Kelly H. Forest

ORCID: 0000-0003-4420-2758
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About
Contact & Profiles
Research Areas
  • Alzheimer's disease research and treatments
  • Neuroscience and Neuropharmacology Research
  • Cholinesterase and Neurodegenerative Diseases
  • Computational Drug Discovery Methods
  • Genetics and Neurodevelopmental Disorders
  • Amino Acid Enzymes and Metabolism
  • Biochemical effects in animals
  • Occupational and environmental lung diseases
  • Nicotinic Acetylcholine Receptors Study
  • Memory and Neural Mechanisms
  • S100 Proteins and Annexins
  • Advanced Glycation End Products research
  • Nuclear Receptors and Signaling

University of Hawaiʻi at Mānoa
2017-2021

Leeward Community College
2017

University of Hawaii System
2017

Human malignant mesothelioma (MM) is an aggressive cancer linked to asbestos and erionite exposure. We previously reported that High-Mobility Group Box-1 protein (HMGB1), a prototypic damage-associated molecular pattern, drives MM development sustains progression. Moreover, we demonstrated targeting HMGB1 inhibited cell growth motility in vitro, reduced tumor vivo, prolonged survival of MM-bearing mice. Ethyl pyruvate (EP), the ethyl ester pyruvic acid, has been shown be effective inhibitor...

10.18632/oncotarget.15152 article EN Oncotarget 2017-02-07

The c-Jun N-terminal kinase (JNK) signal transduction pathway is implicated in learning and memory. Here, we examined the role of JNK activation mediated by JNK-interacting protein 1 (JIP1) scaffold protein. We compared male wild-type mice with a mouse model harboring point mutation Jip1 gene that selectively blocks JIP1-mediated activation. These mutant exhibited increased NMDAR currents, NMDAR-mediated expression, lower threshold for induction hippocampal long-term potentiation. JIP1 also...

10.1523/jneurosci.1913-17.2018 article EN cc-by-nc-sa Journal of Neuroscience 2018-03-14

High levels (μM) of beta amyloid (Aβ) oligomers are known to trigger neurotoxic effects, leading synaptic impairment, behavioral deficits, and apoptotic cell death. The hydrophobic C-terminal domain Aβ, together with sequences critical for oligomer formation, is essential this neurotoxicity. However, Aβ at low (pM-nM) has been shown function as a positive neuromodulator activity resides in the hydrophilic N-terminal Aβ. An fragment (1-15/16), found cerebrospinal fluid, was also be highly...

10.1111/jnc.14257 article EN publisher-specific-oa Journal of Neurochemistry 2017-11-22

Alzheimer’s disease (AD) is the most common cause of dementia in aging population. Evidence implicates elevated soluble oligomeric Aβ as one primary triggers during prodromic phase leading to AD, effected largely via hyperphosphorylation microtubule-associated protein tau. At low, physiological levels (pM-nM), however, has been found regulate synaptic plasticity a neuromodulator. Through mutational analysis, we core hexapeptide sequence within N-terminal domain (N-Aβcore) accounting for its...

10.3389/fnmol.2021.576038 article EN cc-by Frontiers in Molecular Neuroscience 2021-04-12

Abstract Alzheimer’s disease (AD) is the most common cause of dementia in aging population. Evidence implicates elevated soluble oligomeric Aβ as one primary triggers during prodromic phase leading to AD, effected largely via hyperphosphorylation microtubule-associated protein tau. At low, physiological levels (pM-nM), however, has been found regulate synaptic plasticity a neuromodulator. Through mutational analysis, we core hexapeptide sequence within N-terminal domain (N-Aβcore) accounting...

10.1101/2020.03.17.995191 preprint EN cc-by bioRxiv (Cold Spring Harbor Laboratory) 2020-03-17
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