Tsc2 gene inactivation causes a more severe epilepsy phenotype than Tsc1 inactivation in a mouse model of tuberous sclerosis complex. - Test2 - elhamkhani - TriplyDB

Tsc2 gene inactivation causes a more severe epilepsy phenotype than Tsc1 inactivation in a mouse model of tuberous sclerosis complex.

Tsc2 gene inactivation causes a more severe epilepsy phenotype than Tsc1 inactivation in a mouse model of tuberous sclerosis complex.

http://www.wikidata.org/entity/Q30497818

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Ribosomal Protein S6 Phosphorylation in the Nervous System: From Regulation to Function The neurology of mTOR Potential for treatment of severe autism in tuberous sclerosis complex Finding a better drug for epilepsy: the mTOR pathway as an antiepileptogenic target Inflammatory mechanisms contribute to the neurological manifestations of tuberous sclerosis complex.Convulsive seizures from experimental focal cortical dysplasia occur independently of cell misplacement.Translational Mouse Models of Autism: Advancing Toward Pharmacological Therapeutics.Impaired social interactions and motor learning skills in tuberous sclerosis complex model mice expressing a dominant/negative form of tuberin Single-cell Tsc1 knockout during corticogenesis generates tuber-like lesions and reduces seizure threshold in mice Deletion of Rictor in neural progenitor cells reveals contributions of mTORC2 signaling to tuberous sclerosis complex.Rapamycin reverses impaired social interaction in mouse models of tuberous sclerosis complex.Rapamycin prevents seizures after depletion of STRADA in a rare neurodevelopmental disorder Timing of mTOR activation affects tuberous sclerosis complex neuropathology in mouse models.Leveraging a Sturge-Weber Gene Discovery: An Agenda for Future Research.Hippocampal granule cell pathology in epilepsy - a possible structural basis for comorbidities of epilepsy?Specific disruption of Tsc1 in ovarian granulosa cells promotes ovulation and causes progressive accumulation of corpora lutea The neural crest lineage as a driver of disease heterogeneity in Tuberous Sclerosis Complex and Lymphangioleiomyomatosis.Therapeutic role of mammalian target of rapamycin (mTOR) inhibition in preventing epileptogenesis.Monoallelic germline TSC1 mutations are permissive for T lymphocyte development and homeostasis in tuberous sclerosis complex individuals.mTOR signaling in epilepsy: insights from malformations of cortical development Prolonging the survival of Tsc2 conditional knockout mice by glutamine supplementation.Postnatal neurogenesis generates heterotopias, olfactory micronodules and cortical infiltration following single-cell Tsc1 deletion.Tuberous Sclerosis: A New Frontier in Targeted Treatment of Autism Intermittent dosing of rapamycin maintains antiepileptogenic effects in a mouse model of tuberous sclerosis complex Epilepsy as a neurodevelopmental disorder.Epilepsy and autism: is there a special relationship?Graded loss of tuberin in an allelic series of brain models of TSC correlates with survival, and biochemical, histological and behavioral features.Hypoxia-inducible factor 1a is a Tsc1-regulated survival factor in newborn neurons in tuberous sclerosis complex Differential response of skeletal muscles to mTORC1 signaling during atrophy and hypertrophy.Impact of rapamycin on status epilepticus induced hippocampal pathology and weight gain.Rheb activation in subventricular zone progenitors leads to heterotopia, ectopic neuronal differentiation, and rapamycin-sensitive olfactory micronodules and dendrite hypertrophy of newborn neurons.Advances and Future Directions for Tuberous Sclerosis Complex Research: Recommendations From the 2015 Strategic Planning Conference.A magnetic resonance imaging study of cerebellar volume in tuberous sclerosis complex.The role of dopamine signaling in epileptogenesis.mTOR, a Potential Target to Treat Autism Spectrum Disorder.Mammalian target of rapamycin (mTOR) inhibition: potential for antiseizure, antiepileptogenic, and epileptostatic therapy.A critical review of mTOR inhibitors and epilepsy: from basic science to clinical trials.Mammalian target of rapamycin (mTOR) pathways in neurological diseases.Fetal brain mTOR signaling activation in tuberous sclerosis complex.Early susceptibility for epileptiform activity in malformed cortex

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Tsc2 gene inactivation causes a more severe epilepsy phenotype than Tsc1 inactivation in a mouse model of tuberous sclerosis complex.

http://www.wikidata.org/entity/Q30497818

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2010 nî lūn-bûn

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2010 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2010 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2010年の論文

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Tsc2 gene inactivation causes ...... of tuberous sclerosis complex.

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Tsc2 gene inactivation causes ...... of tuberous sclerosis complex.

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Tsc2 gene inactivation causes ...... of tuberous sclerosis complex.

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Tsc2 gene inactivation causes ...... of tuberous sclerosis complex.

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Human Molecular Genetics

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Tsc2 gene inactivation causes ...... of tuberous sclerosis complex

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Bo Zhang

http://www.w3.org/2001/XMLSchema#string

Ling-Hui Zeng

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Michael J Gambello

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Michael Wong

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Nicholas R Rensing

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P2860

Hamartin, the product of the tuberous sclerosis 1 (TSC1) gene, interacts with tuberin and appears to be localized to cytoplasmic vesicles

Interaction between hamartin and tuberin, the TSC1 and TSC2 gene products

Mutational analysis in a cohort of 224 tuberous sclerosis patients indicates increased severity of TSC2, compared with TSC1, disease in multiple organs

Tuberous sclerosis complex-1 and -2 gene products function together to inhibit mammalian target of rapamycin (mTOR)-mediated downstream signaling

Reversal of learning deficits in a Tsc2+/- mouse model of tuberous sclerosis

Rheb GTPase is a direct target of TSC2 GAP activity and regulates mTOR signaling

TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling

Rheb is a direct target of the tuberous sclerosis tumour suppressor proteins

Molecular genetic and phenotypic analysis reveals differences between TSC1 and TSC2 associated familial and sporadic tuberous sclerosis

A mouse model of tuberous sclerosis: neuronal loss of Tsc1 causes dysplastic and ectopic neurons, reduced myelination, seizure activity, and limited survival

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445-454

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10.1093/HMG/DDQ491

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3

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20

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David H Gutmann

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2010-11-09T00:00:00Z

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47729323

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21062901

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3016907

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