Tamara Romero

Universidad San Pablo CEU

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Verónica Ramos–Mejía

Pfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research

Pedro J. Real

Pfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research

Verónica Ayllón

Pfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research

Rosa Montes

Pfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research

Lourdes López-Onieva

Pfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research

Mar Lamolda

Instituto de Investigación Biosanitaria de Granada

Pablo Menéndez

Josep Carreras Leukaemia Research Institute

T. De Haro Muñoz

Instituto de Investigación Biosanitaria de Granada

M.J. Aguilar Castillo

Instituto de Biología Molecular y Celular de Plantas

M. Molina Zayas

Hospital Jerez Puerta del Sur

Cooperative Institutions

Pfizer-University of Granada-Junta de Andalucía Centre for Genomics and Oncological Research

Universidad de Granada

Instituto de Investigación Biosanitaria de Granada

Parque Tecnológico de la Salud

Hospital Universitario Virgen de las Nieves

Consejo Superior de Investigaciones Científicas

Centro de Investigación Biomédica en Red

Centre for Biomedical Network Research on Rare Diseases

Universidad San Pablo CEU

Universidad Nacional Autónoma de México

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RUNX1cRegulates Hematopoietic Differentiation of Human Pluripotent Stem Cells Possibly in Cooperation with Proinflammatory Signaling

Stem Cells (2017)

Óscar Navarro-Montero Verónica Ayllón Mar Lamolda Lourdes López-Onieva Rosa Montes

Abstract Runt-related transcription factor 1 (Runx1) is a master hematopoietic transcription factor essential for hematopoietic stem cell (HSC) emergence. Runx1-deficient mice die during early embryogenesis due to the inability to establish definitive hematopoiesis. Here, we have used human pluripotent stem cells (hPSCs) as model to study the role of RUNX1 in human embryonic hematopoiesis. Although the three RUNX1 isoforms a, b, and c were induced in CD45+ hematopoietic cells, RUNX1c was the only isoform induced in hematoendothelial progenitors (HEPs)/hemogenic endothelium. Constitutive expression of RUNX1c in human embryonic stem cells enhanced the appearance of HEPs, including hemogenic (CD43+) HEPs and promoted subsequent differentiation into blood cells. Conversely, specific deletion of RUNX1c dramatically reduced the generation of hematopoietic cells from HEPs, indicating that RUNX1c is a master regulator of human hematopoietic development. Gene expression profiling of HEPs revealed a RUNX1c-induced proinflammatory molecular signature, supporting previous studies demonstrating proinflammatory signaling as a regulator of HSC emergence. Collectively, RUNX1c orchestrates hematopoietic specification of hPSCs, possibly in cooperation with proinflammatory signaling.

RUNX1

Proinflammatory cytokine

Hematopoietic stem cell

10.1002/stem.2700

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Citations (20)

Necesidades energéticas en ganado ovino lechero

Tierras. Ovino (2018)

Carlos Fernández Martínez Tamara Romero

Source

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Array-CGH: Possible new cytogenetic alteration

Clinica Chimica Acta (2019)

M.D.M. Del Aguila Garcia Soledad García Chileme M. Molina Zayas Tamara Romero M.J. Aguilar Castillo

10.1016/j.cca.2019.03.1186

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SCL/TAL1-mediated Transcriptional Network Enhances Megakaryocytic Specification of Human Embryonic Stem Cells

Molecular Therapy (2014)

Miguel G. Toscano Óscar Navarro-Montero Verónica Ayllón Verónica Ramos–Mejía Xiomara Guerrero-Carreno

Human embryonic stem cells (hESCs) are a unique in vitro model for studying human developmental biology and represent a potential source for cell replacement strategies. Platelets can be generated from cord blood progenitors and hESCs; however, the molecular mechanisms and determinants controlling the in vitro megakaryocytic specification of hESCs remain elusive. We have recently shown that stem cell leukemia (SCL) overexpression accelerates the emergence of hemato-endothelial progenitors from hESCs and promotes their subsequent differentiation into blood cells with higher clonogenic potential. Given that SCL participates in megakaryocytic commitment, we hypothesized that it may potentiate megakaryopoiesis from hESCs. We show that ectopic SCL expression enhances the emergence of megakaryocytic precursors, mature megakaryocytes (MKs), and platelets in vitro. SCL-overexpressing MKs and platelets respond to different activating stimuli similar to their control counterparts. Gene expression profiling of megakaryocytic precursors shows that SCL overexpression renders a megakaryopoietic molecular signature. Connectivity Map analysis reveals that trichostatin A (TSA) and suberoylanilide hydroxamic acid (SAHA), both histone deacetylase (HDAC) inhibitors, functionally mimic SCL-induced effects. Finally, we confirm that both TSA and SAHA treatment promote the emergence of CD34(+) progenitors, whereas valproic acid, another HDAC inhibitor, potentiates MK and platelet production. We demonstrate that SCL and HDAC inhibitors are megakaryopoiesis regulators in hESCs.

Trichostatin A

Thrombopoiesis

Cord blood

Clonogenic assay

10.1038/mt.2014.196

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Epileptic encephalopathy with phenotype pseudo-Dravet and missense mutation in the GRIN2A gene

Clinica Chimica Acta (2019)

María José Aguilar-Castillo Nicolás Lundahl Ciano-Petersen Tamara Romero A. Spuch G. De Vicente

Stochastic geometry

10.1016/j.cca.2019.03.1272

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Generation and characterization of the human iPSC line PBMC1-iPS4F1 from adult peripheral blood mononuclear cells

Stem Cell Research (2015)

Rosa Montes Tamara Romero Sonia Cabrera Verónica Ayllón José A. López‐Escámez

Here we describe the generation and characterization of the human induced pluripotent stem cell (iPSC) line PBMC1-iPS4F1 from peripheral blood mononuclear cells from a healthy female with Spanish background. We used heat sensitive, non-integrative Sendai viruses containing the reprogramming factors Oct3/4, Sox2, Klf4 and c-Myc, whose expression was silenced in the established iPSC line. Characterization of the PBMC1-iPS4F1 cell line included analysis of typical pluripotency-associated factors at mRNA and protein level, alkaline phosphatase enzymatic activity, and in vivo and in vitro differentiation studies.

KLF4

Reprogramming

10.1016/j.scr.2015.10.009

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Generation of human iPSC line GRX-MCiPS4F-A2 from adult peripheral blood mononuclear cells (PBMCs) with Spanish genetic background

Stem Cell Research (2015)

Sonia Cabrera Ae-Ri Ji Lidia Frejo Verónica Ramos–Mejía Tamara Romero

We have generated iPSCs from peripheral blood mononuclear cells (PBMCs) of a healthy man using heat sensitive and non-integrative Sendai virus containing Sox2, Oct3/4, c-Myc and Klf4. Human GRX-MCiPS4F-A2 cell line was established and characterized through this study.

KLF4

Sendai virus

10.1016/j.scr.2015.07.002

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Hoxa9 and EGFP reporter expression in human Embryonic Stem Cells (hESC) as useful tools for studying human development

Stem Cell Research (2017)

Joan Domingo-Reinés Adolfo López-Ornelas Rosa Montes Tamara Romero Jose Luis Rodriguez-Llamas

HoxA9 is an evolutionarily conserved homeobox gene implicated in embryo development. To study the roles of Hoxa9 during human development we generated a transgenic H9 (hESC) line that overexpresses HoxA9 and the Enhanced Green Fluorescent Protein (EGFP), and a control H9 with a stable expression of the EGFP. The resulting H9-HoxA9-EGFP and H9-EGFP cell lines allow an efficient visualization of hESCs by fluorescent microscopy, quantification by flow cytometry and cell differentiation tracking. Both transgenic cell lines maintained the pluripotent phenotype, the ability to differentiate into all three germ layers and a normal karyotype.

Germ layer

10.1016/j.scr.2017.08.004

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Deletion associated with di George syndrome detected by array-CGH

Clinica Chimica Acta (2019)

M. Molina Zayas M.D.M. Del Aguila Garcia Soledad García Chileme Tamara Romero Carmen García Rabaneda

George (robot)

Regenerative Medicine

Congenital malformations

10.1016/j.cca.2019.03.970

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A-312 Segregation in Two Families of the PCDH19Gene Deletion Associated With Infantile Epileptic Encephalopathy of X-Linked Inheritance and Expression in Female Carriers

Clinical Chemistry (2023)

M. Diaz Tamara Romero Teresa González T de Haro

Abstract Background Developmental and epileptic encephalopathy-9 (DEE9) is an X-linked disorder characterized by seizure onset in infancy and mild to severe intellectual impairment. Autistic and psychiatric features have been reported in some individuals. The disorder affects heterozygous females only; transmitting males are unaffected. We described the segregation in two unrelated families where the proband was clinically affected as a female and another family where the proband was clinically unaffected as a male. Methods Array-CGH analysis was performed by a CGXTM HD v1,1 4-plex array 180 k (PerkinElmer), with an average resolution of 40 kb in the backbone and 20 kb in the regions of interest. Results In the first family a deletion of 809.93 Kilobases was detected in the chromosomal region Xq22.1, which includes the PCDH19 gene, in a 1 year old patient with very early onset seizures, 8 months old, inherited from an asymptomatic father. In the second family, a deletion that includes the entire PCDH19 gene was detected in a 5-year-old male patient referred to genetics for autism spectrum disorder (ASD) and not symptomatic for epilepsy; this deletion was inherited from a mother who had episodes of epilepsy in childhood. Conclusion The aCGH technique is currently the technique of choice to determine the presence of deletions/duplications in genes of interest with high reliability in patients with neurodevelopmental disorders such as epilepsy or ASD. The probands of these two families have been studied for different clinical pathology and in both the deletion of the complete PCDH19 gene has been detected. The PCDH19 gene is expressed in developing human and mouse central nervous system, including the hippocampus and cortex, suggesting a role in cognitive function. Malfunction of the protocadherin19 protein is the cause of epileptic seizures in early childhood, the seizures are mostly focal and cause serial seizures (many seizures that cluster together over a few days). It is a type of epilepsy that usually begins in early childhood. Onset may occur spontaneously or in association with fever. Mutations/deletions of the PCDH19 gene are described to cause Early Childhood Epileptic Encephalopathy, with high but incomplete penetrance. DEE9 affects only females heterozygous for the deletion and is characterised by childhood onset of seizures/epilepsy, usually with mild/severe intellectual disability, with males being healthy carriers. Although the cause is not known specifically, it is thought to be related to X-chromosome silencing that occurs in females heterozygous for this mutation. It causes an autosomal dominant X-linked disorder. Some cases of males with a mosaic PCDH19 mutation/deletion have been found to be affected and it has been suggested that the presence of both the normal gene and the mutated/deleted gene is necessary to develop for this epileptic encephalopathy.

Proband

Pervasive developmental disorder

10.1093/clinchem/hvad097.276

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