Bag1-L is a phosphorylation-dependent coactivator of c-Jun during neuronal apoptosis.

In the nervous system, cell death by apoptosis plays a critical role during normal development and pathological neurodegeneration. Jun N-terminal kinases (JNKs) are essential regulators of neuronal apoptosis. The AP-1 transcription factor c-Jun is phosphorylated at multiple sites within its transactivation domain by the JNKs, and c-Jun phosphorylation is required for JNK-induced neurotoxicity.

A functional site on the human TSH receptor: a potential therapeutic target in Graves' disease.

Objective: Identifying sites on the TSH-receptor that are involved in the pathological stimulation of the thyroid by autoantibodies in Graves' disease would aid the development of new therapies. We tested a series of monoclonal antibodies that recognize the native receptor for their ability to inhibit stimulation of the receptor in vitro.

Patients And Methods: Heterologous cells expressing the recombinant human TSH-receptor were stimulated with TSH or serum samples from 13 Graves' disease patients or the MRC Long-Acting Thyroid Stimulator standard B (LATS-B) and their cAMP responses measured.

Modulation of Graves' disease autoantibody stimulation of recombinant human thyrotrophin receptor.

Background: The cAMP response of porcine thyrocytes to the immunoglobulin (Ig) fraction from Graves' sera is increased if these fractions are prepared with higher than usual concentrations of polyethylene glycol (PEG; 22.5% rather than 13.5%), leading to the suggestion that additional factors might exist in serum which influence the ability of autoantibodies to stimulate thyroid cells.