CB
238 ly, characterization of a putative D(1)-D(2) heteromer-selective ligand, 6-chloro-2,3,4,5-tetrahydro-
240 nal transduction from the stabilized DOR/MOR heteromer, shifted the ED50 for analgesia back to the le
241 The results also indicate that MOR-Gal1R heteromers should be viewed as targets for the treatment
242 R antagonist properties, was identified as a heteromer-specific-biased agonist exhibiting partial ago
245 utants are more sensitive to DH-CBD than are heteromers, suggesting presynaptic GlyRs as a primary ta
246 der a physiological pH of 7.4 with ASIC1a/2a heteromers, suggesting that they may sustain postsynapti
248 studies, we show that CB1R and 5-HT2AR form heteromers that are expressed and functionally active in
249 strated by the analysis of striatal receptor heteromers that control striatal glutamatergic neurotran
250 cate that AdipoR1 and AdipoR2 form homo- and heteromers that present unique interaction behaviors and
251 agonists or selective activation of receptor heteromers, that directly target the altered neurophysio
252 EPOR and the ss-common receptor (CD131) form heteromers (the innate repair receptor; IRR), and exert
253 5 receptors in cultured cells associate as a heteromer, the possibility that such a heteromer could b
255 fication of compounds targeting muOR-deltaOR heteromers through high-throughput screening of a small-
257 hen channels were effectively converted from heteromers to 1a homomers by expressing a fragment corre
258 ur results based on the resistance of LRP5-6 heteromers to a selective inhibitor of E1/2-binding Wnt-
259 auditory brainstem are more vulnerable than heteromers to hyperekplexia mutation-induced impairment.
261 we explored the kinetics of ASIC1a and 1a/2a heteromers to such brief pH transients over a wider [H(+
262 nits to yield both 2:1 and 1:2 ASIC1a:ASIC2a heteromers together with ASIC1a and ASIC2a homomers.
266 dance of evidence demonstrating that KCNQ2/3 heteromers underlie critical potassium conductances, it
274 scence complementation reflecting A(2A)/D(2) heteromers was detected at the cell membrane as well as
275 nces in inactivation between different LRRC8 heteromers, we now used chimeras assembled from isoforms
279 curs with ASIC1a (either as homomers or 1a/3 heteromers), whereas ASIC2a/3 heteromers give much large
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 ternary structure of the A(2A)-D(2) receptor heteromer, which was found to depend on the binding of c
283 as adaptors to transactivate the Gbetagamma heteromers, which then act responsible for cell activati
284 We demonstrate that human MTMR6 forms a heteromer with an enzymatically inactive member myotubul
286 2 (mGlu2) receptor to be assembled as a GPCR heteromer with the serotonin 5-hydroxytryptamine 2A (5-H
287 wn whether AdipoR2 may also form homomers or heteromers with AdipoR1 or if such interactions may be f
288 ovide the first evidence that GPR55 can form heteromers with another 7TM/GPCR and that this interacti
289 we discovered that CB(2) receptors can form heteromers with CB(1) receptors in transfected neuronal
290 We show that HCMV-encoded UL33 and UL78 form heteromers with CCR5 and CXCR4 chemokine receptors in tr
294 ant population of these MORs form functional heteromers with the galanin receptor subtype Gal1 (Gal1R
295 elated envelope protein does not assemble in heteromers with the gammaretrovirus glycoproteins tested
297 We also show that V499G/Y501H prestin forms heteromers with wild-type prestin and that the fast moto
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
301 ents from NMDA receptors, which are obligate heteromers, yielded channels made up of A/C and B/D subu
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