| REV | reticuloendotheliosis virus |
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| ReV | regulator of virion |
| rev | reverse; review; revolution |
| ISG | IFN stimulated genes |
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| mdr | Multidrug resistance genes |
| RRE | REV response element |
| REV | Reticuloendotheliosis virus |
| REV-T | Reticuloendotheliosis virus strain T |
| genes, rev | DNA sequences that form the coding region for a protein that regulates the expression of the viral structural and regulatory proteins in human immunodeficiency virus (HIV). Rev is short for regulator of virion. (12 Dec 1998) |
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| gene products, rev | Trans-acting nuclear proteins whose functional expression are required for HIV viral replication. Specifically, the rev gene products are required for processing and translation of the HIV gag and env mRNAs, and thus rev regulates the expression of the viral structural proteins. Rev can also regulate viral regulatory proteins. A cis-acting antirepression sequence (car) in env, also known as the rev-responsive element (rre), is responsive to the rev gene product. Rev is short for regulator of virion. (12 Dec 1998) |
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| rev | <molecular biology> A regulatory protein produced by HIV within infected cells. Rev helps transport HIV RNA sequences (messenger RNA) out from the nucleus into the cells cytoplasm, where it directs construction of proteins for new virus particles. (11 Jan 1998) |
| breast cancer susceptibility genes | Inherited factors that predispose to breast cancer. Put otherwise, these genes make one more susceptible to the disease and so increase the risk of developing breast cancer. Two of these genes, BRCA1 and BRCA2, have been identified (and prominently publicised). Several other genes (those for the Li-Fraumeni syndrome, Cowden disease, Muir-Torre syndrome, and ataxia-telangiectasia) are also known to predispose to breast cancer. However, since all of these known breast cancer susceptibility genes together do not account for more than a minor fraction (1/5th at most) of breast cancer that clusters in families, it is clear that more breast cancer genes remain to be discovered. (12 Dec 1998) |
| cancer, breast, susceptibility genes | Inherited factors that predispose to breast cancer. Put otherwise, these genes make one more susceptible to the disease and so increase the risk of developing breast cancer. Two of these genes, BRCA1 and BRCA2, have been identified (and prominently publicised). Several other genes (those for the Li-Fraumeni syndrome, Cowden disease, Muir-Torre syndrome, and ataxia-telangiectasia) are also known to predispose to breast cancer. However, since all of these known breast cancer susceptibility genes together do not account for more than a minor fraction (1/5th at most) of breast cancer that clusters in families, it is clear that more breast cancer genes remain to be discovered. (12 Dec 1998) |
| genes | Located in the nucleus of the cell, genes contain hereditary information that is transferred from cell to cell. (09 Oct 1997) |
| genes, abl | Retrovirus-associated DNA sequences (abl) originally isolated from the abelson murine leukaemia virus (ab-mulv). The proto-oncogene abl (c-abl) codes for a protein that is a member of the tyrosine kinase family. The human c-abl gene is located at 9q34.1 on the long arm of chromosome 9. It is activated by translocation to bcr on chromosome 22 in chronic myelogenous leukaemia. (12 Dec 1998) |
| genes, apc | Tumour suppressor genes located in the 5q21 region on the long arm of chromosome 5. The mutation of these genes is associated with familial adenomatous polyposis (apc stands for adenomatous polyposis coli) and gardner's syndrome, as well as some sporadic colourectal cancers. (12 Dec 1998) |
| genes, arac | Regulatory genes which encode a cyclic AMP receptor protein required for l-arabinose utilization in e. Coli. It is an example of positive control or regulation of gene expression in the bacterial operon. (12 Dec 1998) |
| genes, archaeal | The genetic material of archaea. (12 Dec 1998) |
| genes, bacterial | The genetic material of bacteria. (12 Dec 1998) |
| genes, bcl-1 | The B-cell leukaemia/lymphoma-1 genes, associated with various neoplasms when overexpressed. Overexpression results from the t(11;14) translocation, which is characteristic of mantle zone-derived B-cell lymphomas. The human c-bcl-1 gene is located at 11q13 on the long arm of chromosome 18. (12 Dec 1998) |
| genes, bcl-2 | The B-cell leukaemia/lymphoma-2 genes, responsible for blocking apoptosis in normal cells, and associated with follicular lymphoma when overexpressed. Overexpression results from the t(14;18) translocation. The human c-bcl-2 gene is located at 18q24 on the long arm of chromosome 18. (12 Dec 1998) |
| genes, BRCA1 | Tumour suppressor genes located on human chromosome 17q12-21. The mutation of these genes is associated with the formation of familial breast and ovarian cancer. (12 Dec 1998) |
| genes, breast cancer susceptibility | Inherited factors that predispose to breast cancer. Put otherwise, these genes make one more susceptible to the disease and so increase the risk of developing breast cancer. Two of these genes, BRCA1 and BRCA2, have been identified (and prominently publicised). Several other genes (those for the Li-Fraumeni syndrome, Cowden disease, Muir-Torre syndrome, and ataxia-telangiectasia) are also known to predispose to breast cancer. Howeverm, since all of these known breast cancer susceptibility genes together do not account for more than a minor fraction (1/5th at most) of breast cancer that clusters in families, it is clear that more breast cancer genes remain to be discovered. See related entries to: BRCA1; BRCA2; Breast cancer, familial. (12 Dec 1998) |
| genes, cdc | Genes that code for proteins that regulate the cell division cycle. These genes form a regulatory network that culminates in the onset of mitosis by activating the p34cdc2 protein (protein p34cdc2). (12 Dec 1998) |
Synonyms : Gene, art-trs, Gene, rev, Gene, trs-art, Genes, art-trs, Genes, trs-art, art trs Genes, art-trs Gene, rev Gene, trs art Genes, trs-art Gene
제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
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제품명 |
판매사 |
보험코드 | 성분/함량 | 구분/보험급여 |
|---|