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MeSH Review

NIH 3T3 Cells

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Disease relevance of NIH 3T3 Cells


High impact information on NIH 3T3 Cells


Chemical compound and disease context of NIH 3T3 Cells


Biological context of NIH 3T3 Cells


Anatomical context of NIH 3T3 Cells


Associations of NIH 3T3 Cells with chemical compounds

  • These observations demonstrate that two distinct, overexpressed tyrosine kinases can act synergistically to transform NIH 3T3 cells, thus identifying a novel mechanism that can lead to transformation [25].
  • A human CSF-1 receptor containing an "activating" mutation in its extracellular domain (serine for leucine 301) induced morphologic transformation, anchorage-independent growth, and tumorigenicity in mouse NIH 3T3 cells [26].
  • Here we report that functional expression in NIH/3T3 cells of a cardiac clone of another member of the ClC family, ClC-3, results in a large basally active chloride conductance, which is strongly modulated by cell volume and exhibits many properties identical to those of ICl.vol in native cells [27].
  • In NIH-3T3 cells expressing subtype 1 human muscarinic receptors (hm1), the agonist carbachol selectively increased the specific activity and phosphorylation state of epitope-tagged Ras-GRF [28].
  • In NIH 3T3 cells that overexpress the mutant Ras protein His116, which releases bound guanine nucleotide at a constitutively high rate and retains sensitivity to GAP and NF1, the proportion of GTP bound to the His116 protein was not altered by serum or platelet-derived growth factor [29].

Gene context of NIH 3T3 Cells

  • NIH 3T3-EGFR clonal lines, which expressed the EGF at 500- to 1000-fold levels over control NIH 3T3 cells, demonstrated a marked increase in DNA synthesis in response to EGF [17].
  • Finally, 125I-NT-3 binds to NIH 3T3 cells expressing gp145trkB; binding can be competed by NT-3 and BDNF but not by NGF [9].
  • A human clone, c-sis clone 8, which contains all of the v-sis-related sequences present in human DNA, was transcriptionally inactive when transfected into NIH/3T3 cells [30].
  • Treatment of NIH 3T3 cells with a specific inhibitor of p38 suppressed activation of the checkpoint by nocodazole [31].
  • Stat3-mediated transformation of NIH-3T3 cells by the constitutively active Q205L Galphao protein [32].

Analytical, diagnostic and therapeutic context of NIH 3T3 Cells


  1. EWS/FLI1-induced manic fringe renders NIH 3T3 cells tumorigenic. May, W.A., Arvand, A., Thompson, A.D., Braun, B.S., Wright, M., Denny, C.T. Nat. Genet. (1997) [Pubmed]
  2. Transformation of NIH 3T3 cells by microinjection of Ha-ras p21 protein. Stacey, D.W., Kung, H.F. Nature (1984) [Pubmed]
  3. Homology between an endogenous viral LTR and sequences inserted in an activated cellular oncogene. Kuff, E.L., Feenstra, A., Lueders, K., Rechavi, G., Givol, D., Canaani, E. Nature (1983) [Pubmed]
  4. Epidermal-growth-factor-dependent transformation by a human EGF receptor proto-oncogene. Velu, T.J., Beguinot, L., Vass, W.C., Willingham, M.C., Merlino, G.T., Pastan, I., Lowy, D.R. Science (1987) [Pubmed]
  5. Mouse c-myc oncogene is located on chromosome 15 and translocated to chromosome 12 in plasmacytomas. Crews, S., Barth, R., Hood, L., Prehn, J., Calame, K. Science (1982) [Pubmed]
  6. Wildtype Kras2 can inhibit lung carcinogenesis in mice. Zhang, Z., Wang, Y., Vikis, H.G., Johnson, L., Liu, G., Li, J., Anderson, M.W., Sills, R.C., Hong, H.L., Devereux, T.R., Jacks, T., Guan, K.L., You, M. Nat. Genet. (2001) [Pubmed]
  7. Epimorphin: a mesenchymal protein essential for epithelial morphogenesis. Hirai, Y., Takebe, K., Takashina, M., Kobayashi, S., Takeichi, M. Cell (1992) [Pubmed]
  8. The neurotrophic factors brain-derived neurotrophic factor and neurotrophin-3 are ligands for the trkB tyrosine kinase receptor. Soppet, D., Escandon, E., Maragos, J., Middlemas, D.S., Reid, S.W., Blair, J., Burton, L.E., Stanton, B.R., Kaplan, D.R., Hunter, T. Cell (1991) [Pubmed]
  9. The trkB tyrosine protein kinase is a receptor for brain-derived neurotrophic factor and neurotrophin-3. Klein, R., Nanduri, V., Jing, S.A., Lamballe, F., Tapley, P., Bryant, S., Cordon-Cardo, C., Jones, K.R., Reichardt, L.F., Barbacid, M. Cell (1991) [Pubmed]
  10. Platelet-activating factor and retinoic acid synergistically activate the inducible prostaglandin synthase gene. Bazan, N.G., Fletcher, B.S., Herschman, H.R., Mukherjee, P.K. Proc. Natl. Acad. Sci. U.S.A. (1994) [Pubmed]
  11. Natural UAG suppressor glutamine tRNA is elevated in mouse cells infected with Moloney murine leukemia virus. Kuchino, Y., Beier, H., Akita, N., Nishimura, S. Proc. Natl. Acad. Sci. U.S.A. (1987) [Pubmed]
  12. Activating mutations of the c-Ha-ras protooncogene in chemically induced hepatomas of the male B6C3 F1 mouse. Wiseman, R.W., Stowers, S.J., Miller, E.C., Anderson, M.W., Miller, J.A. Proc. Natl. Acad. Sci. U.S.A. (1986) [Pubmed]
  13. In vitro methylation of specific regions of the cloned Moloney sarcoma virus genome inhibits its transforming activity. McGeady, M.L., Jhappan, C., Ascione, R., Vande Woude, G.F. Mol. Cell. Biol. (1983) [Pubmed]
  14. Increase in nitrosourea resistance in mammalian cells by retrovirally mediated gene transfer of bacterial O6-alkylguanine-DNA alkyltransferase. Dumenco, L.L., Warman, B., Hatzoglou, M., Lim, I.K., Abboud, S.L., Gerson, S.L. Cancer Res. (1989) [Pubmed]
  15. Glucocorticoid regulation of the Ha-MuSV p21 gene conferred by sequences from mouse mammary tumor virus. Huang, A.L., Ostrowski, M.C., Berard, D., Hager, G.L. Cell (1981) [Pubmed]
  16. Purified maturation promoting factor phosphorylates pp60c-src at the sites phosphorylated during fibroblast mitosis. Shenoy, S., Choi, J.K., Bagrodia, S., Copeland, T.D., Maller, J.L., Shalloway, D. Cell (1989) [Pubmed]
  17. Overexpression of the human EGF receptor confers an EGF-dependent transformed phenotype to NIH 3T3 cells. Di Fiore, P.P., Pierce, J.H., Fleming, T.P., Hazan, R., Ullrich, A., King, C.R., Schlessinger, J., Aaronson, S.A. Cell (1987) [Pubmed]
  18. Altered growth regulation and enhanced tumorigenicity of NIH 3T3 fibroblasts transfected with protein kinase C-I cDNA. Persons, D.A., Wilkison, W.O., Bell, R.M., Finn, O.J. Cell (1988) [Pubmed]
  19. Point mutation at the ATP binding site of EGF receptor abolishes protein-tyrosine kinase activity and alters cellular routing. Honegger, A.M., Dull, T.J., Felder, S., Van Obberghen, E., Bellot, F., Szapary, D., Schmidt, A., Ullrich, A., Schlessinger, J. Cell (1987) [Pubmed]
  20. Activation of the cellular proto-oncogene product p21Ras by addition of a myristylation signal. Buss, J.E., Solski, P.A., Schaeffer, J.P., MacDonald, M.J., Der, C.J. Science (1989) [Pubmed]
  21. A single nucleotide change in the prolidase gene in fibroblasts from two patients with polypeptide positive prolidase deficiency. Expression of the mutant enzyme in NIH 3T3 cells. Tanoue, A., Endo, F., Kitano, A., Matsuda, I. J. Clin. Invest. (1990) [Pubmed]
  22. Stimulation of alpha 1 (I) procollagen gene expression in NIH-3T3 cells by the human T cell leukemia virus type 1 (HTLV-1) Tax gene. Muñoz, E., Suri, D., Amini, S., Khalili, K., Jiménez, S.A. J. Clin. Invest. (1995) [Pubmed]
  23. Lateral diffusion of an 80,000-dalton glycoprotein in the plasma membrane of murine fibroblasts: relationships to cell structure and function. Jacobson, K., O'Dell, D., August, J.T. J. Cell Biol. (1984) [Pubmed]
  24. Identification of amino acid sequences in the integrin beta 1 cytoplasmic domain implicated in cytoskeletal association. Reszka, A.A., Hayashi, Y., Horwitz, A.F. J. Cell Biol. (1992) [Pubmed]
  25. Synergistic interaction of p185c-neu and the EGF receptor leads to transformation of rodent fibroblasts. Kokai, Y., Myers, J.N., Wada, T., Brown, V.I., LeVea, C.M., Davis, J.G., Dobashi, K., Greene, M.I. Cell (1989) [Pubmed]
  26. A point mutation in the extracellular domain of the human CSF-1 receptor (c-fms proto-oncogene product) activates its transforming potential. Roussel, M.F., Downing, J.R., Rettenmier, C.W., Sherr, C.J. Cell (1988) [Pubmed]
  27. Molecular identification of a volume-regulated chloride channel. Duan, D., Winter, C., Cowley, S., Hume, J.R., Horowitz, B. Nature (1997) [Pubmed]
  28. Phosphorylation-dependent activation of the Ras-GRF/CDC25Mm exchange factor by muscarinic receptors and G-protein beta gamma subunits. Mattingly, R.R., Macara, I.G. Nature (1996) [Pubmed]
  29. Mechanistic aspects of signaling through Ras in NIH 3T3 cells. Zhang, K., Papageorge, A.G., Lowy, D.R. Science (1992) [Pubmed]
  30. Expression of the normal human sis/PDGF-2 coding sequence induces cellular transformation. Gazit, A., Igarashi, H., Chiu, I.M., Srinivasan, A., Yaniv, A., Tronick, S.R., Robbins, K.C., Aaronson, S.A. Cell (1984) [Pubmed]
  31. Activation of the protein kinase p38 in the spindle assembly checkpoint and mitotic arrest. Takenaka, K., Moriguchi, T., Nishida, E. Science (1998) [Pubmed]
  32. Stat3-mediated transformation of NIH-3T3 cells by the constitutively active Q205L Galphao protein. Ram, P.T., Horvath, C.M., Iyengar, R. Science (2000) [Pubmed]
  33. Ras p21 proteins with high or low GTPase activity can efficiently transform NIH/3T3 cells. Lacal, J.C., Srivastava, S.K., Anderson, P.S., Aaronson, S.A. Cell (1986) [Pubmed]
  34. The solution structure of the RING finger domain from the acute promyelocytic leukaemia proto-oncoprotein PML. Borden, K.L., Boddy, M.N., Lally, J., O'Reilly, N.J., Martin, S., Howe, K., Solomon, E., Freemont, P.S. EMBO J. (1995) [Pubmed]
  35. Hsp72 functions as a natural inhibitory protein of c-Jun N-terminal kinase. Park, H.S., Lee, J.S., Huh, S.H., Seo, J.S., Choi, E.J. EMBO J. (2001) [Pubmed]
  36. PATE, a gene expressed in prostate cancer, normal prostate, and testis, identified by a functional genomic approach. Bera, T.K., Maitra, R., Iavarone, C., Salvatore, G., Kumar, V., Vincent, J.J., Sathyanarayana, B.K., Duray, P., Lee, B.K., Pastan, I. Proc. Natl. Acad. Sci. U.S.A. (2002) [Pubmed]
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