Nuestra compañera Beatriz Cicuéndez reconoce que necesita «tener aficiones que la saquen del laboratorio porque investigar engancha».
Tag: lipid metabolism (Page 3 of 8)
We are seeking a highly motivated candidate, who would like to start a scientific career doing their doctoral thesis working in understanding the molecular mechanisms involved in how metabolic alterations can affect the cardiac disease, focusing on cardiac metabolism and how the rest of the organs affect it. This work will be supervised by Dr. Guadalupe Sabio.
We offer incorporation to CNIC via an FPU predoctoral contract (FPU 2021 call).
ELEGIBILITY CRITERIA
- This call is open to applicants from all nationalities holding a Master’s degree in Biomedical Sciences and an academic record with average grade over 8,7 (out of 10).
- An excellent academic record and previous research experience during their undergraduate period will be valued very positively.
- Authorship of publicacions in indexed journal will be valued very positively.
- Candidates must have a solid working knowledge of English.
If you are interested, please send your CV, academic record, a letter of interest and contact details of previous references to Laura Grau (lgrau@cnic.es) indicating in the subject: “FPU2021 Guadalupe Sabio’s lab” no later than December 7th 2021.
Interested candidates will also need to apply officially throught the official governmental application for this predoctoral program (additional information: FPU 2021 call ).
Natáliada Silva Lima, Marcos F. Fondevila, Eva Nóvoa, Xabier Buqué, Maria Mercado-Gómez, Sarah Gallet, Maria J. González-Rellan, Uxia Fernandez, Anne Loyens, Maria Garcia-Vence, Maria del Pilar Chantada-Vazquez, Susana B. Bravo, Patricia Marañon, Ana Senra, Adriana Escudero, Magdalena Leiva, Diana Guallar, Miguel Fidalgo, Pedro Gomes, Marc Claret, Guadalupe Sabio, Marta Varela-Rey, Teresa C. Delgado, Rocio Montero-Vallejo, Javier Ampuero, Miguel López, Carlos Diéguez, Laura Herrero, Dolors Serra, Markus Schwaninger, Vincent Prevo, Rocio Gallego-Duran, Manuel Romero-Gomez, Paula Iruzubieta, Javier Crespo, Maria L. Martinez-Chantar, Carmelo Garcia-Monzon, Agueda Gonzalez-Rodriguez, Patricia Aspichueta & Ruben Nogueiras.
BACKGROUND & AIMS: Autophagy-related gene 3 (ATG3) is an enzyme mainly known for its actions in the LC3 lipidation process, which is essential for autophagy. Whether ATG3 plays a role in lipid metabolism or contributes to nonalcoholic fatty liver disease (NAFLD) remains unknown.
METHODS: By performing a liver proteomic analysis from mice with genetic manipulation of hepatic p63, a regulator of fatty acid metabolism, we identified ATG3 as a new target downstream of p63. ATG3 was evaluated in liver samples of patients with NAFLD. Further, genetic manipulation of ATG3 was performed in human hepatocyte cell lines, primary hepatocytes and in the liver of mice.
RESULTS: ATG3 expression is induced in the liver of animal models and patients with NAFLD (both steatosis and NASH) compared with those without liver disease. Moreover, genetic knockdown of ATG3 in mice and human hepatocytes ameliorates p63- and diet-induced steatosis, while its overexpression increases the lipid load in hepatocytes. The inhibition of hepatic ATG3 improves fatty acid metabolism by reducing c-Jun N-terminal protein kinase 1 (JNK1), which increases sirtuin 1 (SIRT1), carnitine palmitoiltransferase I (CPT1a), and mitochondrial function. Hepatic knockdown of SIRT1 and CPT1a blunts the effects of ATG3 on mitochondrial activity. Unexpectedly, these effects are independent of an autophagic action.
CONCLUSIONS: Collectively, these findings indicate that ATG3 is a novel protein implicated in the development of steatosis.
