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In 1968 Shirley Chisholm became the first Black woman elected to the United States Congress. In 1972 she launched a campaign for the Democratic presidential nomination, breaking another political barrier.
MORE →Reflects the personal views, recollections, and perspective of the author, Mike Davis.
This is a personal recollection on the Move fire on May 13, 1985
Tuberous sclerosis complex 2 (TSC2), also known as tuberin, is a protein that in humans is encoded by the TSC2 gene.
Mutations in this gene lead to tuberous sclerosis. Its gene product is believed to be a tumor suppressor and is able to stimulate specific GTPases. Hamartin coded by the gene TSC1 functions as a facilitator of Hsp90 in chaperoning of tuberin, therefore preventing its ubiquitination and degradation in the proteasome.[5] Alternative splicing results in multiple transcript variants encoding different isoforms of the protein.[6] Mutations in TSC2 can cause lymphangioleiomyomatosis, a disease caused by the enlargement of tissue in the lungs, creating cysts and tumours and causing difficulty breathing. Because tuberin regulates cell size, along with the protein hamartin, mutations to TSC1 and TSC2 genes may prevent the control of cell growth in the lungs of individuals.[5]
Cells from individuals with pathogenic mutations in the TSC2 gene display depletion of lysosomes, impairment of autophagy, and abnormal accumulation of glycogen. Defects in the autophagy-lysosome pathway are associated with excessive ubiquitination and degradation of LC3 and LAMP1/2 proteins.[7]
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.[7]
TSC2 functions within a multi-protein complex known as the TSC complex which consists of the core proteins TSC2, TSC1,[9][10] and TBC1D7.
TSC2 has been reported to interact with several other proteins that are not a part of the TSC complex including:
Source: Wikipedia. Article content is retrieved live through the MediaWiki API.
Tuberous sclerosis complex 2 (TSC2), also known as tuberin, is a protein that in humans is encoded by the TSC2 gene.
Tuberous sclerosis complex (TSC) is a rare, multi-system genetic disorder that causes the growth of benign tumors in various organs, including the brain, kidneys, heart, liver, eyes, lungs, and skin. Symptoms may include seizures, intellectual disability, and developmental delay. TSC has autosomal dominant inheritance, meaning a child with TSC either has one affected parent (about 1/3 of cases) or a spontaneous (de novo) mutation (about 2/3 of cases). It is caused by a mutation of either of two genes, TSC1 and TSC2, which code for the proteins hamartin and tuberin, respectively. TSC2 mutations are more frequent and have usually more severe symptoms. These proteins act as tumor growth suppressors, regulating cell proliferation and differentiation. Without them, tumors are more likely to appear. Life for individuals with TSC varies depending on the severity of the symptoms, but most patients have normal life expectancy through routine medical care. The prevalence of the disease is estimated to be 7 to 12 in 100,000. The disease is often abbreviated to tuberous sclerosis, which refers to the hard swellings in the brains of patients, first described by French neurologist Désiré-Magloire Bourneville in 1880.
Angiomyolipomas are the most common benign tumour of the kidney. Although regarded as benign, angiomyolipomas may grow such that kidney function is impaired or the blood vessels may dilate and burst, leading to bleeding. Angiomyolipomas are strongly associated with the genetic disease tuberous sclerosis, in which most individuals have several angiomyolipomas affecting both kidneys. They are also commonly found in women with the rare lung disease lymphangioleiomyomatosis. Angiomyolipomas are less commonly found in the liver and rarely in other organs. Whether associated with these diseases or sporadic, angiomyolipomas are caused by mutations in either the TSC1 or TSC2 genes, which govern cell growth and proliferation. They are composed of blood vessels, smooth muscle cells, and fat cells. Large angiomyolipomas can be treated with embolisation. Drug therapy for angiomyolipomas is at the research stage. The Tuberous Sclerosis Alliance has published guidelines on diagnosis, surveillance, and management.
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. A combination of symptoms may include seizures, developmental delay, behavioural problems and skin abnormalities, as well as lung and kidney disease. TSC is caused by mutations on either of two genes, TSC1 and TSC2, which encode for the proteins hamartin and tuberin respectively. These proteins act as tumour growth suppressors and regulate cell proliferation and differentiation. Originally regarded as a rare pathological curiosity, it is now an important focus of research into tumour formation and suppression. The history of TSC research is commonly divided into four periods. In the late 19th century, notable physicians working in European teaching hospitals first described the cortical and dermatological manifestations; these early researchers have been awarded with eponyms such as "Bourneville's disease" and "Pringle's adenoma sebaceum". At the start of the 20th century, these symptoms were recognised as belonging to a single medical condition. Further organ involvement was discovered, along with a realisation that the condition was highly variable in its severity. The late 20th century saw great improvements in cranial imaging techniques and the discovery of the two genes. Finally, the start of the 21st century saw the beginning of a molecular understanding of the illness, along with possible non-surgical therapeutic treatments.
Before the 1921 destruction of Tulsa’s Greenwood District, Black residents had created a remarkable center of business and community life. The district included stores, professional offices, entertainment venues and homes owned by Black citizens. Understanding Greenwood means learning what was built—not only what was burned.
MORE →Shirley Chisholm, elected in 1968.
