PMID- 1584230
OWN - NLM
STAT- MEDLINE
DCOM- 19920617
LR  - 20190824
IS  - 0161-5890 (Print)
IS  - 0161-5890 (Linking)
VI  - 29
IP  - 5
DP  - 1992 May
TI  - Egr-1 mRNA expression is independent of regulatory proliferative responses in the 
      immature B cell line WEHI-231.
PG  - 619-24
AB  - We have recently reported cellular growth arrest induced following crosslinking 
      of surface IgM (sIgM) but not surface IgD (sIgD) in the WEHI-231 cell line, 
      representative of the immature B cell stage, and its delta heavy chain (delta) 
      transfectant. An initial report has indicated WEHI-231.7, a subclone of WEHI-231, 
      failed to express Egr-1 mRNA following sIgM crosslinking, in contrast to 
      significant up-regulation found in mature B lymphocytes. The implication for 
      linkage between selective surface immunoglobulin (sIg) signal transduction, 
      expression of immediate/early genes and control of cellular growth imposes an 
      attractive model for induction of immature B cell tolerance. Our investigations 
      examined the relationships between Egr-1 mRNA expression and growth regulation in 
      WEHI-231, WEHI-231.7 and their respective delta-transfectants (WEHI-delta, 
      WEHI-delta 7). We report sIgM and sIgD crosslinking leads to a rapid increase of 
      Egr-1 mRNA expression in WEHI-231 and WEHI-delta but not in the subclone 
      WEHI-231.7 and WEHI-delta 7. Nevertheless, both WEHI-231, WEHI-231.7 and their 
      delta-transfectants demonstrate the ability to induce growth arrest following 
      sIgM but not sIgD crosslinking. Furthermore, we found Egr-1 expression could be 
      achieved by direct activation of protein kinase C (PKC) by phorbol 12-myristate 
      13-acetate (PMA) circumventing the classical sIg activated phosphatidylinositol 
      signal transduction pathway. Our results suggest Egr-1 expression does not 
      directly participate in growth regulation of immature B cell clones but rather is 
      a consequence of signal transduction through sIg.
FAU - Iwabuchi, N
AU  - Iwabuchi N
AD  - Mount Sinai Hospital, Department of Medical Genetics and Immunology, University 
      of Toronto, Ontario, Canada.
FAU - Williams, D B
AU  - Williams DB
FAU - Nguyen, H P
AU  - Nguyen HP
FAU - Hozumi, N
AU  - Hozumi N
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Mol Immunol
JT  - Molecular immunology
JID - 7905289
RN  - 0 (DNA-Binding Proteins)
RN  - 0 (Early Growth Response Protein 1)
RN  - 0 (Egr1 protein, mouse)
RN  - 0 (Immediate-Early Proteins)
RN  - 0 (Immunoglobulin D)
RN  - 0 (Immunoglobulin M)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Antigen, B-Cell)
RN  - 0 (Transcription Factors)
RN  - EC 2.7.11.13 (Protein Kinase C)
RN  - NI40JAQ945 (Tetradecanoylphorbol Acetate)
SB  - IM
MH  - Animals
MH  - B-Lymphocytes/*physiology
MH  - Cell Division
MH  - DNA-Binding Proteins/*genetics
MH  - Early Growth Response Protein 1
MH  - *Immediate-Early Proteins
MH  - Immunoglobulin D/analysis
MH  - Immunoglobulin M/analysis
MH  - Lymphoma/immunology/*metabolism/pathology
MH  - Mice
MH  - Protein Kinase C/physiology
MH  - RNA, Messenger/*analysis
MH  - Receptors, Antigen, B-Cell/analysis
MH  - Signal Transduction
MH  - Tetradecanoylphorbol Acetate/pharmacology
MH  - Transcription Factors/*genetics
MH  - Transfection
MH  - Tumor Cells, Cultured
EDAT- 1992/05/01 00:00
MHDA- 1992/05/01 00:01
CRDT- 1992/05/01 00:00
PHST- 1992/05/01 00:00 [pubmed]
PHST- 1992/05/01 00:01 [medline]
PHST- 1992/05/01 00:00 [entrez]
AID - 10.1016/0161-5890(92)90198-7 [doi]
PST - ppublish
SO  - Mol Immunol. 1992 May;29(5):619-24. doi: 10.1016/0161-5890(92)90198-7.