Disease relevance of Genes, mos

• We have previously shown that the mos gene product, p40mos, produced in Escherichia coli binds ATP and has ATPase activity [1].
• Moloney murine sarcoma virus carries an oncogenic sequence (v-mos) which is homologous to a single copy gene (c-mos) present in the normal cells of several vertebrate species [2].
• We have previously described the inhibition of glucocorticoid-dependent transcription from the mouse mammary tumor virus long terminal repeat promoter by products of the H-ras and v-mos oncogenes [3].
• We concluded that tubulin-disturbing agents induce c-Mos gene expression and activation in SKOV3 ovarian carcinoma cells and that such an effect occurs after mitotic blockade and coincides with drug-induced apoptosis [4].
• Overall, v-mosm1 has greater homology with c-mos than does v-mos124, but mutually exclusive differences between c-mos and each of the v-mos genes preclude linear descent and suggest a common ancestral murine sarcoma virus [5].

High impact information on Genes, mos

• Specific proteolysis of the c-mos proto-oncogene product by calpain on fertilization of Xenopus eggs [6].
• The c-mos proto-oncogene is expressed as a maternal mRNA in oocytes and early embryos of Xenopus laevis, but its translation product pp39mos is detectable only during progesterone-induced oocyte maturation [7].
• The product of the mos proto-oncogene is a serine/threonine kinase that is expressed at high levels in germ cells [8].
• Recently, we showed that mosxe can transform murine NIH3T3 fibroblasts, although it exhibited only 1-2% of the transforming activity of the v-mos oncogene [9].
• Elevated levels of a specific class of nuclear phosphoproteins in cells transformed with v-ras and v-mos oncogenes and by cotransfection with c-myc and polyoma middle T genes [10].

Biological context of Genes, mos

• In order to determine whether the v-mos gene product (v-Mos) causes neoplastic transformation via interaction with cell cycle control elements, we have searched for proteins that interact with v-Mos [11].
• These four strains have an identical 5' junction between the murine leukemia virus env gene and the v-mos gene [12].
• The 3' end of MPSV, including the oncogene-helper junctions, the v-mos gene, and the 3' long terminal repeat, was sequenced and compared with sequences of Mo-MuLV, MSV-124, and the mouse oncogene c-mos [13].
• To explore the role of pp39mos in male germ cell meiosis, we have constructed transgenic mice carrying either the c-Mos or v-Mos genes linked to the human male germ cell-specific phosphoglycerate kinase-2 promoter [14].
• BACKGROUND: The mos proto-oncogene encodes a cytoplasmic serine/threonine-specific protein kinase with crucial function during meiotic cell division in vertebrates [15].

Anatomical context of Genes, mos

• We describe the molecular identification of a gene, designated T1, whose expression in mouse NIH 3T3 cells is strongly induced by the Ha-ras(EJ) and v-mos oncogenes and by serum [16].
• After acute infection of Swiss 3T3 cells with virus containing the v-mos oncogene, cells expressing high levels of v-Mos round up and detach from the monolayer (floating cells), while cells that remain attached express 10-fold lower levels of v-Mos and are transformed [17].

Associations of Genes, mos with chemical compounds

• However, deletion mutants of v-mos which allow initiation of translation at the fourth methionine codon have lost the biological activity of the parental v-mos gene [18].
• Mos gene expression was also induced in SKOV3 cells that were treated with vinblastine but not in those that were treated with camptothecin, etoposide, or cisplatin [4].
• Paclitaxel-induced c-Mos gene expression was completely abrogated by cycloheximide and actinomycin D [4].
• Induction of the c-Mos gene expression and activation were determined by Western blot analysis, immunoprecipitation using a polyclonal anti-mos antibody, reverse transcription-PCR assay, and 32P-ATP incorporation into c-Mos protein or the substrate of glutathione S-transferase mitogen-activated protein kinase kinase, respectively [4].
• Conversely, PC Cl3 cells stably expressing the v-mos oncogene (PC mos) were completely insensitive to the somatostatin antiproliferative effects since somatostatin was unable to stimulate a phosphotyrosine phosphatase activity [19].

Gene context of Genes, mos

• Of particular interest is the homology found between the COOH terminus of the E2 putative protein of the different papillomaviruses and the viral or cellular mos oncogene product [20].
• Deregulation of specific E2F complexes by the v-mos oncogene [21].
• Similarly to cells transformed by ras, a Rat1 subline transformed by the v-mos oncogene was characterized by decreased drug sensitivity [22].
• In the present work, our results show that the rat mos proto-oncogene activates transcriptional activity of MyoD protein [23].
• Mitogen-activated protein kinase activation preceded c-Mos gene induction [4].

References