FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2076867332> ?p ?o ?g. }

• W2076867332 endingPage "209" @default.
• W2076867332 startingPage "193" @default.
• W2076867332 abstract "Expression of rat oncogenic neu receptor, p185T-neu (a growth factor receptor with constitutive tyrosine kinase activity), causes cells to become transformed. Treatment with anti-neu receptor monoclonal antibodies reverts the transformed phenotype by down-modulation of p185T-neu. Monoclonal antibody treatment of cells expressing normal neu receptor, p185C-neu (which lacks constitutive tyrosine kinase activity), does not result in down-modulation of p185C-neu. To understand further the role the biochemical activity of p185T-neu plays in transformation and endocytosis, we created a series of mutations in p185T-neu. We found that fibroblasts expressing the tyrosine kinase-defective mutants cannot form foci in culture, colonies in soft agar, or tumors in immunocompromised mice. To follow the antibody-induced endocytosis of neu receptors expressed in these transfectants, we developed a novel two-color flow cytometric assay and confirmed receptor localization by electron microscopy. Cells were treated with mAb7.16.4 over time. After 4 hr of antibody treatment, less than 50% of full-length p185T-neu and of mutant T691 remained on the cell surface, whereas internal expression of the neu receptors within these cells initially increased and then decreased to the original internal receptor level. In contrast, the level of kinase-deficient mutated neu receptors remaining on the cell surface initially decreased by 35%, but, after 4 hr of antibody treatment, the cell surface expression level returned to approximately the original level. Concurrently, fluctuations in expression levels were seen internally over time as well. These cell lines were also treated with gold-conjugated mAb7.16.4. Using electron microscopy, we consistently found the gold particles within multivesicular bodies of cell lines expressing full-length or mutated neu receptor. These data strongly suggest that the fate of the neu receptor, once internalized, is directed by its tyrosine kinase activity. When the kinase activity of the neu receptor is disrupted, the receptor is internalized but recycled to the cell surface, whereas neu receptors which have constitutive kinase activity are internalized and presumably degraded when engaged with anti-neu receptor mAb. Understanding the regulation of receptor endocytosis, degradation, and recycling will contribute to the development of novel therapeutic protocols to combat human malignancies, particularly those associated with the overexpression of the human homologue of the neu receptor, c-erbB2." @default.
• W2076867332 created "2016-06-24" @default.
• W2076867332 creator A5013002185 @default.
• W2076867332 creator A5021776897 @default.
• W2076867332 creator A5042586488 @default.
• W2076867332 creator A5050260667 @default.
• W2076867332 creator A5057271826 @default.
• W2076867332 creator A5084688558 @default.
• W2076867332 creator A5084918260 @default.
• W2076867332 creator A5085210378 @default.
• W2076867332 creator A5091416723 @default.
• W2076867332 date "1994-02-01" @default.
• W2076867332 modified "2023-09-26" @default.
• W2076867332 title "Demonstration by Two-Color Flow Cytometry That Tyrosine Kinase Activity Is Required for Down-Modulation of the Oncogenic neu Receptor" @default.
• W2076867332 cites W128647466 @default.
• W2076867332 cites W1529444545 @default.
• W2076867332 cites W1574457161 @default.
• W2076867332 cites W158850611 @default.
• W2076867332 cites W1607784649 @default.
• W2076867332 cites W1894641937 @default.
• W2076867332 cites W1963804483 @default.
• W2076867332 cites W1964265039 @default.
• W2076867332 cites W1965372133 @default.
• W2076867332 cites W1968013329 @default.
• W2076867332 cites W1972960760 @default.
• W2076867332 cites W1973033337 @default.
• W2076867332 cites W1973188134 @default.
• W2076867332 cites W1977958044 @default.
• W2076867332 cites W1979443682 @default.
• W2076867332 cites W1983673751 @default.
• W2076867332 cites W1985332851 @default.
• W2076867332 cites W1995337883 @default.
• W2076867332 cites W1995574514 @default.
• W2076867332 cites W1999265691 @default.
• W2076867332 cites W2002530645 @default.
• W2076867332 cites W2006285921 @default.
• W2076867332 cites W2008346047 @default.
• W2076867332 cites W2010225640 @default.
• W2076867332 cites W2010527163 @default.
• W2076867332 cites W2017213758 @default.
• W2076867332 cites W2022022192 @default.
• W2076867332 cites W2023506714 @default.
• W2076867332 cites W2028387622 @default.
• W2076867332 cites W2031933070 @default.
• W2076867332 cites W2032422012 @default.
• W2076867332 cites W2039074795 @default.
• W2076867332 cites W2042169992 @default.
• W2076867332 cites W2044075747 @default.
• W2076867332 cites W2047897111 @default.
• W2076867332 cites W2055963067 @default.
• W2076867332 cites W2064625798 @default.
• W2076867332 cites W2067691363 @default.
• W2076867332 cites W2070360831 @default.
• W2076867332 cites W2072140252 @default.
• W2076867332 cites W2077307648 @default.
• W2076867332 cites W2082431893 @default.
• W2076867332 cites W2084548343 @default.
• W2076867332 cites W2084928785 @default.
• W2076867332 cites W2085344344 @default.
• W2076867332 cites W2085665257 @default.
• W2076867332 cites W2086046274 @default.
• W2076867332 cites W2092429540 @default.
• W2076867332 cites W2103174300 @default.
• W2076867332 cites W2117185170 @default.
• W2076867332 cites W2121997189 @default.
• W2076867332 cites W2126818181 @default.
• W2076867332 cites W2130397500 @default.
• W2076867332 cites W2138466097 @default.
• W2076867332 cites W2151127067 @default.
• W2076867332 cites W2171584014 @default.
• W2076867332 cites W4234411800 @default.
• W2076867332 doi "https://doi.org/10.1089/dna.1994.13.193" @default.
• W2076867332 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/7910024" @default.
• W2076867332 hasPublicationYear "1994" @default.
• W2076867332 type Work @default.
• W2076867332 sameAs 2076867332 @default.
• W2076867332 citedByCount "7" @default.
• W2076867332 crossrefType "journal-article" @default.
• W2076867332 hasAuthorship W2076867332A5013002185 @default.
• W2076867332 hasAuthorship W2076867332A5021776897 @default.
• W2076867332 hasAuthorship W2076867332A5042586488 @default.
• W2076867332 hasAuthorship W2076867332A5050260667 @default.
• W2076867332 hasAuthorship W2076867332A5057271826 @default.
• W2076867332 hasAuthorship W2076867332A5084688558 @default.
• W2076867332 hasAuthorship W2076867332A5084918260 @default.
• W2076867332 hasAuthorship W2076867332A5085210378 @default.
• W2076867332 hasAuthorship W2076867332A5091416723 @default.
• W2076867332 hasConcept C101544691 @default.
• W2076867332 hasConcept C153911025 @default.
• W2076867332 hasConcept C159654299 @default.
• W2076867332 hasConcept C170493617 @default.
• W2076867332 hasConcept C197462201 @default.
• W2076867332 hasConcept C203014093 @default.
• W2076867332 hasConcept C28005876 @default.
• W2076867332 hasConcept C2993002077 @default.
• W2076867332 hasConcept C42362537 @default.
• W2076867332 hasConcept C542903549 @default.
• W2076867332 hasConcept C54355233 @default.

• next