Sabio lab

at the CNIC

Tag: steatosis (page 1 of 2)

María Crespo awarded in the Archimedes Competition

Our lab mate María Crespo has been awarded the second prize in the Archimedes Competition. She will receive a prize of € 2,000.

María Crespo

The competition, organized by the Spanish Ministry of Education, favours the incorporation of young students into the research field by awarding them for their original Master projects of scientific or technological research. On this occasion, more than 350 students throughout Spain participated, of which only 25 went to the final.

Under the supervision of Guadalupe Sabio and Magdalena Leiva, Crespo has studied the circadian rhythm of neutrophil infiltration in the liver and the possible role that these cells play in the regulation of hepatic activity. Through the use of neutropenic mice, she has analyzed the contribution of neutrophils in the progress of non-alcoholic fatty liver disease (NAFLD).

María Crespo among other finalists of the Archimedes Competition.

Laboratory technician

Our group seeks a motivated lab technician with at least two years of experience in histology and genotyping.

The technician will be in charge of the preparation and staining of samples for histology and immunohistochemistry, genotyping of our mouse colony and helping the other members of the lab with their experiments.

We offer a work is an international project currently in expansion developed in an environment with a solid commitment to excellent research

Deadline: 3 October 2017

For more information and application, please visit CNIC’s website.

brown fat

H&E staining of murine brown fat (Photo: Nuria Matesanz/CNIC).

Hepatic p63 regulates steatosis via IKKβ/ER stress

Begoña Porteiro, Marcos F. Fondevila, Teresa C. Delgado, Cristina Iglesias, Monica Imbernon, Paula Iruzubieta, Javier Crespo, Amaia Zabala-Letona, Johan Fernø, Bárbara González-Terán, Nuria Matesanz, Lourdes Hernández-Cosido, Miguel Marcos, Sulay Tovar, Anxo Vidal, Julia Sánchez-Ceinos, Maria M. Malagon, Celia Pombo, Juan Zalvide, Arkaitz Carracedo, Xabier Buque, Carlos Dieguez, Guadalupe Sabio, Miguel López, Patricia Aspichueta, María L. Martínez-Chantar & Ruben Nogueiras.

Pathway proposed to modulate lipid metabolism in liverp53 family members control several metabolic and cellular functions. The p53 ortholog p63 modulates cellular adaptations to stress and has a major role in cell maintenance and proliferation.

Here we show that p63 regulates hepatic lipid metabolism. Mice with liver-specific p53 deletion develop steatosis and show increased levels of p63. Down-regulation of p63 attenuates liver steatosis in p53 knockout mice and in diet-induced obese mice, whereas the activation of p63 induces lipid accumulation. Hepatic overexpression of N-terminal transactivation domain TAp63 induces liver steatosis through IKKβ activation and the induction of ER stress, the inhibition of which rescues the liver functions. Expression of TAp63, IKKβ and XBP1s is also increased in livers of obese patients with NAFLD. In cultured human hepatocytes, TAp63 inhibition protects against oleic acid-induced lipid accumulation, whereas TAp63 overexpression promotes lipid storage, an effect reversible by IKKβ silencing.

Our findings indicate an unexpected role of the p63/IKKβ/ER stress pathway in lipid metabolism and liver disease.


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