Modulation of protein kinase C and Ca2+ lipid‐independent protein kinase in lymphoma induced by moloney murine leukemia virus in BALB/c mice

M. Wolfson, M. Aboud, R. Ofir, Y. Weinstein, S. Segal

Research output: Contribution to journalArticlepeer-review

6 Scopus citations

Abstract

We investigated the possible role of protein kinase C (PKC) in the progression of Moloney murine leukemia virus (Mo‐MuLV)‐induced lymphoma in BALB/c mice. Mice injected with Mo‐MuLV on the first day after birth developed lymphoma within 1 1/2 3 months. The development of lymphoma was characterized by a gradual increase in the number of spleen cells. However, no analogous changes could be detected in the thymuses of these mice, although cells of both organs were found to be virus producers as early as 3‐4 weeks after inoculation. PKC activity, which was assayed in extracts of spleen and thymus cells, declined gradually during the development of lymphoma. Concomitantly with this decline, a progressive appearance of Ca2+/ lipid‐independent protein kinase activity was observed. TPA treatment of intact cells from normal mice reduced the level of soluble PKC activity, while inducing Ca2+/lipid‐independent phosphorylation. By contrast, TPA had no effect on these enzymatic activities in cells derived from leukemic mice. Spleen enlargement caused by injection of a non‐leukemogenic inflammatory agent such as mineral oil was ineffective in this respect, suggesting that the PKC‐Ca2+ /lipid‐independent protein kinase modulation is associated with the virally induced leukemogenesis.

Original languageEnglish
Pages (from-to)589-593
Number of pages5
JournalInternational Journal of Cancer
Volume37
Issue number4
DOIs
StatePublished - 1 Jan 1986

Fingerprint

Dive into the research topics of 'Modulation of protein kinase C and Ca2+ lipid‐independent protein kinase in lymphoma induced by moloney murine leukemia virus in BALB/c mice'. Together they form a unique fingerprint.

Cite this