Linked Life Data

17065146

Source:http://linkedlifedata.com/resource/pubmed/id/17065146

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
52
pubmed:dateCreated
2006-12-25
pubmed:abstractText
Cross-linking of the B cell receptor (BCR) on the immature B lymphoma cell line BKS-2 induces growth inhibition and apoptosis accompanied by rapid down-regulation of the immediate-early gene egr-1. In these lymphoma cells, egr-1 is expressed constitutively and has a prosurvival role, as Egr-1-specific antisense oligonucleotides or expression of a dominant-negative inhibitor of Egr-1 also prevented the growth of BKS-2 cells. Moreover, enhancement of Egr-1 protein with phorbol 12-myristate 13-acetate or an egr-1 expression vector rescued BKS-2 cells from BCR signal-induced growth inhibition. Nuclear run-on and mRNA stability assays indicated that BCR-derived signals act at the transcriptional level to reduce egr-1 expression. Inhibitors of ERK and JNK (but not of p38 MAPK) reduced egr-1 expression at the protein level. Transcriptional regulation appears to have a role because egr-1 promoter-driven luciferase expression was reduced by ERK and JNK inhibitors. Promoter truncation experiments suggested that several serum response elements are required for MAPK-mediated egr-1 expression. Our study suggests that BCR signals reduce egr-1 expression by inhibiting activation of ERK and JNK. Unlike ERK and JNK, p38 MAPK reduces constitutive expression of egr-1. Unlike the immature B lymphoma cells, normal immature B cells did not exhibit constitutive MAPK activation. BCR-induced MAPK activation was modest and transient with a small increase in egr-1 expression in normal immature B cells consistent with their inability to proliferate in response to BCR cross-linking.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
29
pubmed:volume
281
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
39806-18
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:17065146-Animals, pubmed-meshheading:17065146-Cell Differentiation, pubmed-meshheading:17065146-Cell Line, Tumor, pubmed-meshheading:17065146-Down-Regulation, pubmed-meshheading:17065146-Early Growth Response Protein 1, pubmed-meshheading:17065146-Extracellular Signal-Regulated MAP Kinases, pubmed-meshheading:17065146-Female, pubmed-meshheading:17065146-Growth Inhibitors, pubmed-meshheading:17065146-JNK Mitogen-Activated Protein Kinases, pubmed-meshheading:17065146-Lymphoma, B-Cell, pubmed-meshheading:17065146-MAP Kinase Signaling System, pubmed-meshheading:17065146-Mice, pubmed-meshheading:17065146-Mice, Inbred BALB C, pubmed-meshheading:17065146-Mice, Inbred CBA, pubmed-meshheading:17065146-Oligonucleotides, Antisense, pubmed-meshheading:17065146-Receptors, Antigen, B-Cell, pubmed-meshheading:17065146-Retroviridae, pubmed-meshheading:17065146-WT1 Proteins, pubmed-meshheading:17065146-p38 Mitogen-Activated Protein Kinases
pubmed:year
2006
pubmed:articleTitle
The role of MAPKs in B cell receptor-induced down-regulation of Egr-1 in immature B lymphoma cells.
pubmed:affiliation
Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, Kentucky 40536, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural