Y. E. Yu

发表

A mouse model of Down syndrome trisomic for all human chromosome 21 syntenic regions.

George Stoica, Shaomin Li, Allan Bradley, 2010, Human molecular genetics.

Genetic and epigenetic pathways in Down syndrome: Insights to the brain and immune system from humans and mouse models.

B. Tycko, N. Schupf, W. Silverman, 2020, Progress in brain research.

Mouse-based genetic modeling and analysis of Down syndrome.

B. Tycko, W. Mobley, A. Pao, 2016, British medical bulletin.

Down Syndrome Cognitive Phenotypes Modeled in Mice Trisomic for All HSA 21 Homologues

L. V. Lysenko, W. Mobley, Y. E. Yu, 2015, PloS one.

Ugt1a is required for the protective effect of selenium against irinotecan-induced toxicity

Y. Rustum, Y. E. Yu, S. Cao, 2012, Cancer Chemotherapy and Pharmacology.

Triplications of human chromosome 21 orthologous regions in mice result in expansion of megakaryocyte-erythroid progenitors and reduction of granulocyte-macrophage progenitors

G. Stoica, P. Wallace, A. Pao, 2017, Oncotarget.

Homozygous inactivation of the LGI1 gene results in hypomyelination in the peripheral and central nervous systems

J. Cowell, Y. E. Yu, Suash J Sharma, 2010, Journal of neuroscience research.

Lgi1 null mutant mice exhibit myoclonic seizures and CA1 neuronal hyperexcitability.

L. Mei, A. Pao, K. Sossey-Alaoui, 2010, Human molecular genetics.

Increased Insulin Action in SKIP Heterozygous Knockout Mice

A. Bradley, T. Takenawa, A. Pao, 2008, Molecular and Cellular Biology.

Coat Color-Facilitated Efficient Generation and Analysis of a Mouse Model of Down Syndrome Triplicated for All Human Chromosome 21 Orthologous Regions

A. Pao, Tao Yu, Y. E. Yu, 2021, Genes.

Analysis of motor dysfunction in Down Syndrome reveals motor neuron degeneration

S. Wells, B. Kalmar, L. Greensmith, 2018, PLoS genetics.

Neuronal differentiation of NTE-deficient embryonic stem cells.

A. Bradley, A. Pao, Zhongyou Li, 2005, Biochemical and biophysical research communications.

MICER targeting vectors for manipulating the mouse genome.

Chunhong Liu, Y. E. Yu, P. Szurek, 2011, Methods in molecular biology.

Genetic analysis of Down syndrome facilitated by mouse chromosome engineering

W. Mobley, A. Pao, S. Clapcote, 2012, Bioengineered bugs.

Hearing impairment in murine model of Down syndrome

D. Ding, Andrew A. McCall, Y. E. Yu, 2022, Frontiers in Genetics.

Human chromosome 21 orthologous region on mouse chromosome 17 is a major determinant of Down syndrome-related developmental cognitive deficits.

P. Ye, S. Josselyn, W. Mobley, 2014, Human molecular genetics.

Retrotransposition creates sloping shores: a graded influence of hypomethylated CpG islands on flanking CpG sites

Leanne S. Whitmore, P. Ye, Z. Izsvák, 2015, Genome research.

Trans effects of chromosome aneuploidies on DNA methylation patterns in human Down syndrome and mouse models

J. Wegiel, B. Tycko, W. Silverman, 2015, Genome Biology.

Impact of increased APP gene dose in Down syndrome and the Dp16 mouse model

Mariko Sawa, W. Mobley, E. Head, 2021, Alzheimer's & dementia : the journal of the Alzheimer's Association.

Mechanistic Analysis of Age-Related Clinical Manifestations in Down Syndrome

B. Tycko, W. Mobley, R. Salvi, 2021, Frontiers in Aging Neuroscience.

Engineered chromosome-based genetic mapping establishes a 3.7 Mb critical genomic region for Down syndrome-associated heart defects in mice

P. Ye, M. Morishima, A. Pao, 2014, Human Genetics.

Genetic analysis of Down syndrome-associated heart defects in mice

Li Zhang, Antonio Baldini, N. Nowak, 2011, Human Genetics.

Duplication of the entire 22.9 Mb human chromosome 21 syntenic region on mouse chromosome 16 causes cardiovascular and gastrointestinal abnormalities.

N. Nowak, M. Morishima, J. Conroy, 2007, Human molecular genetics.

Mouse Models for Down Syndrome-Associated Developmental Cognitive Disabilities

S. Antonarakis, A. Baldini, W. Mobley, 2011, Developmental Neuroscience.

Deficiencies in the region syntenic to human 21q22.3 cause cognitive deficits in mice

J. Roder, A. Bradley, A. Baldini, 2010, Mammalian Genome.

Evidence that increased Kcnj6 gene dose is necessary for deficits in behavior and dentate gyrus synaptic plasticity in the Ts65Dn mouse model of Down syndrome

Jessica Yu, W. Mobley, Y. E. Yu, 2017, Neurobiology of Disease.

Trans-acting epigenetic effects of chromosomal aneuploidies: lessons from Down syndrome and mouse models

B. Tycko, Y. E. Yu, Zhuo Xing, 2016, Epigenomics.

A Deficiency in the Region Homologous to Human 17q21.33–q23.2 Causes Heart Defects in Mice

A. Bradley, A. Baldini, M. Morishima, 2006, Genetics.

Genetic dissection of the Down syndrome critical region.

Jennifer L. Peresie, W. Mobley, A. Pao, 2015, Human molecular genetics.

Effects of individual segmental trisomies of human chromosome 21 syntenic regions on hippocampal long-term potentiation and cognitive behaviors in mice

J. Roder, A. Baldini, W. Mobley, 2010, Brain Research.

Analysis of mutations in primary and metastatic synovial sarcoma

C. Morrison, Jianmin Wang, Song Liu, 2018, Oncotarget.

CRISPR/Cas9-Facilitated Chromosome Engineering to Model Human Chromosomal Alterations

A. Pao, Y. E. Yu, Zhuo Xing, 2018 .

Dissection of a down syndrome-associated trisomy to separate the gene dosage-dependent and -independent effects of an extra chromosome.

Jianlin Cheng, B. Tycko, Song Liu, 2023, Human molecular genetics.

Mouse Models for Down Syndrome-Associated Developmental Cognitive Disabilities

S. Antonarakis, A. Baldini, W. Mobley, 2011, Developmental Neuroscience.