Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1992 Jan;7(1):95-100.

Cell type and developmental regulation of the fyn proto-oncogene in neural retina

Affiliations
  • PMID: 1741169

Cell type and developmental regulation of the fyn proto-oncogene in neural retina

C A Ingraham et al. Oncogene. 1992 Jan.

Abstract

The product of the proto-oncogene c-fyn (p59fyn) is a non-receptor tyrosine kinase of unknown function. The expression of the p59fyn tyrosine kinase was analysed by immunoperoxidase staining of the different neuronal cell types in the developing chick neural retina. p59fyn was primarily localized in the cell bodies of mature retinal neurons. p59fyn immunoreactivity was most abundant in cell bodies of differentiated ganglion, amacrine and photoreceptor cells. The onset of p59fyn expression in developing photoreceptors occurred coordinately with terminal neuronal differentiation. p59fyn was also found within the outer plexiform layer, which contains synaptic terminals of the photoreceptors. At embryonic stages prior to photoreceptor differentiation, p59fyn was most highly concentrated in the cell bodies of differentiating ganglion and amacrine cells. p59fyn autokinase activity in retinal extracts decreased concomitant with the final stages of maturation of retinal neurons, suggesting that the p59fyn kinase is developmentally regulated. Thus, the expression of p59fyn is regulated in both a developmental and cell type-specific manner. The existence of p59fyn in some of the same neuronal cells as p60c-src suggests the possibility of functional redundancy of these non-receptor tyrosine kinases.

PubMed Disclaimer

Publication types

Substances