Literature DB >> 3261204

Lymphoma models for B-cell activation and tolerance. VII. Pathways in anti-Ig-mediated growth inhibition and its reversal.

G L Warner1, D W Scott.   

Abstract

WEHI-231, CH33, and CH31 are B-cell lymphomas that are inhibited in their growth by crosslinking of surface Ig receptors during early G1. This "negative signaling" process can be prevented or reversed under certain conditions. In the present paper, we use a cell synchronization procedure to demonstrate that activation of protein kinase C (PKC) is not involved in the negative signal for growth, but rather that PKC activation prevents growth inhibition when present early in the cell cycle. Indeed, the prevention of negative signaling is only accomplished by active phorbol esters. Moreover, phorbol esters and a calcium ionophore fail to deliver a negative signal under conditions in which anti-Ig can significantly prevent cell cycle progression into S phase, thereby ruling out synergy between PKC and calcium in growth inhibition. Whether phorbol esters reverse negative signaling by preventing internalization of the immune complex or phosphorylation of a critical intracellular protein is discussed.

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Year:  1988        PMID: 3261204     DOI: 10.1016/0008-8749(88)90173-6

Source DB:  PubMed          Journal:  Cell Immunol        ISSN: 0008-8749            Impact factor:   4.868


  2 in total

1.  Low level exposure to inorganic mercury interferes with B cell receptor signaling in transitional type 1 B cells.

Authors:  R Gill; M J McCabe; A J Rosenspire
Journal:  Toxicol Appl Pharmacol       Date:  2017-06-28       Impact factor: 4.219

2.  Antigen receptor-induced cell cycle arrest in WEHI-231 B lymphoma cells depends on the duration of signaling before the G1 phase restriction point.

Authors:  D M Page; A L DeFranco
Journal:  Mol Cell Biol       Date:  1990-06       Impact factor: 4.272

  2 in total

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