The role of MAPKs in B cell receptor-induced down-regulation of Egr-1 in immature B lymphoma cells.

The role of MAPKs in B cell receptor-induced down-regulation of Egr-1 in immature B lymphoma cells. Research Abstract Details 

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The role of MAPKs in B cell receptor-induced down-regulation of Egr-1 in immature B lymphoma cells. Abstract Text:

Jiyuan Ke,Murali Gururajan,Anupam Kumar,Alan Simmons,Lilia Turcios,Ralph L Chelvarajan,David M Cohen,David L Wiest,John G Monroe,Subbarao Bondada,

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.

The role of MAPKs in B cell receptor-induced down-regulation of Egr-1 in immature B lymphoma cells. Publishing Authors By Initials

J Ke,M Gururajan,A Kumar,A Simmons,L Turcios,RL Chelvarajan,DM Cohen,DL Wiest,JG Monroe,S Bondada,

For similar enzymes and coenzymes: enzymes: transferases: phosphotransferases: phosphotransferases (alcohol group acceptor): protein kinases: protein-serine-threonine kinases: mitogen-activated protein kinases: p38 mitogen-activated protein kinases research abstracts see: enzymes and coenzymes: enzymes: transferases: phosphotransferases: phosphotransferases (alcohol group acceptor): protein kinases: protein-serine-threonine kinases: mitogen-activated protein kinases: p38 mitogen-activated protein kinases research

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The role of MAPKs in B cell receptor-induced down-regulation of Egr-1 in immature B lymphoma cells. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: The Journal of biological chemistry

VOLUME: 281

Page Numbers: 39806-18

Journal Abbreviation: J. Biol. Chem.

ISSN: 0021-9258

DAY: 24

MONTH: 10

YEAR: 2006

The role of MAPKs in B cell receptor-induced down-regulation of Egr-1 in immature B lymphoma cells. Information

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LANGUAGE: eng

NlmUniqueID: 2985121

The role of MAPKs in B cell receptor-induced down-regulation of Egr-1 in immature B lymphoma cells. Keywords Mesh Terms:

KEYWORDS: p38 Mitogen-Activated Protein Kinases

MESH TERMS: physiology

Chemical & Substance for Abstract: The role of MAPKs in B cell receptor-induced down-regulation of Egr-1 in immature B lymphoma cells. Information

Substance Name: p38 Mitogen-Activated Protein Kinases

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for The role of MAPKs in B cell receptor-induced down-regulation of Egr-1 in immature B lymphoma cells.

AFFILIATION: Department of Microbiology, Immunology, and Molecular Genetics, University of Kentucky, Lexington, Kentucky 40536, USA.

Country: United States

AGENCY: United States NCI

GRANT: 5P01CA092372

ACRONYM: CA

MEDLINETA: J Biol Chem

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