scispace - formally typeset
P

Pedro M. Fernández-Salguero

Researcher at University of Extremadura

Publications -  133
Citations -  14624

Pedro M. Fernández-Salguero is an academic researcher from University of Extremadura. The author has contributed to research in topics: Aryl hydrocarbon receptor & Receptor. The author has an hindex of 55, co-authored 129 publications receiving 13795 citations. Previous affiliations of Pedro M. Fernández-Salguero include University of Wisconsin-Madison & National Institutes of Health.

Papers
More filters
Journal ArticleDOI

The T/ebp null mouse: thyroid-specific enhancer-binding protein is essential for the organogenesis of the thyroid, lung, ventral forebrain, and pituitary.

TL;DR: In situ hybridization showed that the T/ebp gene is expressed in the normal thyroid, lung bronchial epithelium, and specific areas of the forebrain during early embryogenesis, establishing that the expression of T/EBP, a transcription factor known to control thyroid-specific gene transcription, is also essential for organogenesis of the thyroid, lungs, ventral forebrain, and pituitary.
Journal ArticleDOI

Immune system impairment and hepatic fibrosis in mice lacking the dioxin-binding Ah receptor

TL;DR: The aryl hydrocarbon (Ah) receptor (AHR) mediates many carcinogenic and teratogenic effects of environmentally toxic chemicals such as dioxin and plays an important role in the development of the liver and the immune system.
Journal ArticleDOI

Aryl-hydrocarbon receptor-deficient mice are resistant to 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced toxicity

TL;DR: Results suggest that the pathological changes induced by TCDD in the liver and thymus are mediated entirely by the AHR, however, it is important to note that at high doses of T CDD, AHR-deficient mice displayed limited vasculitis and scattered single cell necrosis in their lungs and livers, respectively.
Journal ArticleDOI

Role of CYP2E1 in the Hepatotoxicity of Acetaminophen

TL;DR: When cyp2e1 knockout mice were challenged with the common analgesic acetaminophen, they were found to be considerably less sensitive to its hepatotoxic effects than wild-type animals, indicating that this P-450 is the principal enzyme responsible for the metabolic conversion of the drug to its active hepatot toxic metabolite.