Reversion of the transformed phenotype of B16 mouse melanoma: involvement of an 
83 kd cell surface glycoprotein in specific growth inhibition

Wieland, I; Müller, G; Braun, S; Birchmeier, W

doi:10.1016/0092-8674(86)90510-6

Item

ITEM ACTIONSEXPORT

Add to Basket

Local TagsRelease HistoryDetailsSummary

Released

Journal Article

Reversion of the transformed phenotype of B16 mouse melanoma: involvement of an 83 kd cell surface glycoprotein in specific growth inhibition

MPS-Authors

/persons/resource/persons287086

Wieland, I
Birchmeier Group, Friedrich Miescher Laboratory, Max Planck Society;

/persons/resource/persons287088

Müller, G
Birchmeier Group, Friedrich Miescher Laboratory, Max Planck Society;

/persons/resource/persons287084

Braun, S
Birchmeier Group, Friedrich Miescher Laboratory, Max Planck Society;

/persons/resource/persons284673

Birchmeier, W
Birchmeier Group, Friedrich Miescher Laboratory, Max Planck Society;

External Resource

No external resources are shared

Fulltext (restricted access)

There are currently no full texts shared for your IP range.

Fulltext (public)

There are no public fulltexts stored in PuRe

Supplementary Material (public)

There is no public supplementary material available

Citation

Wieland, I., Müller, G., Braun, S., & Birchmeier, W. (1986). Reversion of the transformed phenotype of B16 mouse melanoma: involvement of an 83 kd cell surface glycoprotein in specific growth inhibition. Cell, 47(5), 675-685. doi:10.1016/0092-8674(86)90510-6.

Cite as: https://hdl.handle.net/21.11116/0000-000C-A0B5-2

Abstract

Treating B16 mouse melanoma cells with monoclonal antibody NORM-2 reduces cell growth in tissue culture, agar, and syngeneic mice. We show that the NORM-2 antibody recognizes an integral 83 kd glycoprotein that is mobile in the plane of the plasma membrane of B16 melanoma cells. Expression of the glycoprotein is reduced under conditions that inhibit B16 growth, such as low serum, high cell density, and addition of transforming growth factor-beta. The glycoprotein reappears during S phase, when growth-arrested cells are restimulated. The NORM-2 antigen appears to be involved in growth regulation of B16 melanoma cells both in vitro and in vivo.