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Regulation of autism-relevant behaviors by cerebellar-prefrontal cortical circuits

Nature neuroscience, 2020-09, Vol.23 (9), p.1102

2020

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The Prader-Willi syndrome proteins MAGEL2 and necdin regulate leptin receptor cell surface abundance through ubiquitination pathways

Human molecular genetics, 2017-11, Vol.26 (21), p.4215-4230

2017

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Impaired Hypothalamic Regulation of Endocrine Function and Delayed Counterregulatory Response to Hypoglycemia in Magel2-Null Mice

Endocrinology (Philadelphia), 2011-03, Vol.152 (3), p.967-978

2011

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Preclinical Testing in Translational Animal Models of Prader-Willi Syndrome: Overview and Gap Analysis

Molecular therapy. Methods & clinical development, 2019-06, Vol.13, p.344-358

2019

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Loss of the Prader–Willi obesity syndrome protein necdin promotes adipogenesis

Gene, 2012-04, Vol.497 (1), p.45-51

2012

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A MAGEL2-deubiquitinase complex modulates the ubiquitination of circadian rhythm protein CRY1

PloS one, 2020-04, Vol.15 (4), p.e0230874-e0230874

2020

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Disentangling ingestive behavior-related phenotypes in Prader–Willi syndrome: Integrating information from nonclinical studies and clinical trials to better understand the pathophysiology of hyperphagia and obesity

Physiology & behavior, 2020-05, Vol.219, p.112864-112864, Article 112864

Wevrick, Rachel

2020

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Loss of magel2, a candidate gene for features of Prader-Willi syndrome, impairs reproductive function in mice

PloS one, 2009-01, Vol.4 (1), p.e4291-e4291

2009

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Necdin, a p53 target gene, regulates the quiescence and response to genotoxic stress of hematopoietic stem/progenitor cells

Blood, 2012-08, Vol.120 (8), p.1601-1612

2012

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ROHHAD and Prader-Willi syndrome (PWS): clinical and genetic comparison

Orphanet journal of rare diseases, 2018-07, Vol.13 (1), p.124-124, Article 124

2018

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Magel2 is required for leptin-mediated depolarization of POMC neurons in the hypothalamic arcuate nucleus in mice

PLoS genetics, 2013-01, Vol.9 (1), p.e1003207-e1003207

2013

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Hypothalamic AAV-BDNF gene therapy improves metabolic function and behavior in the Magel2-null mouse model of Prader-Willi syndrome

Molecular therapy. Methods & clinical development, 2022-12, Vol.27, p.131-148

2022

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Claudin-4 forms a paracellular barrier, revealing the interdependence of claudin expression in the loose epithelial cell culture model opossum kidney cells

American Journal of Physiology: Cell Physiology, 2012-12, Vol.303 (12), p.C1278-C1291

2012

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Sleeve gastrectomy leads to weight loss in the Magel2 knockout mouse

Surgery for obesity and related diseases, 2016-12, Vol.12 (10), p.1795-1802

2016

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Regionally reduced brain volume, altered serotonin neurochemistry, and abnormal behavior in mice null for the circadian rhythm output gene Magel2

American journal of medical genetics. Part B, Neuropsychiatric genetics, 2009-12, Vol.150B (8), p.1085-1099

2009

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Targeting the endocannabinoid/CB1 receptor system for treating obesity in Prader–Willi syndrome

Molecular metabolism (Germany), 2016-12, Vol.5 (12), p.1187-1199

2016

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Developmental Abnormalities of Neuronal Structure and Function in Prenatal Mice Lacking the Prader-Willi Syndrome Gene Necdin

The American journal of pathology, 2005-07, Vol.167 (1), p.175-191

2005

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Stochastic loss of silencing of the imprinted Ndn/NDN allele, in a mouse model and humans with prader-willi syndrome, has functional consequences

PLoS genetics, 2013-09, Vol.9 (9), p.e1003752-e1003752

2013

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The Smc5/Smc6/MAGE complex confers resistance to caffeine and genotoxic stress in Drosophila melanogaster

PloS one, 2013-03, Vol.8 (3), p.e59866

2013

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Essential role for the Prader–Willi syndrome protein necdin in axonal outgrowth

Human molecular genetics, 2005-03, Vol.14 (5), p.627-637

2005

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Loss of Necdin impairs myosin activation and delays cell polarization

Genesis (New York, N.Y. : 2000), 2010-09, Vol.48 (9), p.540-553

2010

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Clinical and genetic analysis of children with a dual diagnosis of Tourette syndrome and autism spectrum disorder

Journal of psychiatric research, 2019-04, Vol.111, p.145-153

2019

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Disruption of the mouse necdin gene results in early post-natal lethality

Nature genetics, 1999-10, Vol.23 (2), p.199-202

1999

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Loss of the Prader‐Willi syndrome protein necdin causes defective migration, axonal outgrowth, and survival of embryonic sympathetic neurons

Developmental dynamics, 2008-07, Vol.237 (7), p.1935-1943

2008

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Magel2, a Prader-Willi syndrome candidate gene, modulates the activities of circadian rhythm proteins in cultured cells

Journal of circadian rhythms, 2011-12, Vol.9 (1), p.12-12

2011

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Regulation of autism-relevant behaviors by cerebellar-prefrontal cortical circuits

The Prader-Willi syndrome proteins MAGEL2 and necdin regulate leptin receptor cell surface abundance through ubiquitination pathways

Impaired Hypothalamic Regulation of Endocrine Function and Delayed Counterregulatory Response to Hypoglycemia in Magel2-Null Mice

Preclinical Testing in Translational Animal Models of Prader-Willi Syndrome: Overview and Gap Analysis

Loss of the Prader–Willi obesity syndrome protein necdin promotes adipogenesis

A MAGEL2-deubiquitinase complex modulates the ubiquitination of circadian rhythm protein CRY1

Disentangling ingestive behavior-related phenotypes in Prader–Willi syndrome: Integrating information from nonclinical studies and clinical trials to better understand the pathophysiology of hyperphagia and obesity

Loss of magel2, a candidate gene for features of Prader-Willi syndrome, impairs reproductive function in mice

Necdin, a p53 target gene, regulates the quiescence and response to genotoxic stress of hematopoietic stem/progenitor cells

ROHHAD and Prader-Willi syndrome (PWS): clinical and genetic comparison

Magel2 is required for leptin-mediated depolarization of POMC neurons in the hypothalamic arcuate nucleus in mice

Hypothalamic AAV-BDNF gene therapy improves metabolic function and behavior in the Magel2-null mouse model of Prader-Willi syndrome

Claudin-4 forms a paracellular barrier, revealing the interdependence of claudin expression in the loose epithelial cell culture model opossum kidney cells

Sleeve gastrectomy leads to weight loss in the Magel2 knockout mouse

Regionally reduced brain volume, altered serotonin neurochemistry, and abnormal behavior in mice null for the circadian rhythm output gene Magel2

Targeting the endocannabinoid/CB1 receptor system for treating obesity in Prader–Willi syndrome

Developmental Abnormalities of Neuronal Structure and Function in Prenatal Mice Lacking the Prader-Willi Syndrome Gene Necdin

Stochastic loss of silencing of the imprinted Ndn/NDN allele, in a mouse model and humans with prader-willi syndrome, has functional consequences

The Smc5/Smc6/MAGE complex confers resistance to caffeine and genotoxic stress in Drosophila melanogaster

Essential role for the Prader–Willi syndrome protein necdin in axonal outgrowth

Loss of Necdin impairs myosin activation and delays cell polarization

Clinical and genetic analysis of children with a dual diagnosis of Tourette syndrome and autism spectrum disorder

Disruption of the mouse necdin gene results in early post-natal lethality

Loss of the Prader‐Willi syndrome protein necdin causes defective migration, axonal outgrowth, and survival of embryonic sympathetic neurons

Magel2, a Prader-Willi syndrome candidate gene, modulates the activities of circadian rhythm proteins in cultured cells

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