Loss of Maged1 results in obesity, deficits of social interactions, impaired sexual behavior and severe alteration of mature oxytocin production in the hypothalamus (Q48418722)

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scientific article published on 2 August 2012

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English	Loss of Maged1 results in obesity, deficits of social interactions, impaired sexual behavior and severe alteration of mature oxytocin production in the hypothalamus	scientific article published on 2 August 2012

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scholarly article

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Europe PubMed Central

PubMed publication ID

11 February 2018

http://europepmc.org/abstract/MED/22865874

Loss of Maged1 results in obesity, deficits of social interactions, impaired sexual behavior and severe alteration of mature oxytocin production in the hypothalamus (English)

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Europe PubMed Central

PubMed publication ID

11 February 2018

http://europepmc.org/abstract/MED/22865874

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Jacques L. Michaud

4

object named as

Jacques L Michaud

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Europe PubMed Central

PubMed publication ID

11 February 2018

http://europepmc.org/abstract/MED/22865874

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Carlos Dombret

1

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Europe PubMed Central

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11 February 2018

http://europepmc.org/abstract/MED/22865874

Tuan Nguyen

2

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Europe PubMed Central

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11 February 2018

http://europepmc.org/abstract/MED/22865874

Olivier Schakman

3

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Europe PubMed Central

PubMed publication ID

11 February 2018

http://europepmc.org/abstract/MED/22865874

Hélène Hardin-Pouzet

5

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Europe PubMed Central

PubMed publication ID

11 February 2018

http://europepmc.org/abstract/MED/22865874

Mathieu J M Bertrand

6

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Europe PubMed Central

PubMed publication ID

11 February 2018

http://europepmc.org/abstract/MED/22865874

Olivier De Backer

7

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Europe PubMed Central

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11 February 2018

http://europepmc.org/abstract/MED/22865874

publication date

2 August 2012

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Europe PubMed Central

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11 February 2018

http://europepmc.org/abstract/MED/22865874

Human Molecular Genetics

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11 February 2018

http://europepmc.org/abstract/MED/22865874

21

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Europe PubMed Central

PubMed publication ID

11 February 2018

http://europepmc.org/abstract/MED/22865874

21

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Europe PubMed Central

PubMed publication ID

11 February 2018

http://europepmc.org/abstract/MED/22865874

4703-4717

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Europe PubMed Central

PubMed publication ID

11 February 2018

http://europepmc.org/abstract/MED/22865874

1 reference

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An immunochemical analysis of oxytocin and vasopressin prohormone processing in vivo

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The human MAGEL2 gene and its mouse homologue are paternally expressed and mapped to the Prader-Willi region

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The human necdin gene, NDN, is maternally imprinted and located in the Prader-Willi syndrome chromosomal region

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Prader-Willi syndrome

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Disruption of the mouse Necdin gene results in hypothalamic and behavioral alterations reminiscent of the human Prader-Willi syndrome.

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Inactivation of the mouse Magel2 gene results in growth abnormalities similar to Prader-Willi syndrome

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Impaired hypothalamic regulation of endocrine function and delayed counterregulatory response to hypoglycemia in Magel2-null mice.

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

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The imprinted gene Magel2 regulates normal circadian output

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

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Comparative expression analysis of the MAGED genes during embryogenesis and brain development

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NRAGE, a p75NTR adaptor protein, is required for developmental apoptosis in vivo.

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Maged1, a new regulator of skeletal myogenic differentiation and muscle regeneration.

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Social approach and repetitive behavior in eleven inbred mouse strains

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Automated apparatus for quantitation of social approach behaviors in mice.

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Housing conditions and stimulus females: a robust social discrimination task for studying male rodent social recognition

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Ultrasonic vocalizations: a tool for behavioural phenotyping of mouse models of neurodevelopmental disorders.

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Shank3 mutant mice display autistic-like behaviours and striatal dysfunction

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Abnormal hypothalamic oxytocin system in fibroblast growth factor 8-deficient mice

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Synthesis, Transport, and Release of Posterior Pituitary Hormones

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Biosynthesis of vasopressin, oxytocin, and neurophysins: isolation and characterization of two common precursors (propressophysin and prooxyphysin).

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Social amnesia in mice lacking the oxytocin gene

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A conditional knockout mouse line of the oxytocin receptor.

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Behavioural studies using temporal and spatial inactivation of the oxytocin receptor

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Pharmacologic rescue of impaired cognitive flexibility, social deficits, increased aggression, and seizure susceptibility in oxytocin receptor null mice: a neurobehavioral model of autism

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CD38 is critical for social behaviour by regulating oxytocin secretion

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When MAGE meets RING: insights into biological functions of MAGE proteins

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Interaction of MAGED1 with nuclear receptors affects circadian clock function

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Carboxypeptidase E

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5 Peptidylglycine α-amidating monooxygenase: An ascorbate-requiring enzyme

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Proteolysis in Neuropeptide Processing and Other Neural Functions

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Oxytocin is required for nursing but is not essential for parturition or reproductive behavior

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Pervasive social deficits, but normal parturition, in oxytocin receptor-deficient mice

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Deficiency in mouse oxytocin prevents milk ejection, but not fertility or parturition.

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Male aromatase-knockout mice exhibit normal levels of activity, anxiety and "depressive-like" symptomatology

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Influence of oxytocin on feeding behavior in the rat.

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Oxytocin inhibits food and fluid intake in rats

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Oxytocin and an oxytocin agonist administered centrally decrease food intake in rats

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Sim1 haploinsufficiency causes hyperphagia, obesity and reduction of the paraventricular nucleus of the hypothalamus

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Development of neuroendocrine lineages requires the bHLH-PAS transcription factor SIM1.

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Oxytocin deficiency mediates hyperphagic obesity of Sim1 haploinsufficient mice

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Identifiers

10.1093/HMG/DDS310

1 reference

Europe PubMed Central

PubMed publication ID

11 February 2018

http://europepmc.org/abstract/MED/22865874

PubMed publication ID

1 reference

Europe PubMed Central

PubMed publication ID

11 February 2018

http://europepmc.org/abstract/MED/22865874

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