Linked Life Data

20450475

Source:http://linkedlifedata.com/resource/pubmed/id/20450475

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2010-8-12
pubmed:abstractText
G protein-coupled receptors (GPCRs) comprise a large family of membrane receptors involved in signal transduction. These receptors are linked to a variety of physiological and biological processes such as regulation of neurotransmission, growth, cell differentiation and oncogenesis among others. Some of the effects of GPCRs are known to be mediated by the activation of MAPK pathways. Several GPCRs are also able to transactivate receptors with tyrosine kinase activity (TKR) such as EGFR and HER2 and thus to control DNA synthesis and cell proliferation. The interaction between these receptors not only plays an important physiological role but its disregulation can induce pathological states such as cancer. For this reason, the crosstalk between these two types of receptors can be considered a possible mechanism for cell transformation, tumor progression, reactivation of the metastatic disease, and the acquisition of resistance to therapies targeting TKR receptors. The transactivation of some TKRs by GPCRs is related to the lost of response of TKRs to inhibitors of TK activity, mainly by the activation of the c-Src protein which can directly phosphorylate and activate the cytoplasmic domain of a TKR. For these reason, the dual inhibition of GPCRs and TKRs in some types of cancer has been proposed as a better strategy to kill tumor cells. Increased understanding of the mechanisms that interconnect the two pathways regulated by GPCRs and TKRs may facilitate the design of new therapeutic strategies.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1873-5592
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1169-80
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed-meshheading:20450475-ADAM Proteins, pubmed-meshheading:20450475-Cell Line, Tumor, pubmed-meshheading:20450475-Cell Proliferation, pubmed-meshheading:20450475-Drug Resistance, Neoplasm, pubmed-meshheading:20450475-Humans, pubmed-meshheading:20450475-Inflammation Mediators, pubmed-meshheading:20450475-Matrix Metalloproteinases, pubmed-meshheading:20450475-Membrane Microdomains, pubmed-meshheading:20450475-Mitogen-Activated Protein Kinases, pubmed-meshheading:20450475-Neoplasms, pubmed-meshheading:20450475-Protein-Tyrosine Kinases, pubmed-meshheading:20450475-Receptor, Epidermal Growth Factor, pubmed-meshheading:20450475-Receptor Cross-Talk, pubmed-meshheading:20450475-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:20450475-Receptors, G-Protein-Coupled, pubmed-meshheading:20450475-Signal Transduction
pubmed:year
2010
pubmed:articleTitle
Tyrosine kinase receptor transactivation associated to G protein-coupled receptors.
pubmed:affiliation
Institut d'Investigacions Biomèdiques Agustí Pi y Sunyer, Laboratory of Molecular and Translational Oncology (ICMHO), University of Barcelona, Casanova 143, 08036 Barcelona, Spain. almendro@clinic.ub.es
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't