About: β adrenergic receptor modulated signaling in glioma models: promoting β adrenergic receptor-β arrestin scaffold-mediated activation of extracellular-regulated kinase 1/2 may prove to be a panacea in the treatment of intracranial and spinal malignancy and extra-neuraxial carcinoma

Facets (new session)
Description
Metadata
Settings
- owl:sameAs
- Inference Rule:

About: β adrenergic receptor modulated signaling in glioma models: promoting β adrenergic receptor-β arrestin scaffold-mediated activation of extracellular-regulated kinase 1/2 may prove to be a panacea in the treatment of intracranial and spinal malignancy and extra-neuraxial carcinoma Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	β adrenergic receptor modulated signaling in glioma models: promoting β adrenergic receptor-β arrestin scaffold-mediated activation of extracellular-regulated kinase 1/2 may prove to be a panacea in the treatment of intracranial and spinal malignancy and extra-neuraxial carcinoma
Creator	George, Michael Ghali, George Ghali, Zaki
Source	Medline; PMC
abstract	Neoplastically transformed astrocytes express functionally active cell surface β adrenergic receptors (βARs). Treatment of glioma models in vitro and in vivo with β adrenergic agonists variably amplifies or attenuates cellular proliferation. In the majority of in vivo models, β adrenergic agonists generally reduce cellular proliferation. However, treatment with β adrenergic agonists consistently reduces tumor cell invasive potential, angiogenesis, and metastasis. β adrenergic agonists induced decreases of invasive potential are chiefly mediated through reductions in the expression of matrix metalloproteinases types 2 and 9. Treatment with β adrenergic agonists also clearly reduce tumoral neoangiogenesis, which may represent a putatively useful mechanism to adjuvantly amplify the effects of bevacizumab. Bevacizumab is a monoclonal antibody targeting the vascular endothelial growth factor receptor. We may accordingly designate βagonists to represent an enhancer of bevacizumab. The antiangiogenic effects of β adrenergic agonists may thus effectively render an otherwise borderline effective therapy to generate significant enhancement in clinical outcomes. β adrenergic agonists upregulate expression of the major histocompatibility class II DR alpha gene, effectively potentiating the immunogenicity of tumor cells to tumor surveillance mechanisms. Authors have also demonstrated crossmodal modulation of signaling events downstream from the β adrenergic cell surface receptor and microtubular polymerization and depolymerization. Complex effects and desensitization mechanisms of the β adrenergic signaling may putatively represent promising therapeutic targets. Constant stimulation of the β adrenergic receptor induces its phosphorylation by β adrenergic receptor kinase (βARK), rendering it a suitable substrate for alternate binding by β arrestins 1 or 2. The binding of a β arrestin to βARK phosphorylated βAR promotes receptor mediated internalization and downregulation of cell surface receptor and contemporaneously generates a cell surface scaffold at the βAR. The scaffold mediated activation of extracellular regulated kinase 1/2, compared with protein kinase A mediated activation, preferentially favors cytosolic retention of ERK1/2 and blunting of nuclear translocation and ensuant pro-transcriptional activity. Thus, βAR desensitization and consequent scaffold assembly effectively retains the cytosolic homeostatic functions of ERK1/2 while inhibiting its pro-proliferative effects. We suggest these mechanisms specifically will prove quite promising in developing primary and adjuvant therapies mitigating glioma growth, angiogenesis, invasive potential, and angiogenesis. We suggest generating compounds and targeted mutations of the β adrenergic receptor favoring β arrestin binding and scaffold facilitated activation of ERK1/2 may hold potential promise and therapeutic benefit in adjuvantly treating most or all cancers. We hope our discussion will generate fruitful research endeavors seeking to exploit these mechanisms.
has issue date	2020-04-18(xsd:dateTime)
bibo:doi	10.1007/s11033-020-05427-1
bibo:pmid	32303958
has license	no-cc
sha1sum (hex)	fe1d22b6fd8c5fb558baca6f917760964eb30997
schema:url	https://doi.org/10.1007/s11033-020-05427-1
resource representing a document's title	β adrenergic receptor modulated signaling in glioma models: promoting β adrenergic receptor-β arrestin scaffold-mediated activation of extracellular-regulated kinase 1/2 may prove to be a panacea in the treatment of intracranial and spinal malignancy and extra-neuraxial carcinoma
has PubMed Central identifier	PMC7165076
has PubMed identifier	32303958
schema:publication	Mol Biol Rep
resource representing a document's body	covid:fe1d22b6fd8c5fb558baca6f917760964eb30997#body_text
is schema:about of	named entity 'targeted' named entity 'β adrenergic receptor' named entity 'receptor' named entity 'effectively' named entity 'adrenergic agonists' named entity 'adrenergic agonists' named entity 'potential' named entity 'mediated' named entity 'invasive' named entity 'microtubular' named entity 'effects' named entity 'express' named entity 'modulation' named entity 'compounds' named entity 'INDUCED' named entity 'AUTHORS' named entity 'CANCERS' named entity 'PHOSPHORYLATED' named entity 'FUNCTIONS' named entity 'TARGETED' named entity 'CROSSMODAL' named entity 'FAVORING' named entity 'CELL SURFACE' named entity 'BEVACIZUMAB' named entity 'CELL SURFACE RECEPTOR' covid:arg/fe1d22b6fd8c5fb558baca6f917760964eb30997 named entity 'compared' named entity 'homeostatic' named entity 'antiangiogenic' named entity 'histocompatibility' named entity 'amplifies' named entity 'induces' named entity 'Authors' named entity 'ERK1/2' named entity 'binding' named entity 'promising' named entity 'ERK1/2' named entity 'seeking' named entity 'However' named entity 'vascular endothelial growth factor receptor' named entity 'effectively' named entity 'adrenergic agonists' named entity 'majority' named entity 'promotes' named entity 'ERK1/2' named entity 'astrocytes' named entity 'functionally' named entity 'Constant' named entity 'developing' named entity 'scaffold' named entity 'transformed' named entity 'cytosolic' named entity 'intracranial' named entity 'β adrenergic receptor' named entity 'malignancy' named entity 'immunogenicity' named entity 'β adrenergic receptor' named entity 'DR alpha' named entity 'angiogenesis' named entity 'bevacizumab' named entity 'class II' named entity 'phosphorylated' named entity 'downregulation' named entity 'cellular proliferation' named entity 'arrestin' named entity 'antiangiogenic' named entity 'therapeutic targets' named entity 'β adrenergic receptor' named entity 'extracellular' named entity 'depolymerization' named entity 'arrestin' named entity '1/2' named entity 'scaffold' named entity 'adjuvant' named entity 'arrestin' named entity 'therapeutic' named entity 'therapies' named entity 'cellular differentiation' named entity 'U-105'

Faceted Search & Find service v1.13.91 as of Mar 24 2020

Alternative Linked Data Documents: Sponger | ODE Content Formats:

RDF

ODATA

Microdata

About

OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2024 OpenLink Software