Soluble multimeric Alzheimer beta(1-40) pre-amyloid complexes in dilute solution.

Desensitization of the neurokinin 1 receptor is mediated by the receptor carboxy-terminal region, but is not caused by receptor internalization.

Desensitization of the neurokinin 1 receptor is mediated by the receptor carboxy-terminal region, but is not caused by receptor internalization.

[Anonymous].  1996.  Desensitization of the neurokinin 1 receptor is mediated by the receptor carboxy-terminal region, but is not caused by receptor internalization.. Journal of neurochemistry. 67(6):2362-72.

Stopped-flow kinetics reveal multiple phases of thioflavin T binding to Alzheimer beta (1-40) amyloid fibrils.

The solution structure and dynamics of the pleckstrin homology domain of G protein-coupled receptor kinase 2 (beta-adrenergic receptor kinase 1). A binding partner of Gbetagamma subunits.

The solution structure and dynamics of the pleckstrin homology domain of G protein-coupled receptor kinase 2 (beta-adrenergic receptor kinase 1). A binding partner of Gbetagamma subunits.

[Anonymous].  1998.  The solution structure and dynamics of the pleckstrin homology domain of G protein-coupled receptor kinase 2 (beta-adrenergic receptor kinase 1). A binding partner of Gbetagamma subunits.. The Journal of biological chemistry. 273(5):2835-43.

Structural features of heterotrimeric G-protein-coupled receptors and their modulatory proteins.

Quantification of beta-sheet amyloid fibril structures with thioflavin T.

Screening for pharmacologic inhibitors of amyloid fibril formation.

125I-labeled ApoE binds competitively to beta(1-40) fibrils with pathological chaperone proteins.

125I-labeled ApoE binds competitively to beta(1-40) fibrils with pathological chaperone proteins.

[Anonymous].  2000.  125I-labeled ApoE binds competitively to beta(1-40) fibrils with pathological chaperone proteins.. Amyloid : the international journal of experimental and clinical investigation : the official journal of the International Society of Amyloidosis. 7(2):83-9.

The cerebral proteopathies.

Proteopathy: the next therapeutic frontier?