# TRANSFORMATION BY AVIAN RETICULOENDOTHELIOSIS VIRUS

> **NIH NIH R01** · UNIVERSITY OF TEXAS AT AUSTIN · 1991 · $184,920

## Abstract

Avian reticuloendotheliosis virus (REV-T) is the most virulent of
all retroviruses.  The oncogene of REV-T, v-rel, transforms and
prevents the subsequent differentiation of lymphoid cells at
different stages of B cell development.  REV-T converts normal
cells to a tumorigenic state providing an excellent model for
studies on oncogenic mechanisms.  The v-rel oncogene is distinct
from other known oncogenes and encodes a 59 kDa protein which is
associated with a distinct set of cellular proteins.

There are two pp59v-rel cytosolic complexes which contain the
product of the c-rel proto-oncogene (p75c-rel) and the constitutive
form of heat shock protein 70 (p70hsc).  The major cytosolic
complex is distinct in that it contains a 40 kDa phosphoprotein
(pp40).  Twenty percent of pp59v-rel in the cytosol is not
associated with pp40 but with two high molecular weight proteins
(p115, p124).  Purified pp59v-rel cytosolic complexes contain an
associated serine kinase activity.  Approximately ten percent of
the pp59v-rel is present in nuclear complexes which contains pp40.
In normal avian lymphoid cells p75c-rel is complexed with proteins
of the same apparent molecular mass as those associated with pp59v-
rel in REV-T transformed cells.  The major p75c-rel complex
contains p115 and p124.  The less abundant complex contains p75c-
rel associated with pp40.

The c-rel proto-oncogene and v-rel proteins activate transcription
in yeast and the region responsible for activation is also
necessary for oncogenic transformation by v-rel.  However, in
normal and transformed avian lymphoid cells p75c-rel is a cytosolic
protein.  It is likely p75c-rel is a transactivating factor which
is sequestered in the cytosol of unstimulated lymphoid cells.  When
REV-T transformed cells are exposed to heavy metals, p75c-rel
levels increase and nuclear translocation occurs.  The objectives
of this proposal are to 1) perform mutational analysis on v-rel to
correlate transforming ability with the binding of cellular
proteins to the v-rel protein; 2) determine whether any of these
proteins associated with p75c-rel are involved in nuclear
translocation; 3) molecularly clone and sequence the gene encoding
pp40 and define its tissue specific expression; 4) prepare
monoclonal antibodies against the cellular proteins associated with
pp59v-rel and p75c-rel.

## Key facts

- **NIH application ID:** 3171133
- **Project number:** 2R01CA033192-07A2
- **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:** 1991
- **Award amount:** $184,920
- **Award type:** 2
- **Project period:** 1984-01-01 → 1995-03-31

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/3171133

## Citation

> US National Institutes of Health, RePORTER application 3171133, TRANSFORMATION BY AVIAN RETICULOENDOTHELIOSIS VIRUS (2R01CA033192-07A2). Retrieved via MORVS 2026-10-25 from https://api.morvs.ai/grant/nih/3171133. Licensed CC0.

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