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17 results on '"Kemkem, Yasmine"'

1. TSH Pulses Finely Tune Thyroid Hormone Release and TSH Receptor Transduction

Author

Guillou, Anne, primary, Kemkem, Yasmine, additional, Lafont, Chrystel, additional, Fontanaud, Pierre, additional, Calebiro, Davide, additional, Campos, Pauline, additional, Bonnefont, Xavier, additional, Fiordelisio-Coll, Tatiana, additional, Wang, Ying, additional, Brûlé, Emilie, additional, Bernard, Daniel J, additional, Le Tissier, Paul, additional, Steyn, Frederik, additional, and Mollard, Patrice, additional

Published
2023
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2. SOX2+ sustentacular cells are stem cells of the postnatal adrenal medulla

Author

Santambrogio, Alice, primary, Kemkem, Yasmine, additional, Willis, Thea L, additional, Berger, Ilona, additional, Kastriti, Maria Eleni, additional, Faure, Louis, additional, Russell, John P, additional, Lodge, Emily J, additional, Yianni, Val, additional, Oakey, Rebecca J, additional, Altieri, Barbara, additional, Bornstein, Stefan R, additional, Steenblock, Charlotte, additional, Adameyko, Igor Igorevich, additional, and Andoniadou, Cynthia Lilian, additional

Published
2023
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7. Pituitary stem cells produce paracrine WNT signals to control the expansion of their descendant progenitor cells

Author

P, Russell John, primary, Lim, Xinhong, additional, Santambrogio, Alice, additional, Yianni, Val, additional, Kemkem, Yasmine, additional, Wang, Bruce, additional, Fish, Matthew, additional, Haston, Scott, additional, Grabek, Anaeëlle, additional, Hallang, Shirleen, additional, J, Lodge Emily, additional, L, Patist Amanda, additional, Schedl, Andreas, additional, Mollard, Patrice, additional, Nusse, Roel, additional, and Andoniadou, Cynthia L, additional

Published
2022
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8. Metabolic Stress Impairs Pericyte Response to Optogenetic Stimulation in Pancreatic Islets

Author

Michau, Aurélien, primary, Lafont, Chrystel, additional, Bargi-Souza, Paula, additional, Kemkem, Yasmine, additional, Guillou, Anne, additional, Ravier, Magalie A., additional, Bertrand, Gyslaine, additional, Varrault, Annie, additional, Fiordelisio, Tatiana, additional, Hodson, David J., additional, Mollard, Patrice, additional, and Schaeffer, Marie, additional

Published
2022
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9. Pituitary stem cells produce paracrine WNT signals to control the expansion of their descendant progenitor cells

Author

Russell, John P, primary, Lim, Xinhong, additional, Santambrogio, Alice, additional, Yianni, Val, additional, Kemkem, Yasmine, additional, Wang, Bruce, additional, Fish, Matthew, additional, Haston, Scott, additional, Grabek, Anaëlle, additional, Hallang, Shirleen, additional, Lodge, Emily J, additional, Patist, Amanda L, additional, Schedl, Andreas, additional, Mollard, Patrice, additional, Nusse, Roel, additional, and Andoniadou, Cynthia L, additional

Published
2021
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10. Author response: Pituitary stem cells produce paracrine WNT signals to control the expansion of their descendant progenitor cells

Author

Russell, John P, primary, Lim, Xinhong, additional, Santambrogio, Alice, additional, Yianni, Val, additional, Kemkem, Yasmine, additional, Wang, Bruce, additional, Fish, Matthew, additional, Haston, Scott, additional, Grabek, Anaëlle, additional, Hallang, Shirleen, additional, Lodge, Emily J, additional, Patist, Amanda L, additional, Schedl, Andreas, additional, Mollard, Patrice, additional, Nusse, Roel, additional, and Andoniadou, Cynthia L, additional

Published
2020
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11. Pituitary stem cells produce paracrine WNT signals to control the expansion of their descendant progenitor cells

Author

Russell, John Parkin, primary, Lim, Xinhong, additional, Santambrogio, Alice, additional, Yianni, Val, additional, Kemkem, Yasmine, additional, Wang, Bruce, additional, Fish, Matthew, additional, Haston, Scott, additional, Grabek, Anaëlle, additional, Hallang, Shirleen, additional, Lodge, Emily Jane, additional, Patist, Amanda Louise, additional, Schedl, Andreas, additional, Mollard, Patrice, additional, Nusse, Roeland, additional, and Andoniadou, Cynthia Lilian, additional

Published
2020
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13. Imaging and Manipulating Pituitary Function in the Awake Mouse

Author

Hoa, Ombeline, primary, Lafont, Chrystel, additional, Fontanaud, Pierre, additional, Guillou, Anne, additional, Kemkem, Yasmine, additional, Kineman, Rhonda D, additional, Luque, Raul M, additional, Fiordelisio Coll, Tatiana, additional, Le Tissier, Paul, additional, and Mollard, Patrice, additional

Published
2019
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16. TSH Pulses Finely Tune Thyroid Hormone Release and TSH Receptor Transduction

Author

Guillou, Anne, Kemkem, Yasmine, Lafont, Chrystel, Fontanaud, Pierre, Calebiro, Davide, Campos, Pauline, Bonnefont, Xavier, Fiordelisio-Coll, Tatiana, Wang, Ying, Brûlé, Emilie, Bernard, Daniel J, Le Tissier, Paul, Steyn, Frederik, and Mollard, Patrice

Abstract

Detection of circulating TSH is a first-line test of thyroid dysfunction, a major health problem (affecting about 5% of the population) that, if untreated, can lead to a significant deterioration of quality of life and adverse effects on multiple organ systems. Human TSH levels display both pulsatile and (nonpulsatile) basal TSH secretion patterns; however, the importance of these in regulating thyroid function and their decoding by the thyroid is unknown. Here, we developed a novel ultra-sensitive ELISA that allows precise detection of TSH secretion patterns with minute resolution in mouse models of health and disease. We characterized the patterns of ultradian TSH pulses in healthy, freely behaving mice over the day-night cycle. Challenge of the thyroid axis with primary hypothyroidism because of iodine deficiency, a major cause of thyroid dysfunction worldwide, results in alterations of TSH pulsatility. Induction in mouse models of sequential TSH pulses that mimic ultradian TSH profiles in periods of minutes were more efficient than sustained rises in basal TSH levels at increasing both thyroid follicle cAMP levels, as monitored with a genetically encoded cAMP sensor, and circulating thyroid hormone. Hence, this mouse TSH assay provides a powerful tool to decipher how ultradian TSH pulses encode thyroid outcomes and to uncover hidden parameters in the TSH-thyroid hormone set-point in health and disease.

Published
2024
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17. A splice site variant in MADD affects hormone expression in pancreatic β cells and pituitary gonadotropes.

Author

Pulli K, Saarimäki-Vire J, Ahonen P, Liu X, Ibrahim H, Chandra V, Santambrogio A, Wang Y, Vaaralahti K, Iivonen AP, Känsäkoski J, Tommiska J, Kemkem Y, Varjosalo M, Vuoristo S, Andoniadou CL, Otonkoski T, and Raivio T

Subjects
Humans, Animals, Mice, Male, Gonadotrophs metabolism, Female, RNA Splice Sites genetics, Cell Line, Insulin metabolism, Siblings, Exons genetics, rab3 GTP-Binding Proteins metabolism, rab3 GTP-Binding Proteins genetics, Hypogonadism genetics, Hypogonadism metabolism, Hypogonadism pathology, Insulin-Secreting Cells metabolism
Abstract

MAPK activating death domain (MADD) is a multifunctional protein regulating small GTPases RAB3 and RAB27, MAPK signaling, and cell survival. Polymorphisms in the MADD locus are associated with glycemic traits, but patients with biallelic variants in MADD manifest a complex syndrome affecting nervous, endocrine, exocrine, and hematological systems. We identified a homozygous splice site variant in MADD in 2 siblings with developmental delay, diabetes, congenital hypogonadotropic hypogonadism, and growth hormone deficiency. This variant led to skipping of exon 30 and in-frame deletion of 36 amino acids. To elucidate how this mutation causes pleiotropic endocrine phenotypes, we generated relevant cellular models with deletion of MADD exon 30 (dex30). We observed reduced numbers of β cells, decreased insulin content, and increased proinsulin-to-insulin ratio in dex30 human embryonic stem cell-derived pancreatic islets. Concordantly, dex30 led to decreased insulin expression in human β cell line EndoC-βH1. Furthermore, dex30 resulted in decreased luteinizing hormone expression in mouse pituitary gonadotrope cell line LβT2 but did not affect ontogeny of stem cell-derived GnRH neurons. Protein-protein interactions of wild-type and dex30 MADD revealed changes affecting multiple signaling pathways, while the GDP/GTP exchange activity of dex30 MADD remained intact. Our results suggest MADD-specific processes regulate hormone expression in pancreatic β cells and pituitary gonadotropes.

Published
2024
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