ライフサイエンスコーパス: mGluR6

1 ntibodies against G alpha(o), G gamma 13, or mGluR6).

2 or, ELFN1, for trans-synaptic alignment with mGluR6.

3 to two additional family members: mGluR3 and mGluR6.

4 that normally encodes the glutamate receptor mGluR6.

5 ate this cascade because it colocalizes with mGluR6.

6 ting closure of the channel by glutamate and mGluR6.

7 ces in function, express a single isoform of mGluR6.

8 effect mediated by the metabotropic receptor mGluR6.

9 mediated by a signaling cascade comprised of mGluR6, a G-protein containing G(alphao), and the cation

10 utamate, the metabotropic glutamate receptor mGluR6 activates the heterotrimeric G-protein Galphaobet

11 nding to the metabotropic glutamate receptor mGluR6, activating the G-protein G(o1), and closing an u

12 APB (DL-2-amino-4-phosphonobutyric acid), an mGluR6 agonist, blocks normal, short-latency ON response

13 (TTX), the metabotropic glutamate receptor (mGluR6) agonist, 2-amino-4-phosphonobutyric acid (APB),

14 hat were bathed in a solution containing the mGluR6 agonists L-AP4 or glutamate.

15 BCs) require the G-protein-coupled receptor, mGluR6, an intact G-protein-coupled cascade and the tran

16 eceptor pathway involving glutamate receptor mGluR6 and effector channel TRPM1.

17 All ON cone bipolar cells express mGluR6 and G alpha(o), but only a subset expresses Ret-P

18 ritic tips of ON bipolar neurons, along with mGluR6 and Galpha(o1).

19 nd the post-synaptic bipolar cell components mGluR6 and GPR179 become dissociated, suggesting that la

20 istry and had higher expression of PSD95 and mGluR6 and less GFAP expression compared with fellow unt

21 ation of the metabotropic glutamate receptor mGluR6 and the G protein Go.

22 that dendritic transduction cascade members mGluR6 and TRPM1 appear in tips with different timelines

23 be higher than previously reported, and (c) mGluR6 and TRPM1 are trafficked independently during dev

24 by the same bipolar cells that also express mGluR6, and is concentrated at the same subcellular loca

25 ls, and then displacing the agonist with the mGluR6 antagonist (RS)-a-cyclopropyl-4-phosphonophenylgl

26 However, mGluR6 at the photoreceptor-ON bipolar cell synapse medi

27 These findings suggest novel functions of mGluR6 besides sign inversion at ON bipolar cell dendrit

28 The subsequent decline in PSD95 and mGluR6 between 1 and 12 months in Rs1-KO retina mirrors

29 Upon activation of mGluR6 by glutamate released from photoreceptors, a nons

30 ese results suggest that the deactivation of mGluR6 cascade during the light response may require the

31 h RGS7 and RGS11 controls the ability of the mGluR6 cascade to gate TRPM1.

32 a unique macromolecular organization of the mGluR6 cascade, where principal signaling components are

33 ON-bipolar cells, and disrupts postsynaptic mGluR6 clustering.

34 Although association with both R9AP and mGluR6 contributed to the proteolytic stabilization of t

35 Identification of TRPM1 as a mGluR6-coupled cation channel reveals a key step in visi

36 However, mGluR6 E775K (E781K in humans) suggested no trafficking

37 ve use of metabotropic glutamate receptor 6 (mGluR6) expressed in retinal ON bipolar cells.

38 The metabotropic glutamate receptor (mGluR6), expressed by rod bipolar cells and ON cone bipo

39 mGluR6 expression was limited to the outer plexiform lay

40 ing, key cell types, synaptic structure, and mGluR6 expression were all normal, as was the a-wave of

41 RGS1 was coexpressed in Xenopus oocytes with mGluR6, Galpha(o1), and a GIRK (G-protein-gated inwardly

42 s provide new insight into the regulation of mGluR6-Galpha(o) signaling by the RGS11 x Gbeta(5) x R9A

43 Reconstitution of mGluR6-Galpha(o) signaling in Xenopus oocytes indicates

44 Their involvement in the mGluR6/Galpha(o)/TRPM1 pathway that mediates DBC light r

45 gests that Go may be involved in coupling to mGluR6 in ON-bipolar cells.

46 ating the metabotropic glutamate receptor 6 (mGluR6)-initiated ON response.

47 In the ON bipolar cells, mGluR6 inverts the photoreceptor's signal via a cascade

48 G with dystrophin and the glutamate receptor mGluR6 is disrupted, and the post-synaptic bipolar cell

49 ized metabotropic glutamate receptor type 6 (mGluR6) is postsynaptically localized and expressed only

50 nding to the metabotropic glutamate receptor mGluR6, leading to closure of a cation channel.

51 PSD95 and mGluR6 levels were normal at 1 month on Western blot but

52 s possess a metabotropic glutamate receptor (mGluR6) linked to the control of a G-protein and cGMP-ac

53 These results indicate that mGluR6 may signal through G(o), rather than a transducin

54 Consistent with the ERG, the mGluR6-mediated gating of TRPM1 can be evoked pharmacolo

55 PSD95 (postsynaptic density protein), mGluR6 (metabotropic glutamate receptor subtype 6), reti

56 nd ON responses in retinal ganglion cells of mGluR6-null mice, but they occur at long latency.

57 In mGluR6-null mice, long-latency ON responses are observed

58 achurin is no longer closely associated with mGluR6 or alpha-DG in the Lamb2-null.

59 one terminals were marked with antibodies to mGluR6 or synaptic proteins.

60 is currently the only confirmed function of mGluR6, other functions have been suggested.

61 ting endogenous expression of one of the two mglur6 paralogs in zebrafish.

62 sustained signalling, and modulation of the mGluR6 pathway by cGMP allows the RBC to switch between

63 The mGluR6 pathway modulator cGMP sped the rate of RBC depol

64 entify RGS7 and RGS11 as the key GAPs in the mGluR6 pathway of retinal rod ON bipolar cells that set

65 We investigated five known mGluR6 point mutants that lead to CSNB1 to determine the

66 Disruption of mGluR6 prevented targeting of TRPM1 to the postsynaptic

67 fluorescent protein (EGFP), under control of mGluR6 promoter, was expressed in all and only ON bipola

68 ON pathway block with l-AP-4, the mGluR6 receptor agonist, abolished the S-ON response but

69 postsynaptic DBC dendritic tips, whereas the mGluR6 receptor and RGS7 maintained proper synaptic posi

70 es selective for the C-terminus of the human mGluR6 receptor and used confocal and electron microscop

71 voltage or by depolarizing the RBC with the mGluR6 receptor antagonist (R,S)-alpha-cyclopropyl-4-pho

72 of salamander retina with an agonist for the mGluR6 receptor that is expressed on the dendrites of On

73 that nyctalopin additionally interacts with mGluR6 receptor.

74 on was followed by the discovery of the APB (mGluR6) receptor of On bipolars, the first metabotropic

75 Thus, the mGluR6 receptors of ON bipolar cells lie at about the sa

76 glutamate release (CaV1.4) with postsynaptic mGluR6 receptors.

77 activates metabotropic glutamate receptor 6 (mGluR6) receptors in ON bipolar cells; this leads to act

78 and maintaining a stable localization of the mGluR6-related cascade elements.

79 of retinal ON bipolar cells (ON-BPC), where mGluR6 responds to glutamate released from photoreceptor

80 her, indicating that PDE is not required for mGluR6 signal transduction.

81 results suggest that Ggamma13 contributes to mGluR6 signalling in rod bipolar cells more than in ON c

82 ated by the metabotropic glutamate receptor, mGluR6, that signals via the G-protein Go to control ope

83 complished through a direct association with mGluR6, the glutamate receptor essential for the ON-bipo

84 At the synapse, ELFN1 binds in trans to mGluR6, the postsynaptic receptor on rod ON-bipolar cell

85 This indicates that the coupling of mGluR6 to Go is more efficient and suggests that Go may

86 t in assessing the hypothesis that Go couple mGluR6 to its effector.

87 Thus, Go(alpha) could serve to couple mGluR6 to later stages of its signaling cascade.

88 s in the G-protein heterotrimer that couples mGluR6 to TRPM1.

89 ponse of rod bipolar cells by modulating the mGluR6 transduction cascade.

90 Previous studies of mGluR6 transduction have suggested that the receptor cou

91 l melastatin subfamily M member 1-signaling (mGluR6/TRPM1-signaling) cascade was not properly maintai

92 Ultrastructurally, mGluR6 was located not on the tip of the central element

93 was disrupted in Rs1-KO, and some PSD95 and mGluR6 was mislocalized in the outer nuclear layer (ONL)

94 Levels of PSD95 and mGluR6 were determined by quantitative Western blot.

95 PSD95 and mGluR6 were juxtaposed in the OPL of the Rs1-KO retinas

96 ated by the metabotropic glutamate receptor, mGluR6, which controls the activity of a depolarizing cu

97 cones via metabotropic glutamate receptor 6 (mGluR6), whose cascade is unknown.