Skip to main content
padlock icon - secure page this page is secure

Expression of full length or truncated epidermal growth factor precursor transforms NIH3T3 fibroblasts.

Buy Article:

$42.00 + tax (Refund Policy)

Epidermal growth factor (EGF) is derived from a large precursor (EGFP) of unusual structure. As EGFP remains unprocessed in certain tissues, it is of biological relevance to study its activity. Activation of the EGF receptor by EGF is involved in transformation of NIH3T3 fibroblasts. We isolated clones of NIH3T3 expressing full length, cytoplasmic region deleted or EGF-repeats deleted EGFP. All clones formed colonies in soft agarose and tumors in nude mice. Two clones expressing EGF-repeats deleted EGFP formed more and larger colonies. To conclude, EGFP is biologically active. Deletion of the 8 EGF repeats may enhance anchorage independent growth in NIH3T3.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Document Type: Research Article

Affiliations: Department of Paediatrics, the University of Hong Kong, Queen Mary Hospital, Hong Kong.

Publication date: January 1, 1999

More about this publication?
  • The International Journal of Oncology provides an international forum for the publication of the latest, cutting-edge research in the broad area of oncology and cancer treatment. The journal accepts original high quality works and reviews on all aspects of oncology research including carcinogenesis, metastasis, epidemiology, chemotherapy and viral oncology. Through fair and efficient peer review, the journal is dedicated to publishing top tier research in the field, offering authors rapid publication as well as high standards of copy-editing and production. The International Journal of Oncology is published on a monthly basis in both print and early online.
  • Editorial Board
  • Information for Authors
  • Submit a Paper
  • Subscribe to this Title
  • Information for Advertisers
  • Terms & Conditions
  • Ingenta Connect is not responsible for the content or availability of external websites
  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more