Dr. Manuel Adolfo Sanchez-Martin
Medicine, University of Salamanca, Salamanca, Castille-Leon, Spain
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Academic Career Length
27Years (2000-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications1 April 2008 in Biology of Reproduction
Journal Article
RFRaúl Fernández-Gonzalez
Raúl Fernández-Gonzalez
PMPedro Nuno Moreira
Pedro Nuno Moreira
MPMiriam Pérez-Crespo
Miriam Pérez-Crespo
Manuel Adolfo Sanchez-MartinMRMiguel Ángel Ramírez
Miguel Ángel Ramírez
Alfonso Gutierrez-Adan +5
Genetic and environmental factors produce different levels of DNA damage in spermatozoa. Usually, DNA-fragmented spermatozoa (DFS) are used with intra
1 December 2002 in Human Molecular Genetics
Journal Article
Manuel Adolfo Sanchez-MartinARArancha Rodríguez-García
Arancha Rodríguez-García
JPJesús Pérez-Losada
Jesús Pérez-Losada
ASAna Sagrera
Ana Sagrera
ARAndrew P. Read
Andrew P. Read
ISIsidro Sanchez-Garcia
Isidro Sanchez-GarciaWaardenburg syndrome (WS; deafness with pigmentary abnormalities) is a congenital disorder caused by defective function of the embryonic neural crest. Depending on additional symptoms, WS is classified into four types: WS1, WS2, WS3 and WS4. WS1 and WS3 are caused by mutations in PAX3, whereas WS2 is heterogenous, being caused by mutations in the microphthalmia (MITF) gene in some but not all affected families. The identification of Slugh, a zinc-finger transcription factor expressed in migratory neural crest cells, as the gene responsible for pigmentary disturbances in mice prompted us to analyse the role of its human homologue SLUG in neural crest defects. Here we show that two unrelated patients with WS2 have homozygous deletions in SLUG which result in absence of the SLUG product. We further show that Mitf is present in Slug-deficient cells and transactivates the SLUG promoter, and that Slugh and Kit genetically interact in vivo. Our findings further define the locus heterogeneity of WS2 and point to an essential role of SLUG in the development of neural crest-derived human cell lineages: its absence causes the auditory–pigmentary symptoms in at least some individuals with WS2.
8 July 2011 in The EMBO Journal
Journal Article
YHYurema Herrán
Yurema Herrán
CGCristina Gutiérrez‐Caballero
Cristina Gutiérrez‐Caballero
Manuel Adolfo Sanchez-MartinTHTeresa Hernández
Teresa Hernández
AVAlberto Viera
Alberto VieraAPAlberto M. Pendás
Alberto M. Pendás +5
18 June 2012 in Journal of Cell Biology
Journal Article
Elena LlanoYHYurema Herrán
Yurema Herrán
IGIgnacio García-Tuñón
Ignacio García-TuñónCGCristina Gutiérrez-Caballero
Cristina Gutiérrez-Caballero
ENRIQUE DE ALAVAAPAlberto M. Pendás
Alberto M. Pendás +4
Cohesin is a conserved multisubunit protein complex that participates in chromosome segregation, DNA damage repair, chromatin regulation, and synaptonemal complex (SC) formation. Yeast, but not mice, depleted of the cohesin subunit Rec8 are defective in the formation of the axial elements (AEs) of the SC, suggesting that, in mammals, this function is not conserved. In this paper, we show that spermatocytes from mice lacking the two meiosis-specific cohesin subunits RAD21L and REC8 were unable to initiate RAD51- but not DMC1-mediated double-strand break repair, were not able to assemble their AEs, and arrested as early as the leptotene stage of prophase I, demonstrating that cohesin plays an essential role in AE assembly that is conserved from yeast to mammals.
1 September 2008 in Genes & Development
Journal Article
Elena Llano
Rocío GómezCGCristina Gutiérrez-Caballero
Cristina Gutiérrez-Caballero
YHYurema Herrán
Yurema Herrán
Manuel Adolfo Sanchez-MartinAPAlberto M. Pendás
Alberto M. Pendás +6
Shugoshin-2 (SGOL2) is one of the two mammalian orthologs of the Shugoshin/Mei-S322 family of proteins that regulate sister chromatid cohesion by protecting the integrity of the multiprotein cohesin complexes. This protective system is essential for faithful chromosome segregation during mitosis and meiosis, which is the physical basis of Mendelian inheritance. Regardless of its evolutionary conservation from yeast to mammals, little is known about the in vivo relevance and specific role that SGOL2 plays in mammals. Here we show that disruption of the gene encoding mouse SGOL2 does not cause any alteration in sister chromatid cohesion in embryonic cultured fibroblasts and adult somatic tissues. Moreover, mutant mice develop normally and survive to adulthood without any apparent alteration. However, both male and female Sgol2-deficient mice are infertile. We demonstrate that SGOL2 is necessary for protecting centromeric cohesion during mammalian meiosis I. In vivo, the loss of SGOL2 promotes a premature release of the meiosis-specific REC8 cohesin complexes from anaphase I centromeres. This molecular alteration is manifested cytologically by the complete loss of centromere cohesion at metaphase II leading to single chromatids and physiologically with the formation of aneuploid gametes that give rise to infertility.
15 August 2002 in Blood
Journal Article
JPJesus Pérez-Losada
Jesus Pérez-LosadaManuel Adolfo Sanchez-MartinARArancha Rodrı́guez-Garcı́a
Arancha Rodrı́guez-Garcı́a
MSMaria Luz Sánchez
Maria Luz Sánchez
AOAlberto Orfao
Alberto Orfao
ISIsidro Sánchez-Garcı́a
Isidro Sánchez-Garcı́a
+1
The stem cell factor c-kit signaling pathway (SCF/c-kit) has been previously implicated in normal hematopoiesis, melanogenesis, and gametogenesis through the formation and migration of c-kit+ cells. These biologic functions are also determinants in epithelial–mesenchymal transitions during embryonic development governed by the Snail family of transcription factors. Here we show that the activation of c-kit by SCF specifically induces the expression of Slug, a Snail family member. Slug mutant mice have a cell-intrinsic defect with pigment deficiency, gonadal defect, and impairment of hematopoiesis. Kit+ cells derived from Slug mutant mice exhibit migratory defects similar to those of c-kit+ cells derived from SCF and c-kit mutant mice. Endogenous Slug is expressed in migratory c-kit+ cells purified from control mice but is not present in c-kit+cells derived from SCF mutant mice or in bone marrow cells from W/Wv mice, though Slug is present in spleen c-kit+ cells of W/Wv (mutants expressing c-kit with reduced surface expression and activity). SCF-induced migration was affected in primary c-kit+ cells purified from Slug−/− mice, providing evidence for a role of Slug in the acquisition of c-kit+ cells with ability to migrate. Slug may thus be considered a molecular target that contributes to the biologic specificity to the SCF/c-kit signaling pathway, opening up new avenues for stem cell mobilization.
About Me
M. Sánchez-Martín is currently an Assistant Professor in the Department of Medicine at the University of Salamanca (USAL) and the Head of the Transgenic Facility at USAL and the Institute of Biomedical Research of Salamanca (IBSAL). Dr. Sánchez-Martín completed his undergraduate studies in Biochemistry in 1994, after which he began his predoctoral training focused on malignant blood diseases across three different centers:
- The Hematology Service of the Hospital Clínico Universitario of Salamanca, where he focused on molecular cytogenetics in leukemias.
- The Institute of Microbiology and Biochemistry, where his work centered on modeling leukemia disease in mice.
- The Cancer Research Center, where he studied the role of SNAI2 in neoplastic diseases arising from mesenchymal cells (leukemias, lymphomas, and sarcomas).
Following his predoctoral training, he was awarded a Ph.D. with an "Outstanding Cum Laude" qualification and the Extraordinary Award for his thesis work. As a result of this training, several scientific contributions were published in Q1 scientific journals. He then secured a postdoctoral fellowship from the Spanish Association for Cancer (AECC) and a postdoctoral research position through the Spanish "Ramón y Cajal" Research Program. He attained the Assistant Professor position at USAL in 2010 and the Lecturer position in 2020.
During his pre- and postdoctoral career, he conducted research stays at various national scientific centers, including INIA, CNB, INSTI