B. Hobo

发表

Proteasome subunit proteins and neuropathology in tauopathies and synucleinopathies: Consequences for proteomic analyses

E. Hol, R. D. de Vos, M. Zouambia, 2008, Proteomics.

Expression of a Mutant SEMA3A Protein with Diminished Signalling Capacity Does Not Alter ALS-Related Motor Decline, or Confer Changes in NMJ Plasticity after BotoxA-Induced Paralysis of Male Gastrocnemic Muscle

F. de Winter, J. Verhaagen, B. Hobo, 2017, PloS one.

Portal Semaphorin 3 A in injury and disease : its role at the neuromuscular junction

J. Verhaagen, B. Hobo, E. Moloney, 2022 .

CERTL reduces C16 ceramide, amyloid-β levels, and inflammation in a model of Alzheimer’s disease

M. Mielke, H. D. de Vries, J. Walter, 2020, Alzheimer's research & therapy.

CERTL reduces C16 ceramide, amyloid-β levels, and inflammation in a model of Alzheimer’s disease

M. Mielke, H. D. de Vries, J. Walter, 2020, Alzheimer's Research & Therapy.

Characterization of an immune-evading doxycycline-inducible lentiviral vector for gene therapy in the spinal cord

J. Verhaagen, R. Eggers, B. Hobo, 2022, Experimental Neurology.

Brain Endothelial Cells Control Fertility through Ovarian-Steroid–Dependent Release of Semaphorin 3A

S. Bouret, A. Messina, M. Mazzone, 2014, PLoS biology.

Long-term proteasome dysfunction in the mouse brain by expression of aberrant ubiquitin

E. Hol, K. Li, D. Fischer, 2009, Neurobiology of Aging.

Frame‐shifted amyloid precursor protein found in Alzheimer's disease and Down's syndrome increases levels of secreted amyloid β40

E. Hol, D. Mann, D. Fischer, 2004, Journal of neurochemistry.

Accumulation of aberrant ubiquitin induces aggregate formation and cell death in polyglutamine diseases.

R. Roos, E. Hol, R. D. de Vos, 2004, Human molecular genetics.

Disease‐specific accumulation of mutant ubiquitin as a marker for proteasomal dysfunction in the brain

E. Hol, W. Kamphorst, R. Vos, 2003, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

Alzheimer-associated mutant ubiquitin impairs spatial reference memory

M. Oitzl, D. Fischer, B. Hobo, 2011, Physiology & Behavior.

Alzheimer-associated APP+1 transgenic mice: Frameshift β-amyloid precursor protein is secreted in cerebrospinal fluid without inducing neuropathology

E. Hol, D. Fischer, B. Hobo, 2006, Neurobiology of Aging.

Optimization of adeno-associated viral vector-mediated transduction of the corticospinal tract: comparison of four promoters

J. Fawcett, J. Verhaagen, B. Hobo, 2020, Gene Therapy.

Low levels of mutant ubiquitin are degraded by the proteasome in vivo

D. Fischer, B. Hobo, F. V. van Leeuwen, 2010, Journal of neuroscience research.

Modest proteasomal inhibition by aberrant ubiquitin exacerbates aggregate formation in a Huntington disease mouse model

R. Roos, D. Fischer, B. Hobo, 2010, Molecular and Cellular Neuroscience.

Mutant ubiquitin decreases amyloid β plaque formation in a transgenic mouse model of Alzheimer’s disease

H. Steinbusch, D. Fischer, B. Hobo, 2012, Neurochemistry International.

Frameshifted β-Amyloid Precursor Protein (APP+1) Is a Secretory Protein, and the Level of APP+1 in Cerebrospinal Fluid Is Linked to Alzheimer Pathology*

E. Hol, W. Kamphorst, R. Benne, 2003, Journal of Biological Chemistry.

Small Scale Production of Recombinant Adeno-Associated Viral Vectors for Gene Delivery to the Nervous System.

A. Harvey, E. Ehlert, J. Verhaagen, 2018, Methods in molecular biology.

Frameshift proteins in autosomal dominant forms of Alzheimer disease and other tauopathies

G. Leuba, E. Hol, D. Mann, 2006, Neurology.

Repulsive Guidance Molecule a (RGMa) Induces Neuropathological and Behavioral Changes That Closely Resemble Parkinson's Disease

A. Smit, D. Swaab, R. van Kesteren, 2017, The Journal of Neuroscience.

Alzheimer-associated mutant ubiquitin impairs spatial reference memory

M. Oitzl, D. Fischer, B. Hobo, 2011, Physiology & Behavior.