Disease relevance of Kirsten murine sarcoma virus

• The effect of infecting fibroblasts with Kirsten murine sarcoma virus/murine leukemia virus (Ki-MSV/MLV) on constitutive and IFN-gamma-induced H-2 antigen expression was investigated [1].
• The K-ras gene is the cellular counterpart of the viral ras oncogene in Kirsten murine sarcoma virus, but the N-ras has not yet been found in a retrovirus [2].
• Superinfection of early passage nontumorigenic HBL-100 cells with Kirsten murine sarcoma virus, which contains a Ki-ras oncogene having undergone multiple activating events, induces morphologic alterations and rapidly converts the cells to neoplastic cells, further supporting the hypothesis of multistep carcinogenesis [3].
• Human osteosarcoma (HOS) clonal cells transformed in vitro by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) were characterized, and compared to non-producer HOS cells transformed by Kirsten murine sarcoma virus (Ki-MSV) [4].
• Loss of epidermal growth factor receptor on the renal neoplasm induced in vivo with Xenotropic pseudotype Kirsten murine sarcoma virus [5].

High impact information on Kirsten murine sarcoma virus

• Murine hemopoietic cells were infected in vitro with Harvey or Kirsten sarcoma virus, and then cultured in methylcellulose in the presence of relatively low concentrations of erythropoietin [6].
• Tumor promoters and Kirsten sarcoma virus increase synthesis of a secreted glycoprotein by regulating levels of translatable mRNA [7].
• Addition of Kirsten murine sarcoma virus, which contains a K-ras oncogene, to these cells induced morphological alterations associated with the acquisition of neoplastic properties [8].
• Nucleotide sequence of the oncogene encoding the p21 transforming protein of Kirsten murine sarcoma virus [9].
• Exposure of rat thyroid cells for 1 week to a temperature-sensitive variant of Kirsten murine sarcoma virus (KiMSV) Ras inactivated the thyroglobulin promoter (pTg) [10].

Chemical compound and disease context of Kirsten murine sarcoma virus

• An unusual oxygen-sensitive lactate dehydrogenase isozyme associated with Kirsten murine sarcoma virus in human serum [11].
• In contrast to cells from primary or secondary culture, these cells could be transformed to malignant neoplastic cells by infection with Kirsten murine sarcoma virus containing the Ki-ras oncogene or in one line by the chemical carcinogen, N-methyl-N'-nitro-N-nitrosoguanidine; both of these agents produced a marked proliferative response [12].
• Thyroid hormone modulation of transformation induced by Kirsten murine sarcoma virus [13].
• A nitroquinoline oxide (NQT-3T3-714) and a temperature-sensitive Kirsten sarcoma virus (tsKi-3T3-714) transformant of subclone 714 exhibited transformed phenotypes with respect to morphology and growth properties, but their rates of lactate production and 2-[3H]deoxy-D-glucose (deoxyglucose) uptake were similar to those of the parent cells [14].
• Adhesion has been evaluated for tumor cell populations derived from Kirsten murine sarcoma virus (KiMSV)-transformed BALB/c 3T3 cells responding to substrata coated with intact plasma fibronectin (pFN), a family of related proteolytic fragments from pFN or cellular fibronectins (FNs), and the heparan sulfate-binding platelet factor-4 (PF4) [15].

Biological context of Kirsten murine sarcoma virus

• The homologous sequences are present in multiple copies per diploid rat cellular genome in a variety of different rat cellular dna's. In certain cells that constitutively express only low levels of sequences homologous to Kirsten sarcoma virus, bromodeoxyuridine treatment leads to the expression of high levels of these sequences in RNA [16].
• Rat kidney cells infected with a temperature-sensitive mutant of Kirsten sarcoma virus (Ki-MSV ts 371) expressed Ki-Ras at 37 degrees C but not at 42 degrees C. This expression of the oncogene was accompanied by an increase in the activity of ornithine decarboxylase (ODC) and the accumulation of putrescine [17].

Anatomical context of Kirsten murine sarcoma virus

• MEP proteins synthesized by normal NIH 3T3 cells or NIH cells transformed with Kirsten sarcoma virus displayed a similar low affinity for the receptor and were found to possess oligosaccharide species with two phosphomonoester moieties [18].
• Subsequent infection of these cells with Kirsten murine sarcoma virus containing an activated Ki-ras oncogene induces at least a 10-20-fold increase in PTHRP expression and production of both adult and fetal immortalized cell lines in the presence of the same growth factors [19].
• In this report, we show that when human osteosarcoma derived clonal cells (TE 85 clone F-5) (HOS), which are immortalized and nontumorigenic, undergo transformation following infection by Kirsten murine sarcoma virus (K-HOS) or by a chemical carcinogen [N-methyl-N-nitro-N-nitrosoguanidine (MNNG-HOS)], the smooth muscle MLC-2 mRNA is repressed [20].

Gene context of Kirsten murine sarcoma virus

• A derivative cell, KC, resulted from Kirsten murine sarcoma virus transformation, and these cells no longer require EGF for their growth [21].
• The binding of EGF to transformed cell in vivo with Xenotropic pseudotype Kirsten murine sarcoma virus was abolished [5].
• Nonfunctional epidermal growth factor receptor in cells transformed by Kirsten sarcoma virus [22].
• Synthesis and secretion of plasminogen activators and collagenases in human cells transformed by Kirsten murine sarcoma virus and N-methyl-N'-nitro-N-nitrosoguanidine [23].
• Similar induction of MEP RNA is seen after treatment with platelet-derived growth factor or transformation with Kirsten sarcoma virus [24].

References