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Full-Text Articles in Life Sciences
A Pdz-Interacting Domain In Cftr Is An Apical Membrane Polarization Signal, Bryan D. Moyer, Jerod Denton, Katherine H. Karlson, Donna Reynolds, Shusheng Wang, John E. Mickle, Michael Milewski, Garry R. Cutting, William B. Guggino, Min Li, Bruce A. Stanton
A Pdz-Interacting Domain In Cftr Is An Apical Membrane Polarization Signal, Bryan D. Moyer, Jerod Denton, Katherine H. Karlson, Donna Reynolds, Shusheng Wang, John E. Mickle, Michael Milewski, Garry R. Cutting, William B. Guggino, Min Li, Bruce A. Stanton
Dartmouth Scholarship
Polarization of the cystic fibrosis transmembrane conductance regulator (CFTR), a cAMP-activated chloride channel, to the apical plasma membrane of epithelial cells is critical for vectorial transport of chloride in a variety of epithelia, including the airway, pancreas, intestine, and kidney. However, the motifs that localize CFTR to the apical membrane are unknown. We report that the last 3 amino acids in the COOH-terminus of CFTR (T-R-L) comprise a PDZ-interacting domain that is required for the polarization of CFTR to the apical plasma membrane in human airway and kidney epithelial cells. In addition, the CFTR mutant, S1455X, which lacks the 26 …
Dynactin Is Required For Microtubule Anchoring At Centrosomes, N J. Quintyne, S. R. Gill, D M. Eckley, C L. Crego, D A. Compton, T A. Schroer
Dynactin Is Required For Microtubule Anchoring At Centrosomes, N J. Quintyne, S. R. Gill, D M. Eckley, C L. Crego, D A. Compton, T A. Schroer
Dartmouth Scholarship
The multiprotein complex, dynactin, is an integral part of the cytoplasmic dynein motor and is required for dynein-based motility in vitro and in vivo. In living cells, perturbation of the dynein–dynactin interaction profoundly blocks mitotic spindle assembly, and inhibition or depletion of dynein or dynactin from meiotic or mitotic cell extracts prevents microtubules from focusing into spindles. In interphase cells, perturbation of the dynein–dynactin complex is correlated with an inhibition of ER-to-Golgi movement and reorganization of the Golgi apparatus and the endosome–lysosome system, but the effects on microtubule organization have not previously been defined. To explore this question, we overexpressed …
Mechanisms Of Immunotherapeutic Intervention By Anti-Cd40l (Cd154) Antibody In An Animal Model Of Multiple Sclerosis, Laurence M. Howard, Amy J. Miga, Carol L. Vanderlugt, Mauro C. Dal Canto, John D. Laman, Randolph J. Noelle, Stephen D. Miller
Mechanisms Of Immunotherapeutic Intervention By Anti-Cd40l (Cd154) Antibody In An Animal Model Of Multiple Sclerosis, Laurence M. Howard, Amy J. Miga, Carol L. Vanderlugt, Mauro C. Dal Canto, John D. Laman, Randolph J. Noelle, Stephen D. Miller
Dartmouth Scholarship
Relapsing experimental autoimmune encephalomyelitis (R-EAE) in the SJL mouse is a Th1-mediated autoimmune demyelinating disease model for human multiple sclerosis and is characterized by infiltration of the central nervous system (CNS) by Th1 cells and macrophages. Disease relapses are mediated by T cells specific for endogenous myelin epitopes released during acute disease, reflecting a critical role for epitope spreading in the perpetuation of chronic central CNS pathology. We asked whether blockade of the CD40–CD154 (CD40L) costimulatory pathway could suppress relapses in mice with established R-EAE. Anti-CD154 antibody treatment at either the peak of acute disease or during remission effectively blocked …