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1  P321A was coexpressed with RAMP1, RAMP2, or RAMP3.
2                                We found that RAMP3, a component of the receptor for the neuropeptide
3 led receptor, paired with a RAMP1, RAMP2, or RAMP3 accessory subunit, respectively, which increases a
4 medullin receptors are comprised of RAMP2 or RAMP3 (AM1R and AM2R, respectively) and calcitonin recep
5 1 (AMY(1)R), human RAMP2 (AMY(2)R), or human RAMP3 (AMY(3)R).
6 drenomedullin (AM), is comprised of RAMP2 or RAMP3 and calcitonin receptor-like receptor (CRLR).
7 as to identify other interaction partners of RAMP3 and determine their role in CRLR-RAMP3 trafficking
8 ssays and mutational analysis indicated that RAMP3 and NHERF-1 interact via a PDZ type I domain on NH
9                                  The role of RAMP3 and NSF in AM2R recycling was confirmed in rat mes
10 mesangial cells, where RNA interference with RAMP3 and pharmacological inhibition of NSF both resulte
11                               Because RAMP2, RAMP3, and CLR transduce the signaling of the two potent
12 MP2 is required for survival, mice that lack RAMP3 appear normal until old age, at which point they h
13                                Specifically, RAMP3 association with atypical chemokine receptor 3 (AC
14 g secretin receptor expression competing for RAMP3 association with the calcitonin receptor-like rece
15                                              RAMP3 association with this receptor was shown to be cap
16 Z type I domain present in the C terminus of RAMP3, but not in RAMP1 or RAMP2, leads to protein-prote
17 cretin receptor associates specifically with RAMP3, but not with RAMP1 or RAMP2.
18                       Mutational analysis of RAMP3, by deletion and point mutations, indicated that t
19 ellular CGRP signalling through the receptor RAMP3-CALCRL restricted the differentiation of T(H)2 cel
20 ue temporal features, reveal how AM2/IMD and RAMP3 collaborate to shape CLR signaling, and have signi
21 ubule cells endogenously expressing the CRLR-RAMP3 complex and NHERF-1, the CRLR-RAMP complex desensi
22 NHERF-1 indicated that NHERF-1 inhibits CRLR/RAMP3 complex internalization by tethering the complex t
23 leimide-sensitive factor (NSF) with the CRLR-RAMP3 complex, but not CRLR-RAMP1 or CRLR-RAMP2 complex,
24 strates that the Wap super-enhancer controls Ramp3, despite three separating CTCF sites.
25 ce with reduced expression of RAMP2 (but not RAMP3) display remarkable subfertility.
26  replaced with the corresponding region from RAMP3, dual topology was retained but MRAP was inactive.
27 XCR4 and ACKR3 is reduced in the presence of RAMP3 due to complex formation at the cell surface.
28 raction between CGRP produced by neurons and RAMP3 expressed on T cells enhanced the anti-viral IFNga
29  during acute viral infection, which acts on RAMP3-expressing T cells to induce an effective anti-vir
30                                              RAMP3 expression biased the receptor toward Ca(2+) mobil
31  distal CTCF-binding site results in loss of Ramp3 expression in non-mammary tissues.
32 g kinetics to the AM2/IMD mid-region and the RAMP3 extracellular domain (ECD).
33 n adrenomedullin-1 (AM(1)) receptor, and CLR/RAMP3 forms an adrenomedullin-2 (AM(2)) receptor.
34 th targeted deletions of either the RAMP2 or RAMP3 gene.
35 tor activity-modifying proteins (RAMPs), and RAMP3 has been shown to facilitate ACKR3's recycling pro
36    Therefore, to determine whether RAMP2 and RAMP3 have distinct functions in vivo, we generated mice
37 ertheless, our studies reveal that RAMP2 and RAMP3 have distinct physiological functions throughout e
38 on in mice results in elevated expression of Ramp3 in mammary tissue through augmented promoter-enhan
39 quently, genetic deletion of either ACKR3 or RAMP3 in mice abolishes directed cell migration of retin
40 s, indicate a novel function for NHERF-1 and RAMP3 in the internalization of the AM receptor and sugg
41  These results indicate a novel function for RAMP3 in the post-endocytic sorting of the AM-R and sugg
42                                              RAMP3 inhibits ligand-stimulated internalization of ACKR
43 GPCR interaction map suggests that RAMP1 and RAMP3 interact with the same set of GPCRs, which implies
44 t new insights into the structural basis for RAMP3 interaction with a family B G protein-coupled rece
45 t mutations, indicated that the PDZ motif of RAMP3 interacts with NSF to cause the change in traffick
46                                     Instead, RAMP3 is required for the rapid recycling of ACKR3 to th
47 hat AM2/IMD is kinetically selective for CLR-RAMP3, known as the AM(2)R, and we define the structural
48 oth glucose and insulin tolerance tests in a Ramp3 KO mouse model.
49 ed on combined expression level of HN1, RAN, RAMP3, KRT19, and TAF9, was associated with disease-spec
50 AP residues 29-37 conferred dual topology to RAMP3, normally in an Nexo/Ccyt orientation.
51                         Knock-down of either RAMP3 or NHERF-1 by RNA interference technology enabled
52                         It is now known that RAMP3 protein-protein interactions regulate the recyclin
53 ing G protein coupling, the interaction with RAMP3 reduced activation of the cognate Galpha(s) but in
54 tivity-modifying proteins 2 and 3 (RAMP2 and RAMP3), respectively.
55 LR when co-expressed with RAMP1 and RAMP2 or RAMP3, respectively, intermedin represents a nonselectiv
56          Co-expression of CRLR with RAMP2 or RAMP3 resulted in a response with the pharmacological pr
57 f HAECs with CRLR or RAMP2, but not RAMP1 or RAMP3, siRNAs abolished protection by IMD (1 nmol l(-)(1
58 ) and receptor activity modifying protein 3 (RAMP3) to inhibit glycolysis and induce reactive oxygen
59 rs of RAMP3 and determine their role in CRLR-RAMP3 trafficking.
60 stronger interaction between the CTR and the RAMP3 transmembrane domains yielded a more stable AMY(3)
61 e of NHERF-1, although the AM receptor (CRLR/RAMP3) undergoes desensitization, the internalization of
62             However, mRNA encoding RAMP2 and RAMP3 was also detected in the gastrointestinal tract, D
63 expression of ADM receptors Crlr, Ramp2, and Ramp3 was increased (p < 0.05) in P-HFHS dams.
64 nes encoding human ADM2 receptor (CALCRL and RAMP3) was altered in participants with inflammatory bow
65               IMD and CRLR, RAMP1, RAMP2 and RAMP3 were expressed in all cell types.When cells were t
66  insulin secretion when cells overexpressing RAMP3 were stimulated with GLP-1.
67 ne Adrenomedullin and its receptor component Ramp3, which activate PKA and its downstream effector cA
68                  The interaction of RAMP2 or RAMP3 with CLR induces conformational variation in the j
69  looking at reduced expression of endogenous RAMP3, with a loss of sensitivity to GLP-1 in both gluco
70 he GLP-1 receptor was found to interact with RAMP3, with the heterodimer able to bind agonists at the