PP2A-B55 phosphatase counteracts Ki-67-dependent chromosome individualization during mitosis

Autor: María Sanz-Flores, Miguel Ruiz-Torres, Cristina Aguirre-Portolés, Aicha El Bakkali, Beatriz Salvador-Barberó, Carolina Villarroya-Beltri, Sagrario Ortega, Diego Megías, Daniel W. Gerlich, Mónica Álvarez-Fernández, Marcos Malumbres

Publikováno v: Cell Reports, Vol 43, Iss 7, Pp 114494- (2024)

Summary: Cell cycle progression is regulated by the orderly balance between kinase and phosphatase activities. PP2A phosphatase holoenzymes containing the B55 family of regulatory B subunits function as major CDK1-counteracting phosphatases during mi

Externí odkaz: https://doaj.org/article/77cd2f50a74c44d8a02a9ad8b144ca93

ISGylation controls exosome secretion by promoting lysosomal degradation of MVB proteins

Autor: Carolina Villarroya-Beltri, Francesc Baixauli, María Mittelbrunn, Irene Fernández-Delgado, Daniel Torralba, Olga Moreno-Gonzalo, Sara Baldanta, Carlos Enrich, Susana Guerra, Francisco Sánchez-Madrid

Publikováno v: Nature Communications, Vol 7, Iss 1, Pp 1-11 (2016)

Multivesicular bodies (MVB) are endosomal compartments that can either fuse with the plasma membrane for the secretion of exosomes, or fuse with the lysosome and be degraded along with their contents. Here, the authors show that ISGylation of the MVB

Externí odkaz: https://doaj.org/article/1b2e7f717e724460ac0843fd8652dd65

Biallelic germline mutations in MAD1L1 induce a syndrome of aneuploidy with high tumor susceptibility

Autor: Carolina Villarroya-Beltri, Ana Osorio, Raúl Torres-Ruiz, David Gómez-Sánchez, Marianna Trakala, Agustin Sánchez-Belmonte, Fátima Mercadillo, Begoña Hurtado, Borja Pitarch, Almudena Hernández-Núñez, Antonio Gómez-Caturla, Daniel Rueda, José Perea, Sandra Rodríguez-Perales, Marcos Malumbres, Miguel Urioste

Publikováno v: Science advances. 8(44)

Germline mutations leading to aneuploidy are rare, and their tumor-promoting properties are mostly unknown at the molecular level. We report here novel germline biallelic mutations in MAD1L1 , encoding the spindle assembly checkpoint (SAC) protein MA

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dff4ffeb5c2938a24256fd6d33155821
https://pubmed.ncbi.nlm.nih.gov/36322655

Mitotic Checkpoint Imbalances in Familial Cancer

Autor: Carolina Villarroya-Beltri, Marcos Malumbres

Publikováno v: Cancer research. 82(19)

Summary Numerical chromosomal aberrations are highly frequent in cancer cells. However, tumor-associated mutations in regulators of the mitotic machinery that controls chromosome segregation are rather rare. By sequencing families with hereditary can

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8ecbfb559069b21327c174f0d3c2dd1a
https://pubmed.ncbi.nlm.nih.gov/35913887

Priming of dendritic cells by DNA-containing extracellular vesicles from activated T cells through antigen-driven contacts

Autor: María Mittelbrunn, Francesc Baixauli, Angel Luis Jaso-Tamame, Inmaculada Jorge, Johan Garaude, Gloria González-Aseguinolaza, Noa B. Martín-Cófreces, Miguel Vicente-Manzanares, José Antonio Enríquez, Salvador Iborra, Carolina Villarroya-Beltri, Irene Fernández-Delgado, Rebeca Acín-Pérez, Ana Latorre-Pellicer, Francisco Sánchez-Madrid, Daniel Torralba

Publikováno v: Repisalud
Instituto de Salud Carlos III (ISCIII)
Biblos-e Archivo. Repositorio Institucional de la UAM
instname
Digital.CSIC. Repositorio Institucional del CSIC
Repositorio Institucional de la Consejería de Sanidad de la Comunidad de Madrid
Consejería de Sanidad de la Comunidad de Madrid
Nature Communications, Vol 9, Iss 1, Pp 1-17 (2018)
Nature Communications

Interaction of T cell with antigen-bearing dendritic cells (DC) results in T cell activation, but whether this interaction has physiological consequences on DC function is largely unexplored. Here we show that when antigen-bearing DCs contact T cells

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d9392ca650bf15c65212f0417d48062d
http://hdl.handle.net/20.500.12105/6572