Incorporation of the unnatural amino acid p-benzoyl-L-phenylalanine (Bpa) into a G protein-coupled receptor in its native context

被引：0
|
作者：
Umanah, G.
Huang, L. Y.
Schultz, P. G.
Naider, F.
Becker, J. M.
机构：
[1] Univ Tennessee, Dept Microbiol, Knoxville, TN 37996 USA
[2] Scripps Res Inst, Dept Chem, La Jolla, CA 92037 USA
[3] CUNY Coll Staten Isl, Dept Chem, Staten Isl, NY 10301 USA
来源：
BIOPOLYMERS | 2007年 / 88卷 / 04期
关键词：
D O I：
暂无
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
引用
收藏
页码：522 / 522
页数：1
相关论文
共 40 条
  • [31] Biochemical and mutagenic analysis of a G protein-coupled receptor:: Photocrosslinking of the tridecapeptide α-Factor into Ste2p of Saccharomyces cerevisiae reveals contact points between the peptide and its receptor binding site
    Naider, Fred
    Son, Cagdas A.
    Sargsyan, Hasmik
    Becker, Jeffrey M.
    Peptides 2004, Proceedings: BRIDGES BETWEEN DISCIPLINES, 2005, : 93 - 95
  • [32] The G Protein-coupled Receptor Family C Group 6 Subtype A (GPRC6A) Receptor Is Involved in Amino Acid-induced Glucagon-like Peptide-1 Secretion from GLUTag Cells
    Oya, Manami
    Kitaguchi, Tetsuya
    Pais, Ramona
    Reimann, Frank
    Gribble, Fiona
    Tsuboi, Takashi
    JOURNAL OF BIOLOGICAL CHEMISTRY, 2013, 288 (07) : 4513 - 4521
  • [33] BIOPHYSICAL AND MUTAGENIC ANALYSIS OF A G PROTEIN-COUPLED RECEPTOR: PHOTOCROSSLINKING OF THE TRIDECAPEPTIDE ALPHA-FACTOR INTO STE2P OF SACCHAROMYCES CEREVISIAE REVEALS CONTACT POINTS BETWEEN THE PEPTIDE AND ITS RECEPTOR BINDING SITE
    Naider, F.
    Son, C.
    Sargsyan, H.
    Becker, J. M.
    JOURNAL OF PEPTIDE SCIENCE, 2004, 10 : 105 - 105
  • [34] Identification of a transferable two-amino-acid motif (GT) present in the C-terminal tail of the human lutropin receptor that redirects internalized G protein-coupled receptors from a degradation to a recycling pathway
    Galet, C
    Min, L
    Narayanan, R
    Kishi, M
    Weigel, NL
    Ascoli, M
    MOLECULAR ENDOCRINOLOGY, 2003, 17 (03) : 411 - 422
  • [35] RETRACTION: Metalloprotease cleavage of the N terminus of the orphan G protein-coupled receptor GPR37L1 reduces its constitutive activity (Retraction of Vol 9, art no RA36, 2016)
    Coleman, James L. J.
    Tony Ngo
    Schmidt, Johannes
    Mrad, Nadine
    Liew, Chu Kong
    Jones, Nicole M.
    Graham, Robert M.
    Smith, Nicola J.
    SCIENCE SIGNALING, 2019, 12 (612)
  • [36] Activation of the G Protein-Coupled Bile Acid Receptor TGR5 Modulates the HCP5/miR-139-5p/DDIT4 Axis to Antagonize Cervical Cancer Progression
    Su, Jia
    Zhao, Yiqi
    Chen, Wei-Dong
    Wang, Yan-Dong
    INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 2024, 25 (16)
  • [37] G protein-coupled bile acid receptor 1 reduced hepatic immune response and inhibited NFκB, PI3K/AKT, and PKC/P38 MAPK signaling pathway in hybrid grouper
    Xu, Jia
    Cao, Junming
    Tan, Beiping
    Xie, Shiwei
    JOURNAL OF ANIMAL SCIENCE, 2023, 101
  • [38] Berberine attenuates high glucose-induced fibrosis by activating the G protein-coupled bile acid receptor TGR5 and repressing the S1P2/MAPK signaling pathway in glomerular mesangial cells
    Yang, Zhiying
    Li, Jie
    Xiong, Fengxiao
    Huang, Junying
    Chen, Cheng
    Liu, Peiqing
    Huang, Heqing
    EXPERIMENTAL CELL RESEARCH, 2016, 346 (02) : 241 - 247
  • [39] Human immature monocyte-derived dendritic cells express the G protein-coupled receptor GPR105 (KIAA0001, P2Y14) and increase intracellular calcium in response to its agonist, uridine diphosphoglucose
    Skelton, L
    Cooper, M
    Murphy, M
    Platt, A
    JOURNAL OF IMMUNOLOGY, 2003, 171 (04): : 1941 - 1949
  • [40] G Protein-Coupled Receptor APJ and Its Ligand Apelin Act Downstream of Cripto to Specify Embryonic Stem Cells Toward the Cardiac Lineage Through Extracellular Signal-Regulated Kinase/p70S6 Kinase Signaling Pathway
    D'Aniello, Cristina
    Lonardo, Enza
    Iaconis, Salvatore
    Guardiola, Ombretta
    Liguoro, Anna Maria
    Liguori, Giovanna L.
    Autiero, Monica
    Carmeliet, Peter
    Minchiotti, Gabriella
    CIRCULATION RESEARCH, 2009, 105 (03) : 231 - U65
1234