| proto-oncogene proteins c-mos | Cellular proteins encoded by the c-mos genes (genes, mos). They function in the cell cycle to maintain maturation-promoting factor in the active state and have protein-serine/threonine kinase activity. Oncogenic transformation can take place when c-mos proteins are expressed at the wrong time. (12 Dec 1998) |
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| proto-oncogene proteins c-myc | Cellular DNA-binding proteins encoded by the c-myc genes. They are normally involved in nucleic acid metabolism and in mediating the cellular response to growth factors. Elevated and deregulated (constitutive) expression of c-myc proteins can cause tumourigenesis. (12 Dec 1998) |
| proto-oncogene proteins c-raf | <enzyme> A class of serine-threonine kinases involved in cellular signal transduction. Included in this class are the proto-oncogene proteins mil and raf. Raf is a component of a signal transduction pathway leading to increased gene expression through the c-jun DNA binding site, ap1. Registry number: EC 2.7.10.- (12 Dec 1998) |
| dominant oncogene | <genetics, molecular biology, oncology> A gene that stimulates cell proliferation and can drastically increase the risk of cancer development when present in a single copy. (09 Oct 1997) |
| oncogene | <molecular biology, oncology> Mutated and/or overexpressed version of a normal gene of animal cells (the proto-oncogene) that in a dominant fashion can release the cell from normal restraints on growth and thus alone or in concert with other changes, convert a cell into a tumour cell. (18 Nov 1997) |
| oncogene protein gp140(v-fms) | Transforming glycoprotein coded by the fms oncogene from the susan mcdonough strain of feline sarcoma virus (sm-fesv). The oncogene protein v-fms lacks sequences, which, in the highly homologous proto-oncogene protein c-fms (csf-1 receptor), normally serve to regulate its tyrosine kinase activity. The missing sequences in v-fms mimic the effect of ligand and lead to constitutive cell growth. The protein gp120(v-fms) is post-translationally modified to generate gp140(v-fms). (12 Dec 1998) |
| oncogene protein p21(ras) | Transforming protein encoded by ras oncogenes. Point mutations in the cellular ras gene (c-ras) can also result in a mutant p21 protein that can transform mammalian cells. Oncogene protein p21(ras) has been directly implicated in human neoplasms, perhaps accounting for as much as 15-20% of all human tumours. (12 Dec 1998) |
| oncogene protein p55(v-myc) | Transforming protein coded by myc oncogenes. The v-myc protein has been found in several replication-defective avian retrovirus isolates which induce a broad spectrum of malignancies. (12 Dec 1998) |
| oncogene protein p65(gag-jun) | Transforming protein coded by jun oncogenes (genes, jun). This is a gag-onc fusion protein of about 65 kD derived from avian sarcoma virus. V-jun lacks a negative regulatory domain that regulates transcription in c-jun. (12 Dec 1998) |
| oncogene protein pp60(v-src) | <chemical> Tyrosine-specific protein kinase encoded by the v-src oncogene of rous sarcoma virus. The transforming activity of pp60(v-src) depends on both the lack of a critical carboxy-terminal tyrosine phosphorylation site at position 527, and the attachment of pp60(v-src) to the plasma membrane which is accomplished by myristylation of its n-terminal glycine. Chemical name: Kinase (phosphorylating), protein pp60src (12 Dec 1998) |
| oncogene proteins | Proteins coded by oncogenes. They include proteins resulting from the fusion of an oncogene and another gene (oncogene proteins, fusion). (12 Dec 1998) |
| oncogene proteins, fusion | The translation products of the fusion between an oncogene and another gene. The latter may be of viral or cellular origin. (12 Dec 1998) |
| oncogene proteins v-abl | Transforming proteins encoded by the abl oncogenes. Oncogenic transformation of c-abl to v-abl occurs by insertional activation that results in deletions of specific n-terminal amino acids. (12 Dec 1998) |
| oncogene proteins v-erba | Transforming proteins encoded by erba oncogenes from the avian erythroblastosis virus. They are truncated versions of c-erba, the thyroid hormone receptor (receptors, thyroid hormone) that have retained both the DNA-binding and hormone-binding domains. Mutations in the hormone-binding domains abolish the transcriptional activation function. V-erba acts as a dominant repressor of c-erba, inducing transformation by disinhibiting proliferation. (12 Dec 1998) |
| oncogene proteins v-erbb | Transforming proteins encoded by erbb oncogenes from the avian erythroblastosis virus. The protein is a truncated form of the egf receptor (receptors, epidermal growth factor-urogastrone) whose kinase domain is constitutively activated by deletion of the ligand-binding domain. (12 Dec 1998) |