Role of hepatic cytochromes P450 in bioactivation of the anticancer drug ellipticine: Studies with the hepatic NADPH:Cytochrome P450 reductase null mouse

2008 ◽  
Vol 226 (3) ◽  
pp. 318-327 ◽  
Author(s):  
Marie Stiborová ◽  
Volker M. Arlt ◽  
Colin J. Henderson ◽  
C. Roland Wolf ◽  
Věra Kotrbová ◽  
...  
Keyword(s):  
Anticancer Drug ◽  
Cytochromes P450 ◽  
Null Mouse ◽  
P450 Reductase ◽  
Nadph:Cytochrome P450 Reductase

scholarly journals Role of Hepatic Cytochrome P450s in the Pharmacokinetics and Toxicity of Cyclophosphamide: Studies with the Hepatic Cytochrome P450 Reductase Null Mouse

2005 ◽  
Vol 65 (10) ◽  
pp. 4211-4217 ◽  
Author(s):  
Georgia J. Pass ◽  
Dianne Carrie ◽  
Michael Boylan ◽  
Sally Lorimore ◽  
Eric Wright ◽  
...  
Keyword(s):  
Cytochrome P450 ◽  
Cytochrome P450s ◽  
Null Mouse ◽  
Cytochrome P450 Reductase ◽  
P450 Reductase ◽  
Hepatic Cytochrome

Drug Interactions with Angiotensin Receptor Blockers: Role of Human Cytochromes P450

2016 ◽  
Vol 17 (7) ◽  
pp. 681-691 ◽  
Author(s):  
Ruirui Yang ◽  
Zhiqiang Luo ◽  
Yang Liu ◽  
Mohan Sun ◽  
Ling Zheng ◽  
...  
Keyword(s):  
Drug Interactions ◽  
Cytochromes P450 ◽  
Angiotensin Receptor Blockers ◽  
Angiotensin Receptor ◽  
Receptor Blockers

scholarly journals Pathogenic role of Fgf23 in Dmp1-null mice

2008 ◽  
Vol 295 (2) ◽  
pp. E254-E261 ◽  
Author(s):  
Shiguang Liu ◽  
Jianping Zhou ◽  
Wen Tang ◽  
Rochelle Menard ◽  
Jian Q. Feng ◽  
...  
Keyword(s):  
Growth Retardation ◽  
Matrix Protein ◽  
Serum Levels ◽  
Serum Phosphate ◽  
Hypophosphatemic Rickets ◽  
Null Mouse ◽  
Matrix Mineralization ◽  
Severe Growth ◽  
Inactivating Mutations

Autosomal recessive hypophosphatemic rickets (ARHR), which is characterized by renal phosphate wasting, aberrant regulation of 1α-hydroxylase activity, and rickets/osteomalacia, is caused by inactivating mutations of dentin matrix protein 1 ( DMP1). ARHR resembles autosomal dominant hypophosphatemic rickets (ADHR) and X-linked hypophosphatemia (XLH), hereditary disorders respectively caused by cleavage-resistant mutations of the phosphaturic factor FGF23 and inactivating mutations of PHEX that lead to increased production of FGF23 by osteocytes in bone. Circulating levels of FGF23 are increased in ARHR and its Dmp1-null mouse homologue. To determine the causal role of FGF23 in ARHR, we transferred Fgf23 deficient/enhanced green fluorescent protein (eGFP) reporter mice onto Dmp1-null mice to create mice lacking both Fgf23 and Dmp1. Dmp1−/− mice displayed decreased serum phosphate concentrations, inappropriately normal 1,25(OH)2D levels, severe rickets, and a diffuse form of osteomalacia in association with elevated Fgf23 serum levels and expression in osteocytes. In contrast, Fgf23−/− mice had undetectable serum Fgf23 and elevated serum phosphate and 1,25(OH)2D levels along with severe growth retardation and focal form of osteomalacia. In combined Dmp1−/−/Fgf23−/−, circulating Fgf23 levels were also undetectable, and the serum levels of phosphate and 1,25(OH)2D levels were identical to Fgf23−/− mice. Rickets and diffuse osteomalacia in Dmp1-null mice were transformed to severe growth retardation and focal osteomalacia characteristic of Fgf23-null mice. These data suggest that the regulation of extracellular matrix mineralization by DMP1 is coupled to renal phosphate handling and vitamin D metabolism through a DMP1-dependent regulation of FGF23 production by osteocytes.

Enzyme-Mediated Protein Haptenation of Dapsone and Sulfamethoxazole in Human Keratinocytes: I. Expression and Role of Cytochromes P450

2006 ◽  
Vol 319 (1) ◽  
pp. 488-496 ◽  
Author(s):  
Piyush M. Vyas ◽  
Sanjoy Roychowdhury ◽  
Farah D. Khan ◽  
Thomas E. Prisinzano ◽  
Jatinder Lamba ◽  
...  
Keyword(s):  
Cytochromes P450 ◽  
Human Keratinocytes
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