Citation: Jt. Yabe et al., REGULATION OF NEUROFILAMENT AXONAL-TRANSPORT BY PHOSPHORYLATION IN OPTIC AXONS IN-SITU - INVOLVEMENT OF THE MICROTUBULE MOTOR PROTEIN KINESIN, Molecular biology of the cell, 9, 1998, pp. 924-924
Citation: Fj. Ekinci et Tb. Shea, CALCIUM INFLUX FOLLOWING BETA-AMYLOID EXPOSURE IS MEDIATED BY MITOGEN-ACTIVATED PROTEIN (MAP) KINASE, Molecular biology of the cell, 9, 1998, pp. 2804-2804
Citation: Cl. Tupper et Tb. Shea, TRANSFORMING-GROWTH-FACTOR BETA-2 CAN EXERT PROTECTION TOWARDS AND EXACERBATION OF BETA-AMYLOID TOXICITY DEPENDING UPON GROWTH-FACTOR CONCENTRATION AND LENGTH OF EXPOSURE, Neuroscience research communications, 22(2), 1998, pp. 83-89
Citation: Tb. Shea et M. Didier, BIPHASIC EFFECTS OF PHOSPHATASE INHIBITION ON ACCUMULATION OF TAU-PHOSPHO-ISOFORMS IN CULTURED CEREBELLAR NEURONS, Neuroscience research communications, 22(1), 1998, pp. 39-44
Citation: Tb. Shea et al., BETA-AMYLOID INDUCED HYPERPHOSPHORYLATION OF TAU IN HUMAN NEUROBLASTOMA-CELLS INVOLVES MAP KINASE, Neuroscience research communications, 22(1), 1998, pp. 45-49
Citation: Jj. Boyce et Tb. Shea, DIVERGENT INFLUENCES OF PROTEIN-KINASE-C ISOFORMS ON INTRACELLULAR LEVELS OF PHOSPHORYLATED AND NONPHOSPHORYLATED TAU-IMMUNOREACTIVITY, Neuroscience research communications, 22(1), 1998, pp. 51-57
Citation: Mj. Surprenant et Tb. Shea, INDUCTION OF MORPHOLOGICAL-DIFFERENTIATION OF NEUROBLASTOMA-CELLS BY A MITOTIC INHIBITOR - NEURITOGENESIS IS A DEFAULT PATHWAY INVOKED BY DEVELOPMENTAL WITHDRAWAL OF NEUROBLASTS FROM THE MITOTIC-CYCLE, Neuroscience research communications, 22(1), 1998, pp. 59-62
Citation: C. Jung et al., NEUROFILAMENT SUBUNITS CAN UNDERGO AXONAL-TRANSPORT WITHOUT INCORPORATION INTO TRITON-INSOLUBLE STRUCTURES, Cell motility and the cytoskeleton, 40(1), 1998, pp. 44-58
Citation: Tb. Shea et Cm. Cressman, A 26-30 KDA DEVELOPMENTALLY-REGULATED TAU-ISOFORM LOCALIZED WITHIN NUCLEI OF MITOTIC HUMAN NEUROBLASTOMA-CELLS, International journal of developmental neuroscience, 16(1), 1998, pp. 41-48
Citation: Tb. Shea et al., REGIONAL DECLINE IN NEUROFILAMENT AXONAL-TRANSPORT IS MEDIATED BY NEUROFILAMENT PHOSPHORYLATION AND RESULTANT DISSOCIATION FROM A KINESIN-BASED TRANSPORT-SYSTEM - POTENTIAL RELATIONSHIP WITH AMYOTROPHIC-LATERAL-SCLEROSIS, Annals of neurology, 44(3), 1998, pp. 80-80
Citation: C. Jung et Tb. Shea, REGIONAL DECLINE IN NEUROFILAMENT AXONAL-TRANSPORT - CORRELATION WITHNF-H PHOSPHORYLATION, Molecular biology of the cell, 8, 1997, pp. 1619-1619
Citation: J. Yabe et al., NONUNIFORM DISTRIBUTION OF SOLUBLE AND INSOLUBLE NEUROFILAMENT IMMUNOREACTIVITY IN GROWING AXONS, Molecular biology of the cell, 8, 1997, pp. 1621-1621
Citation: Tb. Shea et al., ALUMINUM INHIBITS NEUROFILAMENT ASSEMBLY, CYTOSKELETAL INCORPORATION,AND AXONAL-TRANSPORT - DYNAMIC NATURE OF ALUMINUM-INDUCED PERIKARYAL NEUROFILAMENT ACCUMULATIONS AS REVEALED BY SUBUNIT TURNOVER, Molecular and chemical neuropathology, 32(1-3), 1997, pp. 17-39
Citation: S. Pundreddy et Tb. Shea, AD-LIKE TAU-PHOSPHORYLATION IN HUMAN NEUROBLASTOMA-CELLS FOLLOWING PKC HYPERACTIVATION IS MEDIATED BY MAP KINASE, Neuroscience research communications, 21(3), 1997, pp. 173-177
Citation: Tb. Shea et I. Fischer, PHOSPHORYLATION OF HIGH-MOLECULAR-WEIGHT-TAU WITHIN NEUROBLASTOMA ANDUNDER CELL-FREE CONDITIONS RETARDS ITS ELECTROPHORETIC MIGRATION AND GENERATES AD-LIKE IMMUNOREACTIVITY, Neuroscience research communications, 21(3), 1997, pp. 195-201
Citation: Fj. Ekinci et Tb. Shea, SELECTIVE ACTIVATION BY BRYOSTATIN-1 DEMONSTRATES UNIQUE ROLES FOR PKC-EPSILON IN NEURITE EXTENSION AND TAU-PHOSPHORYLATION, International journal of developmental neuroscience, 15(7), 1997, pp. 867-874
Citation: Jj. Boyce et Tb. Shea, PHOSPHORYLATION EVENTS MEDIATED BY PROTEIN-KINASE-C-ALPHA AND PROTEIN-KINASE-EPSILON PARTICIPATE IN REGULATION OF TAU-STEADY-STATE LEVELS AND GENERATION OF CERTAIN ALZHEIMER-LIKE PHOSPHO-EPITOPES, International journal of developmental neuroscience, 15(3), 1997, pp. 295-307
Citation: Tb. Shea, PHOSPHOLIPIDS ALTER TAU CONFORMATION, PHOSPHORYLATION, PROTEOLYSIS, AND ASSOCIATION WITH MICROTUBULES - IMPLICATION FOR TAU FUNCTION UNDER NORMAL AND DEGENERATIVE CONDITIONS, Journal of neuroscience research, 50(1), 1997, pp. 114-122
Citation: Tb. Shea et al., BETA-AMYLOID AND IONOPHORE A23187 EVOKE TAU-HYPERPHOSPHORYLATION BY DISTINCT INTRACELLULAR PATHWAYS - DIFFERENTIAL INVOLVEMENT OF THE CALPAIN PROTEIN-KINASE-C SYSTEM, Journal of neuroscience research, 49(6), 1997, pp. 759-768
Citation: Tb. Shea et al., TRITON-SOLUBLE PHOSPHOVARIANTS OF THE HEAVY NEUROFILAMENT SUBUNIT IN DEVELOPING AND MATURE MOUSE CENTRAL-NERVOUS-SYSTEM, Journal of neuroscience research, 48(6), 1997, pp. 515-523
Citation: Tb. Shea, RESTRICTION OF MU-M-CALCIUM-REQUIRING CALPAIN ACTIVATION TO THE PLASMA-MEMBRANE IN HUMAN NEUROBLASTOMA-CELLS - EVIDENCE FOR REGIONALIZED INFLUENCE OF A CALPAIN ACTIVATOR PROTEIN, Journal of neuroscience research, 48(6), 1997, pp. 543-550
Authors:
GRYNSPAN F
GRIFFIN WB
MOHAN PS
SHEA TB
NIXON RA
Citation: F. Grynspan et al., CALPAINS AND CALPASTATIN IN SH-SY5Y NEUROBLASTOMA-CELLS DURING RETINOIC ACID-INDUCED DIFFERENTIATION AND NEURITE OUTGROWTH - COMPARISON WITH THE HUMAN BRAIN CALPAIN SYSTEM, Journal of neuroscience research, 48(3), 1997, pp. 181-191
Authors:
TUPPER C
PUNDREDDY S
PRABHAKAR S
CHANG M
SHEA TB
Citation: C. Tupper et al., BETA-AMYLOID AND IONOPHORE-MEDIATED CALCIUM INFLUX EVOKE TAU-HYPERPHOSPHORYLATION BY DISTINCT AND COMMON INTRACELLULAR PATHWAYS - DIFFERENTIAL INVOLVEMENT OF THE CALPAIN PROTEIN-KINASE-C SYSTEM, Journal of neurochemistry, 69, 1997, pp. 47-47