| GnRH | Gonadotropin Releasing Hormone [HP 1898, 2034] = LHRH = Go... |
|---|---|
| AXL | anexelekto [oncogene]; axillary lymphoscintigraphy |
| c-onc | cellular oncogene |
| ONC | oncogene; oncology; Orthopaedic Nursing Certificate; over-the-needle catheter |
| src | Rous sarcoma oncogene |
| c-onc | cellular oncogene |
|---|---|
| GRO-alpha | Growth Regulated Oncogene-alpha |
| GROalpha | Growth-related oncogene-alpha |
| 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) |
|---|---|
| genes, erba | Retrovirus-associated DNA sequences (erythroblastosis virus, avian, hence erba) originally isolated from the avian erythroblastosis virus. The c-erba proto-oncogene encodes the thyroid hormone receptors (receptors, thyroid hormone). Two distinct c-erba proto-oncogenes have been identified, erba-alpha and erba-beta, each giving rise to at least two proteins. Erba-alpha is located at 17q21 on the long arm of chromosome 17. Erba-beta is located at 3p24 on the short arm of chromosome 3. The v-erba oncogene potentiates cell transformation through inhibition of spontaneous differentiation of cells already transformed by the v-erbb gene and eliminates growth requirements of transformed erythroblasts. (12 Dec 1998) |
| recessive oncogene | <molecular biology> A single copy of this gene issufficient to suppress cell proliferation, the loss of both copies of the gene contributes to cancer formation. (09 Oct 1997) |
| viral oncogene | <molecular biology> A viral gene that contributes to cancer development in vertebrate hosts. (09 Oct 1997) |
| cellular oncogene | <molecular biology> A normal gene that, when mutated or improperly expressed, can cause cancer to develop. (09 Oct 1997) |
| c-oncogene | <molecular biology> A normal gene which has a tumour-producing insert that may have originated from a virus in it, turning it into a proto-oncogene. When these genes are sufficiently mutated, amplified, or over-expressed (transcribed too many times), they can begin to produce cancers. (05 Jan 1998) |
| proto-oncogene | <molecular biology> The normal, cellular equivalent of an oncogene, thus usually a gene involved in the signalling or regulation of cell growth. In general, cellular proto-oncogenes are prefixed with a c, rather than their abnormal viral counterparts, that are prefixed with a v, for example c myc and v myc. They are fragments of DNA, related to oncogenes but are the normal switches used to control growth and tissue repair. (06 Oct 1997) |
| proto-oncogene protein p21(ras) | Cellular protein encoded by the c-ras genes. The protein has GTPase activity and is involved in transmembrane signal transduction as a guanine nucleotide binding protein. Elevated levels of p21 c-ras have been associated with neoplasia. (12 Dec 1998) |
| proto-oncogene protein pp60(c-src) | <enzyme> Membrane-associated tyrosine-specific kinase encoded by the c-src genes. It has an important role in cellular growth control. Truncation of carboxy-terminal residues in pp60(c-src) leads to pp60(v-src) which has the ability to transform cells. This kinase pp60 c-src should not be confused with csk, also known as c-src kinase. Registry number: EC 2.7.1.- (12 Dec 1998) |
| proto-oncogene proteins | Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity. (12 Dec 1998) |
| proto-oncogene proteins c-abl | Membrane proteins encoded by the c-abl genes. They exhibit tyrosine kinase activity and play a role in normal haematopoiesis especially of the myeloid lineage. Oncogenic transformation of c-abl arises when specific n-terminal amino acids are deleted, releasing the kinase from negative regulation. (12 Dec 1998) |
| proto-oncogene proteins c-bcl-2 | Membrane proteins encoded by the bcl-2 genes and serving as a potent inhibitor of cell death by apoptosis. The proteins are found on mitochondrial, microsomal, and nuclear membrane sites within many cell types. Overexpression of bcl-2 proteins, due to a translocation of the gene, is associated with follicular lymphoma. (12 Dec 1998) |
| proto-oncogene proteins c-erbb-2 | Cellular proteins in the epidermal growth factor receptor family encoded by the c-erbb genes. These proteins are overexpressed in a significant portion of adenocarcinomas found at various sites, especially in the breast. Gene amplification appears to be the predominant method leading to overexpression. (12 Dec 1998) |
| proto-oncogene proteins c-fos | Cellular DNA-binding proteins encoded by the c-fos genes (genes, fos). They are involved in growth-related transcriptional control. C-fos combines with c-jun (proto-oncogene proteins c-jun) to form a c-fos/c-jun heterodimer (transcription factor ap-1) that binds to the tre (tpa-responsive element) in promoters of certain genes. (12 Dec 1998) |
| proto-oncogene proteins c-jun | Cellular DNA-binding proteins encoded by the c-jun genes (genes, jun). They are involved in growth-related transcriptional control. There appear to be three distinct functions: dimerization (with c-fos), DNA-binding, and transcriptional activation. Oncogenic transformation can take place by constitutive expression of c-jun. (12 Dec 1998) |
제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
|---|
제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
|---|