Chloramphenicol O-Acetyltransferase
"Chloramphenicol O-Acetyltransferase" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus,
MeSH (Medical Subject Headings). Descriptors are arranged in a hierarchical structure,
which enables searching at various levels of specificity.
An enzyme that catalyzes the acetylation of chloramphenicol to yield chloramphenicol 3-acetate. Since chloramphenicol 3-acetate does not bind to bacterial ribosomes and is not an inhibitor of peptidyltransferase, the enzyme is responsible for the naturally occurring chloramphenicol resistance in bacteria. The enzyme, for which variants are known, is found in both gram-negative and gram-positive bacteria. EC 2.3.1.28.
| Descriptor ID |
D015500
|
| MeSH Number(s) |
D08.811.913.050.134.170
|
| Concept/Terms |
Chloramphenicol O-Acetyltransferase- Chloramphenicol O-Acetyltransferase
- Chloramphenicol O Acetyltransferase
- O-Acetyltransferase, Chloramphenicol
- Chloramphenicol Transacetylase
- Transacetylase, Chloramphenicol
- CAT Enzyme
- Enzyme, CAT
- Chloramphenicol Acetyltransferase
- Acetyltransferase, Chloramphenicol
|
Below are MeSH descriptors whose meaning is more general than "Chloramphenicol O-Acetyltransferase".
Below are MeSH descriptors whose meaning is more specific than "Chloramphenicol O-Acetyltransferase".
This graph shows the total number of publications written about "Chloramphenicol O-Acetyltransferase" by people in this website by year, and whether "Chloramphenicol O-Acetyltransferase" was a major or minor topic of these publications.
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| Year | Major Topic | Minor Topic | Total |
|---|
| 1995 | 0 | 5 | 5 |
| 1996 | 0 | 5 | 5 |
| 1997 | 0 | 2 | 2 |
| 1999 | 0 | 3 | 3 |
| 2000 | 0 | 1 | 1 |
| 2004 | 0 | 1 | 1 |
| 2005 | 0 | 2 | 2 |
| 2007 | 0 | 1 | 1 |
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Below are the most recent publications written about "Chloramphenicol O-Acetyltransferase" by people in Profiles.
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EGR-1 forms a complex with YAP-1 and upregulates Bax expression in irradiated prostate carcinoma cells. Oncogene. 2009 Feb 26; 28(8):1121-31.
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Changes in apparent free energy of helix-helix dimerization in a biological membrane due to point mutations. J Mol Biol. 2007 Aug 10; 371(2):422-34.
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Human progesterone receptor displays cell cycle-dependent changes in transcriptional activity. Mol Cell Biol. 2005 Apr; 25(8):2885-98.
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Inhibition of the 26S proteasome blocks progesterone receptor-dependent transcription through failed recruitment of RNA polymerase II. J Steroid Biochem Mol Biol. 2005 Mar; 94(4):337-46.
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Nucleotide excision repair as a marker for susceptibility to tobacco-related cancers: a review of molecular epidemiological studies. Mol Carcinog. 2005 Feb; 42(2):65-92.
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Inhibition of proliferation and induction of apoptosis by 25-hydroxyvitamin D3-3beta-(2)-Bromoacetate, a nontoxic and vitamin D receptor-alkylating analog of 25-hydroxyvitamin D3 in prostate cancer cells. Clin Cancer Res. 2004 Dec 01; 10(23):8018-27.
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HS2 enhancer function is blocked by a transcriptional terminator inserted between the enhancer and the promoter. J Biol Chem. 2004 Dec 03; 279(49):51704-13.
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Dual regulation of MMP-2 expression by the type 1 insulin-like growth factor receptor: the phosphatidylinositol 3-kinase/Akt and Raf/ERK pathways transmit opposing signals. J Biol Chem. 2004 May 07; 279(19):19683-90.
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ATF is important to late S phase-dependent regulation of DNA topoisomerase IIalpha gene expression in HeLa cells. Cancer Lett. 2002 Oct 08; 184(1):81-8.
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The function of multiple IkappaB : NF-kappaB complexes in the resistance of cancer cells to Taxol-induced apoptosis. Oncogene. 2002 Sep 19; 21(42):6510-9.