Muscle atrophy in transgenic mice expressing a human TSC1 transgene (Q24304304)

ALG2 alpha-1,3/1,6-mannosyltransferase

GOA release 2020-03-11

1 reference

GOA release 2020-03-11

author name string

Min Wan

1

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Xiaohui Wu

2

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Kun-Liang Guan

3

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Min Han

4

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Yuan Zhuang

5

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Tian Xu

Molecular mechanisms modulating muscle mass

6

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language of work or name

English

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publication date

16 October 2006

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published in

FEBS Letters

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volume

580

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issue

24

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page(s)

5621-7

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cites work

1 reference

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The IGF-1/PI3K/Akt pathway prevents expression of muscle atrophy-induced ubiquitin ligases by inhibiting FOXO transcription factors

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Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy

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Mediation of IGF-1-induced skeletal myotube hypertrophy by PI(3)K/Akt/mTOR and PI(3)K/Akt/GSK3 pathways.

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Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo

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Dwarfism, impaired skin development, skeletal muscle atrophy, delayed bone development, and impeded adipogenesis in mice lacking Akt1 and Akt2.

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Drosophila Tsc1 functions with Tsc2 to antagonize insulin signaling in regulating cell growth, cell proliferation, and organ size

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Akt regulates growth by directly phosphorylating Tsc2

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TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling

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Identification of the tuberous sclerosis complex-2 tumor suppressor gene product tuberin as a target of the phosphoinositide 3-kinase/akt pathway

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Germ-line mutational analysis of the TSC2 gene in 90 tuberous-sclerosis patients

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

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Insulin activation of Rheb, a mediator of mTOR/S6K/4E-BP signaling, is inhibited by TSC1 and 2

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

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

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The tuberous sclerosis-1 (TSC1) gene product hamartin suppresses cell growth and augments the expression of the TSC2 product tuberin by inhibiting its ubiquitination

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Tuberin phosphorylation regulates its interaction with hamartin. Two proteins involved in tuberous sclerosis

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TSC2 mediates cellular energy response to control cell growth and survival

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Tsc tumour suppressor proteins antagonize amino-acid-TOR signalling

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Hyperinnervation of neuromuscular junctions caused by GDNF overexpression in muscle

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A protein kinase B-dependent and rapamycin-sensitive pathway controls skeletal muscle growth but not fiber type specification

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Functional inactivation of the IGF-I and insulin receptors in skeletal muscle causes type 2 diabetes

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Dystrophin expression in the mdx mouse after localised and systemic administration of a morpholino antisense oligonucleotide

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Tsc2 is not a critical target of Akt during normal Drosophila development

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TSC1 and TSC2 tumor suppressors antagonize insulin signaling in cell growth

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gigas, a Drosophila homolog of tuberous sclerosis gene product-2, regulates the cell cycle

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A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance

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inferred from DOI database lookup

7 January 2021

based on heuristic

E-box sites and a proximal regulatory region of the muscle creatine kinase gene differentially regulate expression in diverse skeletal muscles and cardiac muscle of transgenic mice

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inferred from DOI database lookup

7 January 2021

based on heuristic

Muscle creatine kinase sequence elements regulating skeletal and cardiac muscle expression in transgenic mice

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