Disease relevance of 3T3 Cells

• The EGF-RTA conjugate was toxic to 3T3 cells at concentrations (10(-9)--10(-11) M) similar to those at which EGF exerts its biological activity and within an order of magnitude of the toxicity of ricin [1].
• The SV-40-transformed Balb/c 3T3 line (SVT2) contains four times less vinculin than the parental 3T3 cells, and the rat adenocarcinoma BSp73ASML has no detectable vinculin [2].
• Mouse fibroblasts transformed by simian virus 40 (SV3T3 cells) are characterized by cyclic AMP and cyclic GMP levels, respectively, about half and twice those found in growing untransformed 3T3 cells [3].
• A second phosphotyrosine-containing protein has been detected in both Rous sarcoma virus and Abelson murine leukemia virus-transformed 3T3 cells, but was absent from normal 3T3 cells and 3T3 cells transformed by various other viruses [4].
• Although the amount of labeled p53 was increased in simian virus 40-transformed and methylcholanthrene-induced mouse sarcoma cells, the amount of p53 labeled during a 3-h pulse in Moloney virus- and Rous sarcoma virus-transformed cells and untransformed 3T3 cells was similar [5].

High impact information on 3T3 Cells

• Overexpression of tsg101 antisense transcripts in naive 3T3 cells resulted in cell transformation and increased stathmin-specific mRNA [6].
• Ectopic expression of the gas1 gene by microinjection in normal and transformed NIH 3T3 cell lines with the notable exception of SV40-transformed 3T3 cells leads to inhibition of DNA synthesis [7].
• PC12 cells were cultured on monolayers of control 3T3 cells or 3T3 cells expressing transfected N-cadherin or NCAM [8].
• The autoantigen La, a known transcription termination factor of RNA polymerase III, was purified to homogeneity from mouse 3T3 cells and calf thymus by different isolation procedures [9].
• A chicken-yeast chimeric beta-tubulin DNA was introduced into 3T3 cells using the transfection vector pSV2 [10].

Chemical compound and disease context of 3T3 Cells

• Toxicity of the EGF-RTA conjugate on 3T3 cells was competed by EGF and was blocked by antibodies to RTA, but not by lactose or antibodies to the ricin B chain (RTB) [1].
• Uptake of alpha-aminoisobutyric acid, by membrane vesicles derived principally from the plasma membrane and endoplasmic reticulum of mouse 3T3 cells transformed by simian virus 40, is stimulated by sodium chloride [11].
• An 85,000-molecular-weight polypeptide (85K polypeptide) has previously been identified as a common substrate for tyrosine phosphorylation upon polyomavirus middle T transformation or upon platelet-derived growth factor stimulation of 3T3 cells [12].
• Isolated myelin from adult rat spinal cord was adsorbed to polylysine-coated culture dishes and tested as a substrate for peripheral neurons, neuroblastoma cells, or 3T3 cells [13].
• Tumor virus transformed 3T3 cells (SV3T3 and Py3T3) grow quite well in suspension culture and transport leucine both in monolayer and suspension through a high affinity system, with a high Vmax value [14].

Biological context of 3T3 Cells

• Synergistic stimulation of S6 ribosomal protein phosphorylation and DNA synthesis by epidermal growth factor and insulin in quiescent 3T3 cells [15].
• Similarly, after treatment of 3T3 cells with the tumor-promoter phorbol myristate acetate, which induces a transformation-like phenotype, the cells no longer respond to PDGF as a chemoattractant but retain their migratory response to fibronectin [16].
• Increased cAMP levels promoted by PDGF acting through stimulation of E-type prostaglandin synthesis may contribute to signal the initiation of cell proliferation in 3T3 cells [17].
• Inhibitors of protein synthesis block the progression of quiescent 3T3 cells through G1 into S phase; however these drugs do not block the induction of KC and JE by PDGF [18].
• When added to cultures under hitherto optimum conditions for epidermal cell growth [in the presence of supporting 3T3 cells and epidermal growth factor (EGF)], most of the agents exert an effect of considerable magnitude, the toxin being the most potent [19].

Anatomical context of 3T3 Cells

• This assay shows that a variety of widely used tissue culture cells (mouse L cells, mouse 3T3 cells, chick embryo fibroblasts) have a tubulin content which corresponds to approximately 2.5--3.3% of their total protein [20].
• The identification of calmodulin-binding sites on mitochondria in cultured 3T3 cells [21].
• Phagokinetic tracks of 3T3 cells: parallels between the orientation of track segments and of cellular structures which contain actin or tubulin [22].
• This report demonstrates that a significant portion of the mitogenic activity for 3T3 cells secreted by cultured human alveolar and peritoneal macrophages is due to a molecule (or molecules) similar to platelet-derived growth factor (PDGF) [23].
• CRABP was present at a high level in all 3T3 cell types but was absent in all NRK cell lines [24].

Associations of 3T3 Cells with chemical compounds

• SSV-transformed cells have reduced numbers of high-affinity 125I-PDGF receptors; PDGF/p28v-sis receptor was purified from SSV-NIH 3T3 cells and retained active protein tyrosine kinase activity stimulated by PDGF [25].
• Cyclic AMP-mediated control of lipogenic enzyme synthesis during adipose differentiation of 3T3 cells [26].
• A transformed BHK cell lacking hypoxanthine guanosine phosphoribosyl tranferase, which was used an an indicator, was found to incorporate 3H-hypoxanthine when in prolonged (20 hr) or brief (1 hr) contact with donor 3T3 cells, whether the latter were in a quiescent layer of in the region of stimulation at the edge of a wound [27].
• Interruption of the adipose conversion of 3T3 cells by biotin deficiency: differentiation without triglyceride accumulation [28].
• In contrast, the neurohypophyseal hormone vasopressin, which is mitogenic for 3T3 cells, fails to synergize with TPA to stimulate DNA synthesis, ornithine decarboxylase activity or 2-deoxyglucose uptake [29].

Gene context of 3T3 Cells

• Here we report that Rb can repress c-fos expression and AP-1 transcriptional activity in both serum-induced and cycling 3T3 cells [30].
• Furthermore, Shh and downstream Shh signal transducers specifically induce ES enhancer/luciferase reporters in Shh-responsive 3T3 cells [31].
• Surprisingly, although B7h is expressed in unstimulated B cells, its expression is induced in both 3T3 cells and embryonic fibroblasts treated with TNFalpha, and it is upregulated in nonlymphoid tissues of mice treated with LPS, a potent activator of TNFalpha [32].
• Expression of a c-myc promoter driven CAT gene, transfected into quiescent 3T3 cells, is stimulated by serum addition whereas an identical gene containing mutations in the E2F binding sites is not responsive [33].
• Contrary to c-jun and junB transcription, which are strongly stimulated by serum or TPA treatment of quiescent 3T3 cells, junD transcription is not significantly stimulated in these conditions [34].

Analytical, diagnostic and therapeutic context of 3T3 Cells

• In addition, medium conditioned by continually paced myocytes contained significantly more bFGF measured by ELISA and more mitogenic activity for 3T3 cells, activity that could be reduced by a neutralizing anti-bFGF antibody [35].
• In addition to the plasma membrane, CBP35 could also be found intracellularly, as revealed by immunofluorescence studies of fixed and permeabilized 3T3 cells [36].
• Using indirect immunofluorescence, we have found that epidermal growth factor (EGF), at 100 ng/ml, induces centrosomal separation within 20 min in HeLa and 3T3 cells [37].
• Treatment of quiescent BALB/c mouse 3T3 cells with murine interferon alpha/beta (IFN-alpha/beta) (1000 units/ml) leads to the appearance at 4 hr of 1.7-kilobase 2',5'-oligoadenylate (2',5'-OAS)mRNA as detected by Northern blot analysis [38].
• Antisense RNA complementary to c-fos mRNA was produced in mouse 3T3 cells by gene transfer techniques [39].

References