Cytochrome P450 1B1 mRNA untranslated regions interact to inhibit protein translation

2009 ◽  
Vol 49 (2) ◽  
pp. 190-199 ◽  
Author(s):  
Andrea H. Devlin ◽  
Paul Thompson ◽  
Tracy Robson ◽  
Stephanie R. McKeown
Keyword(s):  
Cytochrome P450 ◽  
Protein Translation ◽  
Untranslated Regions ◽  
Cytochrome P450 1B1 ◽  
Inhibit Protein Translation

scholarly journals Effect of RIP Overexpression on Abiotic Stress Tolerance and Development of Rice

2021 ◽  
Vol 22 (3) ◽  
pp. 1434
Author(s):  
Pieter Wytynck ◽  
Jeroen Lambin ◽  
Simin Chen ◽  
Sinem Demirel Asci ◽  
Isabel Verbeke ◽  
...  
Keyword(s):  
Methyl Jasmonate ◽  
Stress Responses ◽  
Abiotic Stress Tolerance ◽  
Protein Translation ◽  
Ribosome Inactivating Proteins ◽  
Close Proximity ◽  
Inhibit Protein Translation ◽  
Plant Ribosomes ◽  
A Cell ◽  
Type 3

Ribosome-inactivating proteins (RIPs) are a class of cytotoxic enzymes that can inhibit protein translation by depurinating rRNA. Most plant RIPs are synthesized with a leader sequence that sequesters the proteins to a cell compartment away from the host ribosomes. However, several rice RIPs lack these signal peptides suggesting they reside in the cytosol in close proximity to the plant ribosomes. This paper aims to elucidate the physiological function of two nucleocytoplasmic RIPs from rice, in particular, the type 1 RIP referred to as OsRIP1 and a presumed type 3 RIP called nuRIP. Transgenic rice lines overexpressing these RIPs were constructed and studied for developmental effects resulting from this overexpression under greenhouse conditions. In addition, the performance of transgenic seedlings in response to drought, salt, abscisic acid and methyl jasmonate treatment was investigated. Results suggest that both RIPs can affect methyl jasmonate mediated stress responses.

Cytochrome P450 1B1: a novel anticancer therapeutic target

2005 ◽  
Vol 1 (2) ◽  
pp. 259-263 ◽  
Author(s):  
Morag CE McFadyen ◽  
Graeme I Murray
Keyword(s):  
Cytochrome P450 ◽  
Therapeutic Target ◽  
Cytochrome P450 1B1

Cytochrome P450 1B1 polymorphisms and risk of renal cell carcinoma in men

Tumor Biology ◽  
2014 ◽  
Vol 35 (10) ◽  
pp. 10223-10230 ◽  
Author(s):  
Inik Chang ◽  
Shinichiro Fukuhara ◽  
Darryn K. Wong ◽  
Ankurpreet Gill ◽  
Yozo Mitsui ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cytochrome P450 ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Cytochrome P450 1B1

scholarly journals Cytochrome P450 1B1 Contributes to Renal Dysfunction and Damage Caused by Angiotensin II in Mice

Hypertension ◽  
2012 ◽  
Vol 59 (2) ◽  
pp. 348-354 ◽  
Author(s):  
Brett L. Jennings ◽  
Larry J. Anderson ◽  
Anne M. Estes ◽  
Fariborz A. Yaghini ◽  
Xiao R. Fang ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Angiotensin Ii ◽  
Renal Dysfunction ◽  
Cytochrome P450 1B1

Immunochemical detection of N-acetyltransferase 1 and cytochrome P450 1B1 proteins in human prostate

2003 ◽  
Vol 2 (6) ◽  
pp. 27
Author(s):  
S.Z Al-Buheissi ◽  
V Kumar ◽  
H.R.H Patel ◽  
R.L Bryan ◽  
R.A Miller ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Human Prostate ◽  
Cytochrome P450 1B1 ◽  
Immunochemical Detection

Abstract 252: 6ß-Hydroxytestosterone, A Cytochrome P450 1B1 Metabolite of Testosterone, Enhances Angiotensin II-Induced Pressor Effect in Male Mice

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Ajeeth K Pingili ◽  
Brett L Jennings ◽  
Nayaab S Khan ◽  
Kafait U Malik
Keyword(s):  
Cytochrome P450 ◽  
Endothelial Dysfunction ◽  
Ros Production ◽  
Oxygen Species ◽  
Pressor Effect ◽  
Ang Ii ◽  
Male Mice ◽  
Cytochrome P450 1B1 ◽  
Induced Hypertension ◽  
Novel Target

Androgens have been implicated in the development of hypertension and castration minimizes the pressor effect of angiotensin (Ang) II. Previously we showed that Ang II-induced hypertension and associated pathophysiological changes are diminished in male cytochrome P450 (CYP) 1B1 gene disrupted mice. Since CYP1B1 metabolizes testosterone to 6β-hydroxytestosterone (6β-OHT); this study was conducted to determine its contribution in modulation of Ang II-induced hypertension. Eight weeks old male Cyp1b1+/+ and Cyp1b1-/- mice were either castrated or injected with 6β-OHT (15 μg/g, i.p. every 3rd day) or vehicle (DMSO, 50 μl), infused with Ang II (700 ng/kg/min) or vehicle for 2 weeks, and systolic blood pressure (SBP) was measured by tail cuff. Castration attenuated Ang II-induced increase in SBP in both Cyp1b1+/+ (184 ± 6 vs. 129 ± 4 mmHg, P < 0.05) and Cyp1b1-/- mice (150 ± 6 vs. 129 ± 4 mmHg, P < 0.05). In Cyp1b1+/+ mice, 6β-OHT did not alter Ang II-induced increase in SBP (184 ± 6 vs. 180 ± 8 mmHg, P < 0.05), but enhanced it in Cyp1b1-/- mice (150 ± 6 vs. 172 ± 8 mmHg, P < 0.05). Castration improved endothelial dysfunction associated with Ang II-induced hypertension in Cyp1b1+/+ mice, as demonstrated by increased relaxation of the aorta to acetylcholine. No endothelial dysfunction was observed in Cyp1b1-/- mice given Ang II with or without castration. In Cyp1b1+/+ mice, 6β-OHT did not alter Ang II-induced endothelial dysfunction, however, in Cyp1b1-/- mice infused with Ang II, 6β-OHT caused endothelial dysfunction. We have shown that Ang II-induced hypertension is associated with increased vascular production of reactive oxygen species (ROS) in Cyp1b1+/+ mice, and this increase is attenuated in Cyp1b1-/- mice, as measured by dihydroethidium fluorescence. In both Cyp1b1+/+ and Cyp1b1-/- mice given Ang II, castration abolished the increased ROS production. In Cyp1b1+/+ mice, 6β-OHT did not alter levels of ROS produced by Ang II, however, 6β-OHT further increased ROS production in Cyp1b1-/- mice given Ang II. These data suggest that 6β-OHT, a CYP1B1 metabolite of testosterone, contributes to the hypertensive effect of Ang II in male mice. Moreover, CYP1B1 could serve as a novel target for the development of agents for the treatment of androgen-mediated hypertension.

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