Linked Life Data

12947395

Source:http://linkedlifedata.com/resource/pubmed/id/12947395

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
37
pubmed:dateCreated
2003-8-29
pubmed:abstractText
Within the last 15 years, multiple new signal transduction pathways within cells have been discovered. Many of these pathways belong to what is now termed 'the mitogen-activated protein kinase (MAPK) superfamily.' These pathways have been linked to the growth factor-mediated regulation of diverse cellular events such as proliferation, senescence, differentiation and apoptosis. Based on currently available data, exposure of cells to ionizing radiation and a variety of other toxic stresses induces simultaneous compensatory activation of multiple MAPK pathways. These signals play critical roles in controlling cell survival and repopulation effects following irradiation, in a cell-type-dependent manner. Some of the signaling pathways activated following radiation exposure are those normally activated by mitogens, such as the 'classical' MAPK (also known as the ERK) pathway. Other MAPK pathways activated by radiation include those downstream of death receptors and procaspases, and DNA-damage signals, including the JNK and P38 MAPK pathways. The expression and release of autocrine growth factor ligands, such as (transforming growth factor alpha) and TNF-alpha, following irradiation can also enhance the responses of MAPK pathways in cells and, consequently, of bystander cells. Thus, the ability of radiation to activate MAPK signaling pathways may depend on the expression of multiple growth factor receptors, autocrine factors and Ras mutation. Enhanced basal signaling by proto-oncogenes such as K-/H-/N-RAS may provide a radioprotective and growth-promoting signal. In many cell types, this may be via the PI3K pathway; in others, this may occur through nuclear factor-kappa B or multiple MAPK pathways. This review will describe the enzymes within the known MAPK signaling pathways and discuss their activation and roles in cellular radiation responses.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0950-9232
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5885-96
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
MAPK pathways in radiation responses.
pubmed:affiliation
Department of Radiation Oncology, Virginia Commonwealth University, Richmond, VA 23298-0058, USA. pdent@hsc.vcu.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Review, Research Support, Non-U.S. Gov't