| MYT1L haploinsufficiency in human neurons and mice causes autism-associated phenotypes that can be reversed by genetic and pharmacologic intervention. | MYT1L haploinsufficiency in human neurons and mice causes autism-associated phenotypes that can be reversed by genetic and pharmacologic intervention.
Weigel B, Tegethoff JF, Grieder SD, Lim B, Nagarajan B, Liu YC, Truberg J, Papageorgiou D, Adrian-Segarra JM, Schmidt LK, Kaspar J, Poisel E, Heinzelmann E, Saraswat M, Christ M, Arnold C, Ibarra IL, Campos J, Krijgsveld J, Monyer H, Zaugg JB, Acuna C, Mall M., Free PMC Article | 11/16/2023 |
| 2p25.3 microduplications involving MYT1L: further phenotypic characterization through an assessment of 16 new cases and a literature review. | 2p25.3 microduplications involving MYT1L: further phenotypic characterization through an assessment of 16 new cases and a literature review.
Bouassida M, Egloff M, Levy J, Chatron N, Bernardini L, Le Guyader G, Tabet AC, Schluth-Bolard C, Brancati F, Giuffrida MG, Dard R, Clorennec J, Coursimault J, Vialard F, Hervé B., Free PMC Article | 08/9/2023 |
| Co-Occurrence of Fragile X Syndrome with a Second Genetic Condition: Three Independent Cases of Double Diagnosis. | Co-Occurrence of Fragile X Syndrome with a Second Genetic Condition: Three Independent Cases of Double Diagnosis.
Tabolacci E, Pomponi MG, Remondini L, Pietrobono R, Orteschi D, Nobile V, Pucci C, Musto E, Pane M, Mercuri EM, Neri G, Genuardi M, Chiurazzi P, Zollino M., Free PMC Article | 02/19/2022 |
| MYT1L-associated neurodevelopmental disorder: description of 40 new cases and literature review of clinical and molecular aspects. | MYT1L-associated neurodevelopmental disorder: description of 40 new cases and literature review of clinical and molecular aspects.
Coursimault J, Guerrot AM, Morrow MM, Schramm C, Zamora FM, Shanmugham A, Liu S, Zou F, Bilan F, Le Guyader G, Bruel AL, Denommé-Pichon AS, Faivre L, Tran Mau-Them F, Tessarech M, Colin E, El Chehadeh S, Gérard B, Schaefer E, Cogne B, Isidor B, Nizon M, Doummar D, Valence S, Héron D, Keren B, Mignot C, Coutton C, Devillard F, Alaix AS, Amiel J, Colleaux L, Munnich A, Poirier K, Rio M, Rondeau S, Barcia G, Callewaert B, Dheedene A, Kumps C, Vergult S, Menten B, Chung WK, Hernan R, Larson A, Nori K, Stewart S, Wheless J, Kresge C, Pletcher BA, Caumes R, Smol T, Sigaudy S, Coubes C, Helm M, Smith R, Morrison J, Wheeler PG, Kritzer A, Jouret G, Afenjar A, Deleuze JF, Olaso R, Boland A, Poitou C, Frebourg T, Houdayer C, Saugier-Veber P, Nicolas G, Lecoquierre F. | 01/22/2022 |
| A web-based survey on various symptoms of computer vision syndrome and the genetic understanding based on a multi-trait genome-wide association study. | A web-based survey on various symptoms of computer vision syndrome and the genetic understanding based on a multi-trait genome-wide association study.
Yoshimura K, Morita Y, Konomi K, Ishida S, Fujiwara D, Kobayashi K, Tanaka M., Free PMC Article | 10/23/2021 |
| The neuronal transcription factor Myt1L interacts via a conserved motif with the PAH1 domain of Sin3 to recruit the Sin3L/Rpd3L histone deacetylase complex. | The neuronal transcription factor Myt1L interacts via a conserved motif with the PAH1 domain of Sin3 to recruit the Sin3L/Rpd3L histone deacetylase complex.
Marcum RD, Radhakrishnan I., Free PMC Article | 05/8/2021 |
| Nine newly identified individuals refine the phenotype associated with MYT1L mutations. | Nine newly identified individuals refine the phenotype associated with MYT1L mutations.
Windheuser IC, Becker J, Cremer K, Hundertmark H, Yates LM, Mangold E, Peters S, Degenhardt F, Ludwig KU, Zink AM, Lessel D, Bierhals T, Herget T, Johannsen J, Denecke J, Wohlleber E, Strom TM, Wieczorek D, Bertoli M, Colombo R, Hempel M, Engels H. | 03/27/2021 |
| MYT1L: A systematic review of genetic variation encompassing schizophrenia and autism. | MYT1L: A systematic review of genetic variation encompassing schizophrenia and autism.
Mansfield P, Constantino JN, Baldridge D., Free PMC Article | 02/20/2021 |
| The crucial role of DNA-dependent protein kinase and myelin transcription factor 1-like protein in the miR-141 tumor suppressor network. | The crucial role of DNA-dependent protein kinase and myelin transcription factor 1-like protein in the miR-141 tumor suppressor network.
Wang B, Li D, Yao Y, Heyns M, Kovalchuk A, Ilnytskyy Y, Rodriguez-Juarez R, Bronson RT, Metz GAS, Kovalchuk O, Kovalchuk I., Free PMC Article | 09/5/2020 |
| Our finding supports the association of MYT1L mutations with early-onset syndromic obesity. The identification of novel monogenic forms of childhood-onset obesity will provide insights to the involved genetic and biologic pathways. | A novel MYT1L mutation in a patient with severe early-onset obesity and intellectual disability.
Loid P, Mäkitie R, Costantini A, Viljakainen H, Pekkinen M, Mäkitie O. | 09/14/2019 |
| Myt1l was a critical mediator of induced neuron cell reprogramming. | Myt1l induced direct reprogramming of pericytes into cholinergic neurons.
Liang XG, Tan C, Wang CK, Tao RR, Huang YJ, Ma KF, Fukunaga K, Huang MZ, Han F., Free PMC Article | 07/20/2019 |
| Here we demonstrate that re-expression of Myt1 or Myt1l in glioblastoma (GBM) cell lines slows proliferation, that expression of both is lower in more aggressive sub-types of glioma, and that reduced expression correlates with poor prognosis in both GBM and low grade glioma, and our data suggest that Myt1 and Myt1l directly repress expression of YAP1, a protein which promotes proliferation and GBM growth. | Myt1 and Myt1l transcription factors limit proliferation in GBM cells by repressing YAP1 expression.
Melhuish TA, Kowalczyk I, Manukyan A, Zhang Y, Shah A, Abounader R, Wotton D., Free PMC Article | 06/1/2019 |
| wide analyses of the effects of Myt1 and Myt1l expression in a glioblastoma cell line suggest that the two proteins have largely similar effects on endogenous gene expression. Transcriptional repression is likely mediated by binding to DNA via the known consensus site, whereas this site is not associated with the transcriptional start sites of genes with higher expression in the presence of Myt1 or Myt1l. | Analysis of transcriptional activity by the Myt1 and Myt1l transcription factors.
Manukyan A, Kowalczyk I, Melhuish TA, Lemiesz A, Wotton D. | 03/2/2019 |
| (1) MYT1L is required for neuronal differentiation and identified ID1 as a target. (2) Although MYT1L prevented expression of ID1, it induced expression of a large number of terminal differentiation genes. (3) Consistently, expression of MYT1L in the human brain coincided with neuronal maturation and inversely correlated with that of ID1 and ID3 throughout the lifespan. | Associations of the Intellectual Disability Gene MYT1L with Helix-Loop-Helix Gene Expression, Hippocampus Volume and Hippocampus Activation During Memory Retrieval.
Kepa A, Martinez Medina L, Erk S, Srivastava DP, Fernandes A, Toro R, Lévi S, Ruggeri B, Fernandes C, Degenhardt F, Witt SH, Meyer-Lindenberg A, Poncer JC, Martinot JL, Paillère Martinot ML, Müller CP, Heinz A, Walter H, Schumann G, Desrivières S., Free PMC Article | 08/4/2018 |
| This study demonstrates that MYT1L variants are associated with syndromic obesity in humans. The mechanism is related to dysregulated expression of neurodevelopmental genes and altered development of the neuroendocrine hypothalamus | MYT1L mutations cause intellectual disability and variable obesity by dysregulating gene expression and development of the neuroendocrine hypothalamus.
Blanchet P, Bebin M, Bruet S, Cooper GM, Thompson ML, Duban-Bedu B, Gerard B, Piton A, Suckno S, Deshpande C, Clowes V, Vogt J, Turnpenny P, Williamson MP, Alembik Y, Clinical Sequencing Exploratory Research Study Consortium, Deciphering Developmental Disorders Consortium, Glasgow E, McNeill A., Free PMC Article | 10/14/2017 |
| Haplotype-dependent allele-specific methylation of MYT1L gene is associated with neurological disorders. | Mechanisms and Disease Associations of Haplotype-Dependent Allele-Specific DNA Methylation.
Do C, Lang CF, Lin J, Darbary H, Krupska I, Gaba A, Petukhova L, Vonsattel JP, Gallagher MP, Goland RS, Clynes RA, Dwork A, Kral JG, Monk C, Christiano AM, Tycko B., Free PMC Article | 05/20/2017 |
| Our data strongly strengthen the hypothesis that MYT1L is the causal gene for the observed syndromal intellectual disability. | Refinement of the critical 2p25.3 deletion region: the role of MYT1L in intellectual disability and obesity.
De Rocker N, Vergult S, Koolen D, Jacobs E, Hoischen A, Zeesman S, Bang B, Béna F, Bockaert N, Bongers EM, de Ravel T, Devriendt K, Giglio S, Faivre L, Joss S, Maas S, Marle N, Novara F, Nowaczyk MJ, Peeters H, Polstra A, Roelens F, Rosenberg C, Thevenon J, Tümer Z, Vanhauwaert S, Varvagiannis K, Willaert A, Willemsen M, Willems M, Zuffardi O, Coucke P, Speleman F, Eichler EE, Kleefstra T, Menten B. | 02/27/2016 |
| Report shows that the first histidine of Cys2His2Cys domains is involved in a functionally important hydrogen bonding interaction. | A role for hydrogen bonding in DNA recognition by the non-classical CCHHC type zinc finger, NZF-1.
Besold AN, Amick DL, Michel SL., Free PMC Article | 01/31/2015 |
| MYT1L rs17039396 variants are associated with clinical outcome in gastric cancer. | Clinical significance of MYT1L gene polymorphisms in Chinese patients with gastric cancer.
Zhang Y, Zhu H, Zhang X, Gu D, Zhou X, Wang M, Cao C, Zhang X, Wu X, Gong W, Tang Y, Zhou J, Tang C, Zhang Z, Chen J., Free PMC Article | 05/24/2014 |
| MYT1L and the SNTG2 genes within the reported region could probably relate to the phenotypic discordance of the monozygotic twins. | Monozygotic twins discordant for submicroscopic chromosomal anomalies in 2p25.3 region detected by array CGH.
Rio M, Royer G, Gobin S, de Blois MC, Ozilou C, Bernheim A, Nizon M, Munnich A, Bonnefont JP, Romana S, Vekemans M, Turleau C, Malan V. | 01/4/2014 |
| Data indicate that reintroduction of A2BP1 or Myt1L in glioblastoma multiforme (GBM) cell lines and glioma stem cells profoundly inhibited tumorigenesis. | From the Cover: Neutralization of terminal differentiation in gliomagenesis.
Hu J, Ho AL, Yuan L, Hu B, Hua S, Hwang SS, Zhang J, Hu T, Zheng H, Gan B, Wu G, Wang YA, Chin L, DePinho RA., Free PMC Article | 12/21/2013 |
| A meta-analysis of four recently published studies that together provide strong evidence for an association between variably sized microduplications involving the MYT1L gene and schizophrenia. | Microduplications disrupting the MYT1L gene (2p25.3) are associated with schizophrenia.
Lee Y, Mattai A, Long R, Rapoport JL, Gogtay N, Addington AM., Free PMC Article | 11/17/2012 |
| Results from this study indicate that the 2p25.3 duplication disrupting PXDN and MYT1L is a potential autism-causing variant in the pedigree reported here and should receive further consideration as a candidate for autism | Germline mosaic transmission of a novel duplication of PXDN and MYT1L to two male half-siblings with autism.
Meyer KJ, Axelsen MS, Sheffield VC, Patil SR, Wassink TH., Free PMC Article | 08/18/2012 |
| Findings suggest that MYT1L may represent a susceptibility gene for schizophrenia in the Han Chinese population and show that a specific SNP may increase susceptibility in females. | Association study of myelin transcription factor 1-like polymorphisms with schizophrenia in Han Chinese population.
Li W, Wang X, Zhao J, Lin J, Song XQ, Yang Y, Jiang C, Xiao B, Yang G, Zhang HX, Lv LX. | 06/2/2012 |
| MYT1L deletion gives a nonspecific clinical phenotype shared by patients with 2p25.3 deletions, with only intellectual disability and obesity/overweight being present in all patients. | MYT1L is a candidate gene for intellectual disability in patients with 2p25.3 (2pter) deletions.
Stevens SJ, van Ravenswaaij-Arts CM, Janssen JW, Klein Wassink-Ruiter JS, van Essen AJ, Dijkhuizen T, van Rheenen J, Heuts-Vijgen R, Stegmann AP, Smeets EE, Engelen JJ. | 02/11/2012 |