# TRANSFORMATION BY AVIAN RETICULOENDOTHELIOSIS VIRUS

> **NIH NIH R01** · UNIVERSITY OF TEXAS AT AUSTIN · 1989 · $126,881

## Abstract

Avian reticuloendotheliosis virus (REV-T) is a replication-defective
retrovirus that transforms very immature lymphoid cells and induces a fatal
lymphomatosis within 7-10 days.  REV-T is the only retrovirus which
immortalizes cells and converts them to a tumorigenic state in a helper
virus independent fashion.  REV-T contains a single oncogene, v-rel, which
is distinct from all other known oncogenes and is responsible for
transformation.  Uninfected vertebrate cells and Drosophila contain a
sequence related to the v-rel oncogene.  Polyclonal antisera to the v-rel
protein synthesized in E. coli immunoprecipitates a phosphoprotein with a
molecular weight of 57 kDa which is located in the cytosol of transformed
cells.  Preliminary studies indicate that the v-rel protein may possess Mn+
dependent protein kinase activity capable of autophosphorylation.

One of our specific aims will be to characterize the enzymes activity
associated with the v-rel protein.  To demonstrate whether the kinase
activity is intrinsic to v-rel protein the entire v-rel gene and deletion
mutants will be expressed in E. coli and the products assaysed for kinase
activity.  Deletion mutants which lack kinase activity will also be tested
for their ability to transform lymphoid cells in vitro.  We will determine
whether the transforming protein is a serine/threonine or tyrosine protein
kinase.  We propose to identify potential cellular substrates of the v-rel
kinase.  Monoclonal antibodies will be developed to characterize functional
domains and identify potential cellular substrates.  A correlation has been
observed between REV-T provirus copy number, level of v-rel transcription,
and extent of immunoglobulin gene rearrangements in REV-T transformed
lymphoid cells.  We propose to define whether the level of v-rel expression
indirectly influences the phenotype of the REV-T transformed lymphoid
cells.  We propose to identify the produce of the c-rel proto-oncogene and
compare its enzyme activity and substrate specificity to the viral
transforming protein.  The expression of c-rel will also be studied during
early avian embryogenesis to define its role in the control of cell
proliferation and differentiation.

## Key facts

- **NIH application ID:** 3171137
- **Project number:** 5R01CA033192-06
- **Recipient organization:** UNIVERSITY OF TEXAS AT AUSTIN
- **SAM.gov UEI:** V6AFQPN18437
- **Principal Investigator:** HENRY R BOSE
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 1989
- **Award amount:** $126,881
- **Award type:** 5
- **Project period:** 1984-01-01 → 1989-12-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3171137

## Citation

> US National Institutes of Health, RePORTER application 3171137, TRANSFORMATION BY AVIAN RETICULOENDOTHELIOSIS VIRUS (5R01CA033192-06). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3171137. Licensed CC0.

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