G. Hook

发表

Molecular Features of CA-074 pH-Dependent Inhibition of Cathepsin B.

W. Gerwick, Anthony J. O’Donoghue, Vivian V. H. Hook, 2022, Biochemistry.

Selective Neutral pH Inhibitor of Cathepsin B Designed Based on Cleavage Preferences at Cytosolic and Lysosomal pH Conditions.

D. Wolan, W. Gerwick, Anthony J. O’Donoghue, 2021, ACS chemical biology.

Genetic cathepsin B deficiency reduces beta-amyloid in transgenic mice expressing human wild-type amyloid precursor protein.

C. Peters, T. Reinheckel, M. Kindy, 2009, Biochemical and biophysical research communications.

Cysteine protease inhibitors effectively reduce in vivo levels of brain β-amyloid related to Alzheimer's disease

M. Kindy, G. Hook, V. Hook, 2007, Biological chemistry.

Cathepsin B Gene Knockout Improves Behavioral Deficits and Reduces Pathology in Models of Neurologic Disorders

C. Peters, T. Reinheckel, Vivian V. H. Hook, 2022, Pharmacological Reviews.

Cathepsin B inhibition blocks neurite outgrowth in cultured neurons by regulating lysosomal trafficking and remodeling

H. Qing, Vivian V. H. Hook, G. Hook, 2020, Journal of neurochemistry.

Penetrating Traumatic Brain Injury Triggers Dysregulation of Cathepsin B Protein Levels Independent of Cysteine Protease Activity in Brain and Cerebral Spinal Fluid

C. Robertson, Kevin K. W. Wang, J. S. Jacobsen, 2020 .

The cysteine protease cathepsin B is a key drug target and cysteine protease inhibitors are potential therapeutics for traumatic brain injury.

M. Kindy, M. Pierschbacher, Jin Yu, 2014, Journal of neurotrauma.

Cathepsin BGeneKnockout Improves Behavioral Deficits andReduces Pathology inModels of Neurologic Disorders

C. Peters, T. Reinheckel, Vivian V. H. Hook, 2022 .

Cysteine protease inhibitors reduce brain β-amyloid and β-secretase activity in vivo and are potential Alzheimer's disease therapeutics

M. Kindy, G. Hook, V. Hook, 2007 .

Imaging of calcium and aluminum in neurofibrillary tangle-bearing neurons in parkinsonism-dementia of Guam.

R. Garruto, R. Yanagihara, G. Hook, 1984, Proceedings of the National Academy of Sciences of the United States of America.

Cathepsin B is a New Drug Target for Traumatic Brain Injury Therapeutics: Evidence for E64d as a Promising Lead Drug Candidate

M. Kindy, K. Grabstein, G. Hook, 2015, Front. Neurol..

Cysteine Cathepsins in the secretory vesicle produce active peptides: Cathepsin L generates peptide neurotransmitters and cathepsin B produces beta-amyloid of Alzheimer's disease.

M. Kindy, S. Bark, J. Wegrzyn, 2012, Biochimica et biophysica acta.

Inhibition of cathepsin B reduces β-amyloid production in regulated secretory vesicles of neuronal chromaffin cells: evidence for cathepsin B as a candidate β-secretase of Alzheimer's disease

Katalin F Medzihradszky, Vivian Hook, Matthew Bogyo, 2005, Biological chemistry.

Inhibitors of Cathepsin B Improve Memory and Reduce β-Amyloid in Transgenic Alzheimer Disease Mice Expressing the Wild-type, but Not the Swedish Mutant, β-Secretase Site of the Amyloid Precursor Protein*

M. Kindy, G. Hook, V. Hook, 2008, Journal of Biological Chemistry.

Brain pyroglutamate amyloid-β is produced by cathepsin B and is reduced by the cysteine protease inhibitor E64d, representing a potential Alzheimer's disease therapeutic.

M. Kindy, Jin Yu, G. Hook, 2014, Journal of Alzheimer's disease : JAD.

Cathepsin B in neurodegeneration of Alzheimer's disease, traumatic brain injury, and related brain disorders.

R. Rissman, Michael C Yoon, G. Hook, 2020, Biochimica et biophysica acta. Proteins and proteomics.

Alternative pathways for production of β-amyloid peptides of Alzheimer's disease

H. Demuth, I. Schechter, G. Hook, 2008, Biological chemistry.

Cysteine Proteases as beta-Secretases for Abeta Production in the Major Regulated Secretory Pathway of Neurons: Implications for Therapeutic Strategies in Alzheimer’s Disease

T. Reisine, G. Hook, V. Hook, 2005 .

Deletion of the cathepsin B gene improves memory deficits in a transgenic ALZHeimer's disease mouse model expressing AβPP containing the wild-type β-secretase site sequence.

M. Kindy, Jin Yu, Hong Zhu, 2012, Journal of Alzheimer's disease : JAD.

The cysteine protease inhibitor, E64d, reduces brain amyloid-β and improves memory deficits in Alzheimer's disease animal models by inhibiting cathepsin B, but not BACE1, β-secretase activity.

M. Kindy, G. Hook, V. Hook, 2011, Journal of Alzheimer's disease : JAD.

Cathepsin B Deficiency Improves Memory Deficits and Reduces Amyloid-β in hAβPP Mouse Models Representing the Major Sporadic Alzheimer’s Disease Condition

G. Hook, Mark Kindy, V. Hook, 2023, Journal of Alzheimer's disease : JAD.

Pharmacogenetic features of cathepsin B inhibitors that improve memory deficit and reduce β-amyloid related to Alzheimer's disease

M. Kindy, G. Hook, V. Hook, 2010, Biological chemistry.

Penetrating Traumatic Brain Injury Triggers Subacute Dysregulation of Cathepsin B Protein Levels Independently of Cysteine Protease Activity in Brain and Cerebral Spinal Fluid.

C. Robertson, Kevin K. W. Wang, G. Sarkis, 2020, Journal of neurotrauma.