Cross-talk and modulation of signaling between somatostatin and growth factor receptors

被引:16
作者
Kumar, Ujendra [1 ]
机构
[1] Univ British Columbia, Fac Pharmaceut Sci, Vancouver, BC V6T 1Z3, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
G-protein coupled receptors; Receptor tyrosine kinase; Somatostatin receptors; Signaling; Dimerization; PROTEIN-COUPLED RECEPTORS; BREAST-CANCER CELLS; RESONANCE ENERGY-TRANSFER; EGF-RECEPTOR; TYROSINE PHOSPHORYLATION; ERBB RECEPTORS; RAT PITUITARY; MOLECULAR PHARMACOLOGY; TRASTUZUMAB RESISTANCE; QUANTITATIVE-ANALYSIS;
D O I
10.1007/s12020-011-9524-8
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The process of homo- and/or heterodimerization of G-protein coupled receptors (GPCRs) and receptor tyrosine kinase (RTK) families are crucial for implicating the fundamental properties of receptor proteins including receptor expression, trafficking, and desensitization as well as signal transduction. The members of GPCR and RTK family constitute largest cell surface receptor proteins and regulate physiological functions of cells in response to external and internal stimuli. Notably, GPCRs and RTKs play major role in regulation of several key cellular functions which are associated with several pathological conditions including cancer biology, neurodegenerative and cardiovascular diseases. The focus of this review is to highlight the recent findings on the possible cross-talk between somatostatin receptors (members of GPCR family) and growth factor receptors like epidermal growth factor receptors (members of RTK family). Furthermore, functional consequences of such an interaction in modulation of signaling pathways linked to pathological conditions specifically in cancer are discussed.
引用
收藏
页码:168 / 180
页数:13
相关论文
共 103 条
[71]   Heterodimerization of somatostatin and opioid receptors cross-modulates phosphorylation, internalization, and desensitization [J].
Pfeiffer, M ;
Koch, T ;
Schröder, H ;
Laugsch, M ;
Höllt, V ;
Schulz, S .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (22) :19762-19772
[72]   Monitoring the formation of dynamic G-protein-coupled receptor-protein complexes in living cells [J].
Pfleger, KDG ;
Eidne, KA .
BIOCHEMICAL JOURNAL, 2005, 385 :625-637
[73]   New mechanisms in heptahelical receptor signaling to mitogen activated protein kinase cascades [J].
Pierce, KL ;
Luttrell, LM ;
Lefkowitz, RJ .
ONCOGENE, 2001, 20 (13) :1532-1539
[74]   Neu differentiation factor neuregulin isoforms activate distinct receptor combinations [J].
PinkasKramarski, R ;
Shelly, M ;
Glathe, S ;
Ratzkin, BJ ;
Yarden, Y .
JOURNAL OF BIOLOGICAL CHEMISTRY, 1996, 271 (32) :19029-19032
[75]   HEREGULIN INDUCES TYROSINE PHOSPHORYLATION OF HER4/P180(ERBB4) [J].
PLOWMAN, GD ;
GREEN, JM ;
CULOUSCOU, JM ;
CARLTON, GW ;
ROTHWELL, VM ;
BUCKLEY, S .
NATURE, 1993, 366 (6454) :473-475
[76]   EGF receptor transactivation by G-protein-coupled receptors requires metalloproteinase cleavage of proHB-EGF [J].
Prenzel, N ;
Zwick, E ;
Daub, H ;
Leserer, M ;
Abraham, R ;
Wallasch, C ;
Ullrich, A .
NATURE, 1999, 402 (6764) :884-888
[77]   HETERODIMERIZATION OF EPIDERMAL GROWTH-FACTOR RECEPTOR AND WILD-TYPE OR KINASE-DEFICIENT NEU - A MECHANISM OF INTERRECEPTOR KINASE ACTIVATION AND TRANSPHOSPHORYLATION [J].
QIAN, XL ;
LEVEA, CM ;
FREEMAN, JK ;
DOUGALL, WC ;
GREENE, MI .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1994, 91 (04) :1500-1504
[78]   Inhibition of PI3K and MEK: It Is All about Combinations and Biomarkers [J].
Rexer, Brent N. ;
Ghosh, Ritwik ;
Arteaga, Carlos L. .
CLINICAL CANCER RESEARCH, 2009, 15 (14) :4518-4520
[79]   Overcoming resistance to tyrosine kinase inhibitors Lessons learned from cancer cells treated with EGFR antagonists [J].
Rexer, Brent N. ;
Engelman, Jeffrey A. ;
Arteaga, Carlos L. .
CELL CYCLE, 2009, 8 (01) :18-22
[80]   Receptors for dopamine and somatostatin: Formation of hetero-oligomers with enhanced functional activity [J].
Rocheville, M ;
Lange, DC ;
Kumar, U ;
Patel, SC ;
Patel, RC ;
Patel, YC .
SCIENCE, 2000, 288 (5463) :154-157