Tsc2(+/-) mice develop tumors in multiple sites that express gelsolin and are influenced by genetic background - Wikidata - wikimedia - TriplyDB

Tsc2(+/-) mice develop tumors in multiple sites that express gelsolin and are influenced by genetic background

Tsc2(+/-) mice develop tumors in multiple sites that express gelsolin and are influenced by genetic background

http://www.wikidata.org/entity/Q28507548

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The p38 and MK2 kinase cascade phosphorylates tuberin, the tuberous sclerosis 2 gene product, and enhances its interaction with 14-3-3 The TSC1 tumor suppressor hamartin interacts with neurofilament-L and possibly functions as a novel integrator of the neuronal cytoskeleton Regulation of TSC2 by 14-3-3 binding Signaling by target of rapamycin proteins in cell growth control The tuberous sclerosis complex Reversal of learning deficits in a Tsc2+/- mouse model of tuberous sclerosis Role of FIP200 in cardiac and liver development and its regulation of TNFalpha and TSC-mTOR signaling pathways A novel anesthesia regime enables neurofunctional studies and imaging genetics across mouse strains Mourning Dr. Alfred G. Knudson: the two-hit hypothesis, tumor suppressor genes, and the tuberous sclerosis complex Cell size regulation by the human TSC tumor suppressor proteins depends on PI3K and FKBP38 Pam and its ortholog highwire interact with and may negatively regulate the TSC1.TSC2 complex mTOR signaling in tumorigenesis Association of focal adhesion kinase with tuberous sclerosis complex 2 in the regulation of s6 kinase activation and cell growth Differential cellular expression of neurotrophins in cortical tubers of the tuberous sclerosis complex Brain-expressed X-linked 2 Is Pivotal for Hyperactive Mechanistic Target of Rapamycin (mTOR)-mediated Tumorigenesis Therapeutic trial of metformin and bortezomib in a mouse model of tuberous sclerosis complex (TSC)Feedback inhibition of Akt signaling limits the growth of tumors lacking Tsc2 A germ-line Tsc1 mutation causes tumor development and embryonic lethality that are similar, but not identical to, those caused by Tsc2 mutation in mice Genetic analysis of Pten and Tsc2 functional interactions in the mouse reveals asymmetrical haploinsufficiency in tumor suppression Tuberous sclerosis complex tumor suppressor-mediated S6 kinase inhibition by phosphatidylinositide-3-OH kinase is mTOR independent Target of rapamycin (TOR): an integrator of nutrient and growth factor signals and coordinator of cell growth and cell cycle progression Uterine-specific loss of Tsc2 leads to myometrial tumors in both the uterus and lungs.Both maternal and pup genotype influence ultrasonic vocalizations and early developmental milestones in tsc2 (+/-) mice.Altered ultrasonic vocalizations in a tuberous sclerosis mouse model of autism Rapamycin reverses impaired social interaction in mouse models of tuberous sclerosis complex.mTOR regulates tau phosphorylation and degradation: implications for Alzheimer's disease and other tauopathies.Survey of somatic mutations in tuberous sclerosis complex (TSC) hamartomas suggests different genetic mechanisms for pathogenesis of TSC lesions Selective alterations in glutamate and GABA receptor subunit mRNA expression in dysplastic neurons and giant cells of cortical tubers.Use of serial analysis of gene expression to generate kidney expression libraries.Mouse models of human familial cancer syndromes.Tuberous sclerosis preclinical studies: timing of treatment, combination of a rapamycin analog (CCI-779) and interferon-gamma, and comparison of rapamycin to CCI-779 Rapamycin weekly maintenance dosing and the potential efficacy of combination sorafenib plus rapamycin but not atorvastatin or doxycycline in tuberous sclerosis preclinical models Tsc/mTORC1 signaling in oocytes governs the quiescence and activation of primordial follicles Comparison of three rapamycin dosing schedules in A/J Tsc2+/- mice and improved survival with angiogenesis inhibitor or asparaginase treatment in mice with subcutaneous tuberous sclerosis related tumors Genetic control of renal tumorigenesis by the mouse Rtm1 locus.From mTOR to cognition: molecular and cellular mechanisms of cognitive impairments in tuberous sclerosis.Persistent mTORC1 signaling in cell senescence results from defects in amino acid and growth factor sensing.Lymphangioleiomyomatosis and TSC2-/- cells Animal models of lymphangioleiomyomatosis (LAM) and tuberous sclerosis complex (TSC).Gestational immune activation and Tsc2 haploinsufficiency cooperate to disrupt fetal survival and may perturb social behavior in adult mice.

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Tsc2(+/-) mice develop tumors in multiple sites that express gelsolin and are influenced by genetic background

http://www.wikidata.org/entity/Q28507548

description

1999 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

1999 թվականի սեպտեմբերին հրատարակված գիտական հոդված

@hy

artículu científicu espublizáu en 1999

@ast

im September 1999 veröffentlichter wissenschaftlicher Artikel

@de

scientific journal article

@en

vedecký článok (publikovaný 1999/09/01)

@sk

vědecký článek publikovaný v roce 1999

@cs

wetenschappelijk artikel (gepubliceerd op 1999/09/01)

@nl

наукова стаття, опублікована у вересні 1999

@uk

مقالة علمية (نشرت في سبتمبر 1999)

@ar

name

Tsc2(+/-) mice develop tumors ...... fluenced by genetic background

@ast

Tsc2(+/-) mice develop tumors ...... fluenced by genetic background

@en

Tsc2(+/-) mice develop tumors ...... fluenced by genetic background

@nl

type

label

Tsc2(+/-) mice develop tumors ...... fluenced by genetic background

@ast

Tsc2(+/-) mice develop tumors ...... fluenced by genetic background

@en

Tsc2(+/-) mice develop tumors ...... fluenced by genetic background

@nl

prefLabel

Tsc2(+/-) mice develop tumors ...... fluenced by genetic background

@ast

Tsc2(+/-) mice develop tumors ...... fluenced by genetic background

@en

Tsc2(+/-) mice develop tumors ...... fluenced by genetic background

@nl

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P1433

Journal of Clinical Investigation

P1476

Tsc2(+/-) mice develop tumors ...... fluenced by genetic background

@en

P2093

A. Lueck

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

D. J. Kwiatkowski

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H. B. Warren

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

H. Onda

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

P. W. Marks

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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

The tuberous sclerosis 2 gene product, tuberin, functions as a Rab5 GTPase activating protein (GAP) in modulating endocytosis

Comprehensive mutation analysis of TSC1 and TSC2-and phenotypic correlations in 150 families with tuberous sclerosis.

Predisposition to renal carcinoma in the Eker rat is determined by germ-line mutation of the tuberous sclerosis 2 (TSC2) gene

Identification of the tuberous sclerosis gene TSC1 on chromosome 9q34

Identification and characterization of the tuberous sclerosis gene on chromosome 16

Comprehensive mutational analysis of the TSC1 gene: observations on frequency of mutation, associated features, and nonpenetrance

Hemostatic, inflammatory, and fibroblast responses are blunted in mice lacking gelsolin

Renal carcinogenesis, hepatic hemangiomatosis, and embryonic lethality caused by a germ-line Tsc2 mutation in mice

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687–695

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scholarly article

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1331235

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10.1172/JCI7319

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6

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104

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1999-09-01T00:00:00Z

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12809622

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10491404

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408440

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