Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.28 (chloramphenicol acetyltransferase)
 5,100 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have recently modified a non-fluorescent, non-radioactive histochemical method to detect sulfhydryl (S-H) groups in tissues. This method was originally intended to detect chloramphenicol acetyltransferase (CAT) in transgenic mice. Temporal developmental differences in the keratinization of mouse digits can be seen in the staining pattern of the skin about the toes of neonatal mice. The basal cells of the epidermis exposed to the air show intense staining while the epidermis that is still attached to an adjacent toe shows no staining. The degree of S-H presence can be determined by the tissues' resistance to blocking of the S-H groups by iodoacetic acid. Areas that contain very high numbers of S-H groups still show staining following blocking by iodoacetic acid. We have found that this method shows clear differences in the S-H distribution of various epithelium, including skin, hair, nails, and tongue epithelium.
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PMID:A method to detect areas high in sulfhydryl groups in mouse epithelium. 830 28

The pancreatic cancer cell line, MIA PaCa-2 is not responsive to transforming growth factor beta (TGF-beta) because of a lack of expression of the TGF-beta type II receptor (RII). We show that the lack of RII expression is caused by a deficit of the transcription factor Sp1. Nuclear run-off assays and Western immunoblot showed low levels of transcription and protein levels of Sp1, respectively. Treatment of MIA PaCa-2 cells with the DNA methyl transferase inhibitor, 5-aza-2'-deoxycytidine, resulted in an increase in the rate of Sp1 transcription, in Sp1 protein expression, and in the binding of Sp1 to the RII promoter. Ectopic expression of Sp1 cDNA in MIA PaCa-2 cells led to an increase in RII promoter-chloramphenicol acetyltransferase activity and RII expression. Expression of Sp1 cDNA also caused a reduction in both growth and clonogenicity that was associated with restoration of responsiveness to TGF-beta. Conversely, cells that express RII (BxPC-3 and MIA PaCa-2 Sp1 transfectants) when treated with mithramycin, an inhibitor of Sp1 binding, showed a reduction in RII mRNA expression. The reduction of RII mRNA was attributed to a decrease in RII promoter-chloramphenicol acetyltransferase activity that was associated with a decrease in Sp1 binding to the RII promoter. These data indicate that transcriptional repression of the Sp1 gene in MIA PaCa-2 cells plays a role in the transcriptional inactivation of the RII gene and thus lack of responsiveness to TGF-beta.
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PMID:Reversion of transcriptional repression of Sp1 by 5 aza-2' deoxycytidine restores TGF-beta type II receptor expression in the pancreatic cancer cell line MIA PaCa-2. 1150 78