Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.30.2 (endonuclease)
 18,621 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have recently described a mouse pituitary tumor line, MGH 101A which is derived from a TSH-producing thyrotropic tumor line and now produces only the alpha-subunit of the glycoprotein hormones. In these studies, we have investigated the mechanism for the lack of TSH beta subunit expression in MGH 101A, as well as the failure of triiodothyronine (T3) to regulate alpha-subunit. Southern blot analysis of restriction endonuclease-digested DNA from MGH 101A tumors indicates the presence of a TSH beta gene and an alpha-subunit gene indistinguishable from those in a TSH-producing tumor (TtT 97). In MGH 101A tumors, however, TSH beta gene transcription was minimal (4 +/- 2 ppm) relative to alpha-subunit (283 +/- 29 ppm) and there was no significant difference in transcription after T3 treatment. In contrast, TtT 97 tumors had nearly equal rates of alpha-subunit (375 +/- 25 ppm) gene transcirption, and T3 respectively. The MGH 101A suppressed the transcription of alpha-subunit and TSH beta genes by 76% and 87%, respectively. The MGH 101A tumor contained T3 receptors with a binding affinity (1.54 X 10-10M) similar to receptors on TtT 97 tumors (1.78 X 10-10M), but at a lower concentration (2800 vs. 4000 sites/cell). We conclude that the absence of TSH beta production in MGH 101A tumors is not due to the absence of the TSH beta gene, but perhaps to some other modification of the gene structure. This could also explain the failure of MGH 101A tumors to respond to T3, since they do contain T3 receptors of normal affinity.
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PMID:A non-responsive alpha-secreting thyrotropic tumor contains T3 receptors and a TSH beta gene. 300 38

The 5-bromodeoxyuridine-resistant (BrdUrdr) derivative (F1BGH12C1) of prolactin nonproducing (PRL-) rat pituitary tumor cell-subclone GH12C1, synthesize prolactin (PRL) in the presence of the drug. Analysis of nuclear RNA isolated from BrdUrd treated F1BHG12C1 cells demonstrated several high molecular weight RNA PRL sequences, similar to those observed in the nuclear RNA fraction of PRL producing (PRL+) GH3 cells. No such RNAPRL sequences could be detected in nuclear RNA fraction of untreated F1 BGH12C1 cells. PRL sequences in the genome of GH3 (PRL+), GH12C1 (PRL-) and F1BGH12C1 (PRL-, BrdUrdr) GH cells could be identified by blot analysis in 4.8-5.2kb fragment of restriction endonuclease, Hind III digested DNA. Both PRL+ and PRL- cells seem to have approximately the same level of PRL gene sequences in total cell DNA. However Hind III digested DNA of BrdUrd treated F1BGH12C cells revealed the presence of significantly higher levels of PRL gene sequences, in comparison, to that observed in total DNA of untreated cells. The increased level of PRL gene sequences was dependent on the period of drug treatment and a parallel increase in the cytoplasmic RNAPRL sequences was also observed.
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PMID:Increased level of prolactin gene sequences in bromodeoxyuridine treated GH cells. 711 Oct 26