Results 121 to 130 of about 23,999 (238)
Transient repression of TSC2 expression in the ISC lineage.
A. TSC2 is highly expressed in GFP−, Dl+ ISCs (arrowheads) of 5966GS>GFP flies. Confocal images detecting TSC2 (red, Tritc channel, right panels) and Dl (red, Cy5 channel, left panels) were acquired using sequential scanning to separate Cy5 and TRITC ...
DaeSung Hwangbo (121326) +4 more
core +1 more source
Targeting EZH2 in Cancer: From Molecular Mechanisms to Clinical Translation
The abnormal overexpression or gain‐of‐function mutations of EZH2 play a significant role in cancer occurrence and progression, highlighting the importance and potential of EZH2 as a cancer biomarker. Therefore, screening for effective and safe small‐molecule inhibitors, degraders, and natural compounds targeting EZH2 through preclinical cancer models ...
Xi Zhong +4 more
wiley +1 more source
TSC2 Modulates Actin Cytoskeleton and Focal Adhesion Through TSC1-Binding Domain and the Rac1 GTPase
Tuberous sclerosis complex (TSC) 1 and TSC2 are thought to be involved in protein translational regulation and cell growth, and loss of their function is a cause of TSC and lymphangioleiomyomatosis (LAM).
Goncharov, Dmitry +7 more
core +1 more source
Focal postnatal deletion of Tsc2 causes epilepsy
Introduction Tuberous sclerosis complex (TSC) is a genetic disorder caused by mutations in either the TSC1 or TSC2 genes. These mutations prevent the TSC1/TSC2 protein complex from forming, resulting in
McCoy, Carlie +9 more
openaire +3 more sources
The role of TSC1 and TSC2 proteins in neuronal axons
Tuberous Sclerosis Complex 1 and 2 proteins, TSC1 and TSC2 respectively, participate in a multiprotein complex with a crucial role for the proper development and function of the nervous system. This complex primarily acts as an inhibitor of the mechanistic target of rapamycin (mTOR) kinase, and mutations in either TSC1 or TSC2 cause a ...
Vasiliki Karalis +3 more
openaire +2 more sources
ABSTRACT The high prevalence of gastrointestinal (GI) diseases and their significant impact on the quality of life require new therapeutic strategies. The development of novel therapeutic strategies should prioritize targeting the fundamental pathophysiological mechanisms underlying these diseases, including inflammation, cellular proliferation, and ...
Sayedeh Azimeh Hosseini +7 more
wiley +1 more source
Aging impairs vaccine efficacy through gut microbiota dysbiosis and mTOR hyperactivation, which together drive inflammaging and weaken immune memory. This review highlights the bidirectional microbiota–mTOR axis and proposes that combining mTOR inhibitors with microbiota modulation offers a promising strategy to enhance vaccine responses in older ...
Jiaxuan Li +5 more
wiley +1 more source
Senescent myoblasts exhibit dysregulated Akt/mTORC1 signalling. Antioxidants can alleviate this dysregulation, as well as other downstream senescent phenotypes. Moreover, prolonged antioxidant treatment can selectively induce cell death in senescent myoblasts, suggesting that these cells are more susceptible to reductive stress.
Vladimir Belhac +13 more
wiley +1 more source
TSC1 and TSC2 differentially regulate migration and invasiveness.
A: Representative membrane showing migration of serum-deprived Tsc2+/+, Tsc2−/−, Tsc1+/+, and Tsc1−/− MEFs. Serum-deprived cells were placed on collagen-saturated membranes in serum-free medium, and allowed to migrate in the Boyden chamber for 4 h in the
Melane L. James (652653) +4 more
core +1 more source
TSC2 negatively regulates AdPLA2 expression in rapamycin-insensitive manner in vitro.
(A) Immunoblotting analysis of AdPLA2 and tuberin in TSC2-deficient (TSC2−) and TSCS2-addback (TSC2+) LAM patient-derived cells. Data show the mean of three sets of independent samples. Densitometry analysis of the protein levels of AdPLA2.
Po-Shun Lee (358563) +10 more
core +1 more source

