Pablo Huertas

Research interest

Double strand breaks (DSBs) repair is essential fory and cell death, mutations that hamper it causes the appearance of cancer or several genetically inherited syndromes. DSBs are repaired by two major mechanisms. The ends can be simple re-jo . Despite its importance, the network controlling the choice between both is poorly understood. In my laboratory, we pursue three research lines designed to investigate how such choice between is made, its relevance for survival and disease, and its potential as a therapeutic target for cancer or some genetically inherited disorders.

  1. By biochemical and genetics approaches, we have uncovered new interactors and post-translational modifications of CtIP that affect such regulation.
  2. Using a novel reporter designed in our laboratory wepursuing the characterization of other genes found in our screening.
  3. We are applying the findings we have obtained in the lab to study the role of specific factors in cell survival and fitness during normal development and in the appearance of cancer or rare diseases.


  • CtIP-Specific Roles during Cell Reprogramming Have Long-Term Consequences in the Survival and Fitness of Induced Pluripotent Stem Cells. Gómez-Cabello D, Checa-Rodríguez C, Abad M, Serrano M, Huertas P. Stem Cell Reports. 2016 Dec 27. pii: S2213-6711(16)30299-5. doi: 10.1016/j.stemcr.2016.12.009

  • A genome-wide screening for factors that regulate the balance between recombination and NHEJ uncovers the role of CCAR2 as an antagonist of DNA-end resection. López-Saavedra A, Gómez-Cabello D, Domínguez-Sánchez MS, Mejías-Navarro F, Fernández-Ávila MJ, Martínez-Macías MI, Dinant C, Bartek J, Huertas P. Nature Communication. 2016 Aug 9;7:12364. doi: 10.1038/ncomms12364.

  • Neddylation inhibits CtIP-mediated resection and regulates DNA double strand break repair pathway choice. Jimeno S, Fernández-Avila MJ, Cepeda-García C, Gómez-Cabello D, Cruz-García A, Huertas P. Nucleic Acids Res. 2015 Jan;43(2):987-99. doi: 10.1093/nar/gku1384. Epub 2015 Jan 7..

  • Speed matters: how subtle changes in DNA-end resection rate affect repair. Huertas P., Cruz-García A. Molecular and Cellular Oncology. 2015 May;2:3, e982964.

  • BRCA1 accelerates CtIP-mediated DNA-end resection. Cruz-García A, López Saavedra A, Huertas P. Cell Reports. 2014 Oct 23;9(2):451-9. doi: 10.1016/j.celrep.2014.08.076. Epub 2014 Oct 9..

  • Prognostic value of CtIP/RBBP8 expression in breast cancer.. Soria-Bretones I, Sáez C, Ruíz-Borrego M, Japon MA, Huertas P. Cancer Med. 2013 Dec;2(6):774-83. doi: 10.1002/cam4.141. Epub 2013 Oct 3.

  • New tools to study DNA double strand breaks repair pathway choice. Gomez-Cabello D, Jimeno S, Fernandez-Avila MJ, Huertas P. PLOS One. 2013 Oct 14;8(10):e77206. doi: 10.1371/journal.pone.0077206.

  • CtIP mutations cause Seckel and Jawad syndromes. Qvist P, Huertas P, Jimeno S, Nyegaard M, Jackson SP, Borglum AD. PLOS Genetics . 2011 October e1002310.

Active Grants

Título del proyecto: Relación del Daño en Fase S y los Defectos de Segregación en Mitosis en los Síndromes Recesivos con Microcefalia
Entidad financiado: Junta de Andalucía, (P12-BIO-515)

Título del proyecto: Regulación de la Recombinación en el Contexto Celular
Entidad financiadora: Ministerio de Economía y Competitividad, SAF2016-74855-P

Group members

Group leader:
  • Pablo Huertas Sánchez
  • Dr. Sonia Jimeno
PhD students:
  • Cintia Checa Rodríguez
  • Ana López Saavedra
  • Fernando Mejías Navarro
  • María Rosario Prados Carvajal
  • Isabel Soria Bretones
Master students:
  • María Rosa Camarillo Daza