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1.
Biochem Biophys Res Commun ; 208(2): 637-43, 1995 Mar 17.
Artículo en Inglés | MEDLINE | ID: mdl-7695618

RESUMEN

The high affinity 67-kDa laminin receptor (67LR) is highly expressed in metastatically active human cancers. A 37-kDa polypeptide has been identified as its precursor (37LRP). Antibodies raised against 37LRP-derived synthetic peptides were used in immunogold electron microscopy and immunoblot studies to assess the effect of laminin on expression of the 67LR and the 37LRP. Laminin (15 micrograms/ml) treatment of suspended A2058 human melanoma cells doubled the expression of both 37LRP and the 67LR. Fibronectin had no effect. There was no effect of laminin on the expression of actin or galectin-3. Cycloheximide treatment of cells prior to laminin abrogated its inducible effect. The results suggest that binding of laminin by cell surface laminin receptors induces synthesis of the 37LRP and mature 67LR, with a consequent delivery to the cell surface of more laminin binding proteins for potentiated attachment of the melanoma cell to the basement membrane during invasion and metastasis.


Asunto(s)
Laminina/farmacología , Receptores de Laminina/biosíntesis , Animales , Cicloheximida/farmacología , Humanos , Inmunohistoquímica , Técnicas In Vitro , Melanoma/metabolismo , Ratones , Peso Molecular , Precursores de Proteínas/metabolismo , Células Tumorales Cultivadas
2.
Cell Growth Differ ; 1(5): 217-24, 1990 May.
Artículo en Inglés | MEDLINE | ID: mdl-2150753

RESUMEN

Site-directed mutagenesis of the conserved sequence motifs of p21 generated a group of mutant p21s defective in GTP binding. Some of these mutants were highly transforming, whereas others were transformation defective. Among the latter group, we found two mutants, derived from the v-H-ras oncogene by substituting the asparagine-116 with tyrosine and isoleucine, that exhibited a trans-dominant activity of suppressing the transformed phenotype of NIH3T3 cells induced by a long terminal repeat-linked c-H-ras and a wild-type v-H-ras. They caused reduction of the colony-forming efficiency in soft agar (78% in c-ras-transformed cells; 55% in v-ras cells) and morphological reversion of ras transformants. Subclones of revertants expressed a great excess of mutant p21 relative to the c-ras p21 present in these cells. These mutants were not lethal to NIH3T3 cells. Apparently, defective proteins encoded by suppressor mutants sequestered vital targets for ras function. Suppressor mutants also induced morphological reversion of NIH3T3 cells transformed by src, fes/flp, sis, and fms oncogenes, suggesting that these oncogenes function upstream to ras in the signaling pathways. Cells transformed by mos and a chemical carcinogen were unaffected.


Asunto(s)
Transformación Celular Neoplásica/genética , Proteínas de Unión al GTP/genética , Genes ras , Proteína Oncogénica p21(ras)/genética , Supresión Genética , Animales , Secuencia de Bases , Línea Celular , Transformación Celular Neoplásica/inducido químicamente , Chlorocebus aethiops , Secuencia de Consenso , Metanosulfonato de Etilo , Fibroblastos , Proteínas de Unión al GTP/fisiología , Genes Dominantes , Guanosina Trifosfato/metabolismo , Ratones , Datos de Secuencia Molecular , Mutagénesis Sitio-Dirigida , Proteína Oncogénica p21(ras)/fisiología , Proteínas Oncogénicas/antagonistas & inhibidores , Proteínas Oncogénicas/fisiología , Oncogenes , Proteínas Proto-Oncogénicas p21(ras)/genética , Transducción de Señal/genética
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