ArticleThe Journal of cell biology1990
Isolation and characterization of a 60-70-kD plasma membrane glycoprotein involved in the contact-dependent inhibition of growth.
Article in The Journal of cell biology, 1990. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 51 citations in OpenAlex.
- Article
- The aryl hydrocarbon receptor (AhR) in the regulation of cell-cell contact and tumor growth.Carcinogenesis · 2010Review
- Involvement of Galectin-3 with vascular cell adhesion molecule-1 in growth regulation of mouse BALB/3T3 cells.The Journal of biological chemistry · 2009Article
- Akt phosphorylation of merlin enhances its binding to phosphatidylinositols and inhibits the tumor-suppressive activities of merlin.Cancer research · 2009Article
- The role of cell differentiation in controlling cell multiplication and cancer.Journal of cancer research and clinical oncology · 2008Review
- p38alpha MAPK is required for contact inhibition.Oncogene · 2005Article
- Involvement of protein kinase Cdelta in contact-dependent inhibition of growth in human and murine fibroblasts.Oncogene · 2001Article
- The NF2 tumor suppressor gene product, merlin, mediates contact inhibition of growth through interactions with CD44.Genes & development · 2001Article
- SSeCKS, a major protein kinase C substrate with tumor suppressor activity, regulates G(1)-->S progression by controlling the expression and cellular compartmentalization of cyclin D.Molecular and cellular biology · 2000Article
- Confluence of vascular endothelial cells induces cell cycle exit by inhibiting p42/p44 mitogen-activated protein kinase activity.Molecular and cellular biology · 1999Article
- p16INK4 mediates contact-inhibition of growth.Oncogene · 1999Article
- Growth retardation and early death of beta-1,4-galactosyltransferase knockout mice with augmented proliferation and abnormal differentiation of epithelial cells.The EMBO journal · 1997Article
- Cell-contact mediated modulation of the sialylation of contactinhibin.Glycoconjugate journal · 1995Article
- Expression of DEP-1, a receptor-like protein-tyrosine-phosphatase, is enhanced with increasing cell density.Proceedings of the National Academy of Sciences of the United States of America · 1994Article
- Regulation of Mel-CAM/MUC18 expression on melanocytes of different stages of tumor progression by normal keratinocytes.The American journal of pathology · 1994Article
- Bradykinin-induced growth inhibition of normal rat kidney (NRK) cells is paralleled by a decrease in epidermal-growth-factor receptor expression.The Biochemical journal · 1994Article
- Kinetic resistance to anticancer agents.Cytotechnology · 1993Review
- Chemotactic migration of human diploid fibroblasts is inhibited by contactinhibin.In vitro cellular & developmental biology : journal of the Tissue Culture Association · 1992Article
- Neural cell adhesion molecule mediates contact-dependent inhibition of growth of near-diploid mouse fibroblast cell line m5S/1M.The Journal of cell biology · 1991Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that plasma membrane compounds are involved in the contact-dependent inhibition of growth of human diploid fibroblasts. The purification of the active plasma membrane glycoprotein is described in this report. The glycoprotein has an apparent molecular mass of 60-70 kD and, due to differential sialylation, isoelectric points between pH 5.5. and 6.2. Treatment with sialidase yielded one spot in two-dimensional gel electrophoresis with an isoelectric point of 6.3. After removal of the N-glycosidically linked oligosaccharide chains, the apparent molecular mass is reduced by approximately 22 kD. Treatment was diluted NaOH, which removes the O-glycosidically linked portion of oligosaccharides, resulted in a reduction of the apparent molecular mass by approximately 5 kD. The addition of 50 ng/ml of this glycoprotein-for which the term "contactinhibin" is proposed-in immobilized form to sparsely seeded human fibroblasts resulted in a reversible 70-80% inhibition of growth. The inhibition was not confined to human fibroblasts as other cells were also inhibited, with the exclusion of transformed cells, which are refractory to contactinhibin. The inhibitory activity was abolished by treatment with beta-galactosidase or glycopeptidase F, indicating that the glycan moiety is the biologically active part of the molecule. Confluent cultures treated with antibodies raised against contactinhibin were released from the contact-dependent inhibition of growth. In addition to enhanced saturation density, these cultures exhibited a crisscross growth pattern and the formation of foci. Immunocytochemical studies showed that contactinhibin was associated with vimentin. Furthermore, contactinhibin was found to be not expressed in a species- or organ-specific manner.
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