Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form
As of April 1st VIVO Scientific Profiles will no longer updated for faculty, and the link to VIVO will be removed from the library website. Faculty profile pages will continue to be updated via Interfolio. VIVO will continue being used behind the scenes to update graduate student profiles. Please contact helplib@scripps.edu if you have questions.
How to download citations from VIVO | Alternative profile options

Domains of the qin protein required for oncogenic transformation

Academic Article
uri icon
  • Overview
  • Research
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Chang, H. W.
  • Li, J.
  • Vogt, Peter K.

publication date

  • July 1996

journal

  • Oncogene  Journal

abstract

  • The qin oncogene is a cell-derived insert in the genome of avian sarcoma virus 31 (ASV 31) and functions as the oncogenic determinant of that virus. Overexpression of the viral and cellular versions of the Qin protein (v-Qin and c-Qin) induces oncogenic transformation of chicken embryo fibroblasts (CEF); v-Qin also rapidly induces fibrosarcomas in chickens. Qin proteins can bind to specific DNA sequences and act as transcriptional repressors. In this study, mutants of Qin were constructed in order to determine the molecular domains required for transformation of chicken embryo fibroblasts. Our data indicate that three regions required for transforming activity are located (i) between residues 74-141 at the amino terminus, (ii) in the winged helix domain and (iii) between residues 383-395 at the carboxyl terminus. A Qin mutant with 12 amino acids deleted from the carboxyl terminus (383-395) showed transforming activity that was lower than that of wild type Qin for CEF. Compare to wild type Qin transformants, the mutant transformed cells had a reduced ability for multilayered and for anchorage independent growth. Deletion of 48 amino acids from the carboxyl terminus of the Qin protein (347-395) completely abolished transforming activity. In contrast, deletion of 74 amino acids from the amino terminus did not affect transformation of CEF. However, further deletion of 68 amino acids (74-141) reduced but did not abolish transforming activity. Finally, deletion in the winged helix domain (218-295) completely abrogated oncogenic capacity in CEF. These results suggest that DNA binding and transcriptional repression may be important in Qin-induced oncogenic transformation.

subject areas

  • Animals
  • Avian Proteins
  • Cell Transformation, Neoplastic
  • Chick Embryo
  • Chickens
  • Cloning, Molecular
  • Forkhead Transcription Factors
  • Mutation
  • Oncogene Proteins
  • Peptide Mapping
  • Polymerase Chain Reaction
  • Protein Structure, Secondary
  • Proto-Oncogene Proteins
  • Structure-Activity Relationship
  • Viral Proteins
scroll to property group menus

Research

keywords

  • DNA binding
  • Qin
  • transcriptional repression
  • winged helix domain
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0950-9232

PubMed ID

  • 8710385
scroll to property group menus

Additional Document Info

start page

  • 441

end page

  • 444

volume

  • 13

issue

  • 2

©2022 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support