Papers

Peer-reviewed
3 1999

Requirement of PEST domain tyrosine phosphatase PEP in B cell antigen receptor-induced growth arrest and apoptosis

EUROPEAN JOURNAL OF IMMUNOLOGY
  • K Hasegawa
  • ,
  • H Yajima
  • ,
  • T Katagiri
  • ,
  • M Ogimoto
  • ,
  • Y Arimura
  • ,
  • K Mitomo
  • ,
  • K Mashima
  • ,
  • K Mizuno
  • ,
  • H Yakura

Volume
29
Number
3
First page
887
Last page
896
Language
English
Publishing type
Research paper (scientific journal)
DOI
10.1002/(SICI)1521-4141(199903)29:03<887::AID-IMMU887>3.0.CO;2-9
Publisher
WILEY-V C H VERLAG GMBH

Signaling events leading to B cell growth or apoptosis are beginning to be unravelled, but detailed information is still lacking. To identify signaling molecules involved in B cell antigen receptor (BCR)-initiated pathways, we used the immature B cell line, WEHI-231, to investigate protein tyrosine phosphatases (PTP) whose expression was modulated by BCR ligation. Among the PTP cloned by reverse transcription-PCR, mRNA expression of the proline-, glutamic acid-, serine- and threonine-rich (PEST) domain phosphatase (PEP) was selectively elevated 3.1-fold within 3 h after anti-IgM antibody stimulation. In contrast, expression of another PEST domain phosphatase, PTP-PEST, was unaffected. Western blot analysis revealed that 71 % of PEP was located in the cytosolic fraction, while 29 % was in the membrane fraction. To examine the direct contribution made by PEP to BCR-initiated signal transduction, we transfected an antisense PEP cDNA into WEHI-231 cells. Two stable clones were established in which PEP expression was reduced by 34 % and 47 %, respectively. Strikingly, BCR-mediated inhibition of DNA synthesis was significantly rescued in the clones, and G1 phase cell cycle arrest acid apoptosis were almost completely ablated. Considered collectively,these results indicate that PEP is a positive, crucial regulator in determining B cell fate triggered by BCR engagement.

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Link information
DOI
https://doi.org/10.1002/(SICI)1521-4141(199903)29:03<887::AID-IMMU887>3.0.CO;2-9
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/10092092
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000079149600019&DestApp=WOS_CPL