ABSTRACT
BACKGROUND: Bcl-2 family proteins play a central role in regulating apoptosis. In human, over 20 members of this family have been identified to date. Bfl-1, a member of the Bcl-2 family, has been known to retard apoptosis in various cell lines. However, the function of Bfl-1 remains unclear. METHODS: In order to investigate the Bfl-1 function, we employed yeast two-hybrid system to identify the proteins which are capable of interacting with Bfl-1. The interaction of inhibitor kappaB kinase-beta (IKK-beta) and Bfl-1 was confirmed using glutathione S-transferase pull down assays. To determine which regions of IKK-beta were required for interaction with Bfl-1, we constructed 12 deletion mutants of IKK-beta and 5 deletion mutants of Bfl-1. RESULTS: Bfl-1 interacted with the C-terminal region of IKK-beta which is a subunit of IKK complex, and IKK-beta activity is very important in the NF-kappaB related pathway. In addition, the amino acids 673-745 of IKK-beta were important for Bfl-1 interactions, and amino acids 1-484 of Bfl-1, including Bcl-2 homology domains (BH1, BH2, BH3, BH4), were crucial for IKK-beta interactions. CONCLUSIONS: IKK beta C-terminus contains many serine residues as binding partner of Bfl-1. Our results suggested that Bfl-1 is involved in the NF-kappaB activation through interaction of IKK-beta and Bfl-1. Further studies need to be performed to understand functions of the IKK-beta and Bfl-1 associated with the regulation of the NF-kappaB activation pathway.
Subject(s)
Humans , Amino Acids , Apoptosis , Cell Line , Glutathione Transferase , I-kappa B Kinase , NF-kappa B , Serine , Two-Hybrid System TechniquesABSTRACT
BACKGROUND AND OBJECTIVES: Congenital long QT syndrome (LQTS) is a genetic disease that brings prolongation of the QT interval on an electrocardiogram and leads to syncope and sudden death by a fatal ventricular arrhythmia. In Korea, there have been studies about the clinical characteristics and treatment of LQTS, but there are no studies for the molecular and biological evaluation of its genetic mutation. SUBJECTS AND METHODS: Six nationwide university hospitals and laboratories segregated DNA from the blood of 10 patients diagnosed with LQTS to analyze the genetic mutation. RESULTS: Nine out of ten individuals were female. Eight showed genetic mutations. Three had an abnormality in the KvLQT1, 6 in the HERG and 2 had abnormalities in both KvLQT1 and HERG. None had abnormalities in KCNE1 and 2 showed no abnormalities in KvLQT1, HERG or KCNE1. CONCLUSION: Congenital LQTS shows various genetic mutations, and this indicates the necessity for further organized study in more individuals for confirmation of the relationship between the results of clinical diagnosis and genetic analysis.
Subject(s)
Female , Humans , Arrhythmias, Cardiac , Death, Sudden , Diagnosis , DNA , Electrocardiography , Hospitals, University , Korea , Long QT Syndrome , SyncopeABSTRACT
No abstract available.
Subject(s)
Animals , Rats , Clone Cells , Cloning, Organism , DNA, Complementary , Leptin , Receptors, LeptinABSTRACT
To maintain an adequate airway in a patient with tracheobronchial narrowing coming from various causes, prosthetic tracheobronchial stents provide palliative treatment for narrowed airways where surgical resection is inadvisable. After insertion, precious reported complications were granuloma formation, dysphagia, suction catheter entrapment and fatal massive hemoptysis. We report a case of complication associated with expandible metallic scent with endobronchial stenosis due to tuberculosis.