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Shagreen patches are present in about half of people with TSC, appearing in childhood. [11] They are areas of thick leathery skin that are dimpled like an orange peel, and pigmented, they are usually found on the lower back or nape of the neck, or scattered across the trunk or thighs.
TSC is a rare genetic disease causing benign tumours to grow in the brain and on other vital organs. A combination of symptoms may include seizures, developmental delay, behavioural problems, skin abnormalities, lung and kidney disease.
In 2004, FTC Dam Neck was reorganized and renamed Training Support Center Hampton Roads, to align it with the U.S. Navy's "Revolution In Training". The actual training activity is the Center for Surface Combat Systems, which is headquartered in Dahlgren, Virginia. TSC Hampton Roads supports the training mission, as its name suggests.
Poliosis circumscripta, commonly referred to as a "white forelock", is a condition characterized by localized patches of white hair due to a reduction or absence of melanin in hair follicles. Although traditionally associated with the scalp, poliosis can affect any hairy area on the body, including eyebrows, eyelashes, and beards.
The history of tuberous sclerosis (TSC) research spans less than 200 years. TSC is a rare, multi-system genetic disease that can cause benign tumours to grow on the brain or other vital organs such as the kidneys , heart , eyes , lungs , and skin .
TSC1, TSC2 and TBC1D7 is a multi-protein complex also known as the TSC complex. This complex negatively regulates mTORC1 signaling by functioning as a GTPase-activating protein (GAP) for the small GTPase Rheb, an essential activator of mTORC1. The TSC complex has been implicated as a tumor suppressor.
Subependymal giant cell astrocytoma (SEGA, SGCA, or SGCT) is a low-grade astrocytic brain tumor (astrocytoma) that arises within the ventricles of the brain. [1] It is most commonly associated with tuberous sclerosis complex (TSC).
Pharmacological inhibition of ERK1/2 restores GSK3β activity and protein synthesis levels in a model of tuberous sclerosis. [8]The defective degradation of glycogen by the autophagy-lysosome pathway is, at least in part, independent of impaired regulation of mTORC1 and is restored by the combined use of PKB/Akt and mTORC1 pharmacological inhibitors.