at the CNIO

Category: positions (Page 1 of 3)

Senior researcher (César Nombela grant)

Within the 2024 call of the Talented Research Scientists Recruitment Programme, “César Nombela” grants, we are looking for a scientist who have obtained a PhD between January 1st, 2014 and December 31st, 2021.

The Programme grants a full-time Senior researcher position for 5 years to experienced PhDs who have carried out pre-doctoral and/or post-doctoral stays in an R&D centre outside Spain. Additional funds (up to 200,000 €) will also be granted for the development of the research project.

In order to complete all the necessary internal procedures, please contact Dr Guadalupe Sabio. Applications must be submitted before 6 May 2024.


  • Open to candidates of any nationality (regardless of where the PhD degree was obtained).
  • PhD degree obtained between January 1st, 2014 and December 31st, 2021.
  • Candidates must have been employed in a foreign research centre (as a predoctoral or postdoctoral researcher) for a minimum period of 2 years out of the last five years.

Gross salary: 40,000 € (years 1-3), 47,000 € (years 4-5, in the case that the doctoral researcher has obtained the R3 certificate accrediting the positive evaluation as an established researcher).

Predoctoral contract in metabolism

We are seeking a highly motivated candidate, who would like to start a scientific career doing their doctoral thesis working in understanding p38 kinases role in how the communiation between organs affect the metabolic. This work will be supervised by Dr. Guadalupe Sabio.

We offer incorporation to CNIC via an FPU predoctoral contract. Interested candidates will need to apply before 19 September 2023 in the following CNIC website:

METABOkines: Comunicación celular en el metabolismo: Implicación de la vía de las p38s.



  • This call is open to applicants from all nationalities  holding a Master’s degree in Biomedical Sciences.
  • 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.

Programa CICERONE 2023 para estudiantes de Grado y Máster

Como en años anteriores, nuestro grupo ofrece dos plazas para que estudiantes de Grado y Máster realicen prácticas en nuestro laboratorio entre el 1 de julio y el 15 de septiembre de 2023.

El propósito del programa CICERONE es acercar la investigación biomédica a los estudiantes universitarios para que puedan escoger más adecuadamente su orientación profesional.

Para inscribirse es necesario crear una cuenta en la web del CNIC antes del 28 de abril de 2023.

Enlace Tamaño
Bases de la convocatoria 2023 243 KB
Extracto del BOE 167 KB

Los dos proyectos científicos que ofrecemos este año son:

  • Stress in the brain, metabolic effects: Obesity has become a new pandemic. It is known that obesity induces molecular changes in the brain that are fundamental for the development of diseases and for maintaining excess energy intake. However, little is known about how these changes appear and the molecular mechanisms that mediate them. We will study how modulating stress in the central nervous system induced by high fat diet affects the development of cardiometabolic diseases. For this purpose, genetically modified animals will be used and whole organism metabolism will be evaluated, and how the signalling of this stress in the brain affects the response of distant organs through inter-tissue communication.
  • Role of adipose tissue controling whole body homeostasis: Cardiometabolic diseases (CMDs)—e.g., diabetes, steatohepatitis, and cardiomyopathy— are the leading cause of death worldwide. Adipose tissue (AT) heterogeneity and dysfunction might be involved in the CMD pathogenesis. We have recently demonstrated that i) AT regulates whole-body metabolism independently of obesity and predisposes to hepatic cancer in mice and humans; and ii) molecules secreted by AT trigger liver steatosis and insulin resistance. Our studies suggest that dysfunctional AT communicates with other organs and induces pathogenic adaptive responses through evolutionarily conserved mechanisms (rodent to humans). Our preliminary results show that AT dysfunction caused by mitochondrial alteration induces cardiomyopathy in lean mice, reinforcing that AT has a central role in controlling heart functionality.
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