A5002642642- Thyroid Disorders and Treatments
- Genetics, Aging, and Longevity in Model Organisms
- Neuroscience of respiration and sleep
- Growth Hormone and Insulin-like Growth Factors
- Thyroid Cancer Diagnosis and Treatment
- Plant Molecular Biology Research
- Epigenetics and DNA Methylation
- Ion channel regulation and function
- CRISPR and Genetic Engineering
- Genetics and Neurodevelopmental Disorders
- GDF15 and Related Biomarkers
Columbia University
2021-2024
Universidad Autónoma de Madrid
2009-2013
Consejo Superior de Investigaciones Científicas
2009-2013
Instituto de Investigaciones Biomédicas Sols-Morreale
2012
Mutations of the gene expressing plasma membrane transporter for thyroid hormones MCT8 (SLC16A2) in humans lead to altered hormone levels and a severe neurodevelopmental disorder. Genetically engineered defect Mct8 mice leads similar abnormalities but no obvious impairment brain development or function. In this work we studied relative role blood-brain barrier neuronal cell restricted access T3 target neurons. To end compared effects low doses T4 on cerebellar structure expression wild-type...
Thyroid hormones influence brain development through the control of gene expression. The concentration active hormone T3 in depends on transport blood-brain barrier, mediated part by monocarboxylate transporter 8 (Mct8/MCT8) and activity type 2 deiodinase (D2) generating from T4. relative roles each these pathways regulation expression is not known. To shed light this question, we analyzed thyroid hormone-dependent cerebral cortex mice with inactivated Mct8 (Slc16a2) Dio2 genes, alone or...
Thyroid hormones regulate brain development and function through the control of gene expression, mediated by binding T3 to nuclear receptors. Brain concentration is tightly controlled homeostatic mechanisms regulating transport metabolism T4 T3. We have examined role inactivating enzyme type 3 deiodinase (D3) in regulation 43 thyroid hormone-dependent genes cerebral cortex 30-d-old mice. D3 inactivation increased slightly expression two 22 positively regulated significantly decreased seven...
Mutations of the monocarboxylate transporter 8 (MCT8) cause a severe X-linked intellectual deficit and neurological impairment. MCT8 is specific thyroid hormone (T4 T3) patients also present unusual abnormalities in serum profile concentrations due to altered secretion metabolism T4 T3. Given role hormones brain development, it thought that impairment restricted transport target neurons. In this work we have investigated cerebral mice with Mct8 deficiency. Adult male were infused for 30...
SUMMARY The proto-oncogene c-MYC is a key representative of the MYC transcription factor network regulating growth and metabolism. MML-1 (Myc- Mondo-like) its homolog in C. elegans . functional molecular cooperation between H3 lysine 79 methyltransferase DOT1L was demonstrated several human cancer types, we have earlier discovered connection DOT-1.1. Here, demonstrate critical role DOT1L/DOT-1.1 c-MYC/MML-1 target genes genome-wide by ensuring removal “spent” factors from chromatin nuclear...
The only representative of the MYC superfamily transcription factors in C. elegans, MML-1 (Myc and Mondo-like 1), was shown to promote extended lifespan a variety models regulate some aspects elegans development. This previous research did not involve molecular characterization MML-1. Here we use available mml-1 mutant alleles other reagents demonstrate that is modified by O-GlcNAc, binds promoters genes directly regulated DOT-1.1 histone methyltransferase complex, has role promoting...