Gregory Hook - Concepedia

Author

Gregory Hook

American Life Science Pharmaceuticals (United States)

Also Known As

G L Hook, Gregory Hook, Hook, Gregory

Publications

1.5K

Citations

H-Index

Concepts

All Affiliations

American Life Science Pharmaceuticals (United States)University of Montana University of California San Diego Neurotech (United States)Ralph H. Johnson VA Medical Center

About

Gregory Hook is an author at American Life Science Pharmaceuticals (United States) specializing in medicine, neuroprotection, and neurodegenerative diseases.

Top Concepts

#	Concept	H-Index	Publications	Citations
1	Medicine	7	7	594
2	Biochemistry	4	4	451
3	Natural Sciences	2	2	138
4	Health Sciences	1	1	203
5	Cell Biology	1	1	13

Gregory Hook

Publications

911

Citations

H-Index

Page 1

	Year	Citations
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 Vivian Hook, Mark S. Kindy, Gregory Hook Journal of Biological Chemistry Protein SecretionMolecular BiologyAmyloid Precursor ProteinSynaptic SignalingAlzheimer's Disease	2008	203
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 Vivian Hook, Thomas Toneff, Matthew Bogyo, Biological Chemistry	2005	168
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 Gregory Hook, Vivian Hook, Mark S. Kindy Journal of Alzheimer s Disease Neurodegenerative DiseasesAlzheimer's DiseaseBiochemistryCathepsin BReduces Brain Amyloid-β	2011	110
Genetic cathepsin B deficiency reduces β-amyloid in transgenic mice expressing human wild-type amyloid precursor protein Vivian Hook, Mark S. Kindy, Thomas Reinheckel, Biochemical and Biophysical Research Communications Neurodegenerative DiseasesDisease MechanismGeneticsImmunologyDegenerative Pathology	2009	107
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 Gregory Hook, Jin Yu, Thomas Toneff, Journal of Alzheimer s Disease Molecular BiologyPeptide ScienceBrain Pyroglutamate Amyloid-βSynaptic SignalingAlzheimer's Disease	2014	83
Selective Neutral pH Inhibitor of Cathepsin B Designed Based on Cleavage Preferences at Cytosolic and Lysosomal pH Conditions Michael C. Yoon, Angelo Solania, Zhenze Jiang, ACS Chemical Biology Cleavage PreferencesNeutral Ph SelectivityChemical BiologyBioanalysisProteomics	2021	55
Cysteine protease inhibitors effectively reduce in vivo levels of brain β-amyloid related to Alzheimer's disease Vivian Hook, Mark S. Kindy, Gregory Hook Biological Chemistry	2007	44
Cysteine protease inhibitors reduce brain β-amyloid and β-secretase activity <i>in vivo</i> and are potential Alzheimer's disease therapeutics Gregory Hook, Vivian Hook, Mark S. Kindy Biological Chemistry	2007	39
Molecular Features of CA-074 pH-Dependent Inhibition of Cathepsin B Michael C. Yoon, Mitchell P. Christy, Von V. Phan, Biochemistry	2022	39
Cathepsin B inhibition blocks neurite outgrowth in cultured neurons by regulating lysosomal trafficking and remodeling Muzhou Jiang, Jie Meng, Fan Zeng, Journal of Neurochemistry	2020	27

Page 1