Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: UMLS:C0001511 (
Adhesion
)
5,955
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Recent work indicates that treatments which block adhesion receptors prevent the stabilization of long term potentiation (LTP). The experiments reported here show that brief stimulation of hippocampal NMDA receptors, a triggering event for LTP induction, results in the extracellular proteolysis of two or more members of the Cell
Adhesion
Molecule (CAM) family. This effect is rapid, occurs at a consensus serine protease site, and is selective to NMDA receptors. It is also found in vivo after kainic acid induced
seizures
. Cleavage of adhesive connections could be an early step in the formation of new synaptic configurations.
...
PMID:Activation of NMDA receptors stimulates extracellular proteolysis of cell adhesion molecules in hippocampus. 980 35
Tuberous sclerosis complex (TSC) is a tumor suppressor gene syndrome characterized by
seizures
, mental retardation, autism, and tumors of the brain, kidney, heart, retina, and skin. TSC is caused by mutations in either TSC1 or TSC2, both of which are tumor suppressor genes. Hamartin, the protein product of TSC1, was found to interact with the ezrin-radixin-moesin family of cytoskeletal proteins and to activate the small GTPase Rho. To determine whether tuberin, the TSC2 product, can also activate Rho, we stably expressed full-length human tuberin in two cell types: MDCK cells and ELT3 cells. ELT3 cells lack endogenous tuberin expression. We found that expression of human tuberin in both MDCK and ELT3 cells was associated with an increase in the amount of Rho-GTP, but not in Rac1-GTP or cdc42-GTP. Tuberin expression increased cell adhesion in both cell types, and decreased chemotactic cell migration in ELT3 cells. In MDCK cells, there was a decrease in the amount of total Focal
Adhesion
Kinase (FAK) and an increase in the fraction of phosphorylated FAK. These findings demonstrate for the first time that tuberin activates Rho and regulates cell adhesion and migration. Pathways involving Rho activation may have relevance to the clinical manifestations of TSC, including pulmonary lymphangioleiomyomatosis.
...
PMID:Tuberin, the tuberous sclerosis complex 2 tumor suppressor gene product, regulates Rho activation, cell adhesion and migration. 1246 66