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The Impact of Selenium Deficiency on Cardiovascular Function

International journal of molecular sciences, 2021-10, Vol.22 (19), p.10713

2021

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From Selenium Absorption to Selenoprotein Degradation

Biological trace element research, 2019-11, Vol.192 (1), p.26-37

2019

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From Selenium Absorption to Selenoprotein Degradation

Biological trace element research, 2019-11, Vol.192 (1), p.26-37

2019

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Stress and the Brain: An Emerging Role for Selenium

Frontiers in neuroscience, 2021-04, Vol.15, p.666601-666601

2021

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Cannabinoids, the Heart of the Matter

Journal of the American Heart Association, 2018-07, Vol.7 (14)

2018

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TRPV1 is a component of the atrial natriuretic signaling complex, and using orally delivered antagonists, presents a valid therapeutic target in the longitudinal reversal and treatment of cardiac hypertrophy and heart failure

Channels (Austin, Tex.), 2019-01, Vol.13 (1), p.1-16

2019

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High-fat, Selenium Deficient Diet Reduces Glutathione Peroxidase in the Hearts of Selenocysteine Lyase Knockout Mice

Free radical biology & medicine, 2023-11, Vol.208, p.S95-S96

2023

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New insights on selenoproteins and neuronal function

Free radical biology & medicine, 2022-09, Vol.190, p.55-61

2022

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Thyroid Hormone Status in Mice Lacking Selenium Recycling

Current developments in nutrition, 2024-07, Vol.8, p.103721, Article 103721

2024

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P31-053-23 Selenium Deficiency and Loss of Selenocysteine Lyase Activity Exacerbates Diet-Induced Obesity in Female Mice

Current developments in nutrition, 2023-07, Vol.7, p.101618, Article 101618

2023

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Regulation of presynaptic Ca2+, synaptic plasticity and contextual fear conditioning by a N-terminal β-amyloid fragment

The Journal of neuroscience, 2014-10, Vol.34 (43), p.14210-14218

2014

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Effect of statin treatment in obese selenium-supplemented mice lacking selenocysteine lyase

Molecular and cellular endocrinology, 2021-08, Vol.533, p.111335-111335, Article 111335

2021

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JIP1-Mediated JNK Activation Negatively Regulates Synaptic Plasticity and Spatial Memory

The Journal of neuroscience, 2018-04, Vol.38 (15), p.3708-3728

2018

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Protection against β‐amyloid neurotoxicity by a non‐toxic endogenous N‐terminal β‐amyloid fragment and its active hexapeptide core sequence

Journal of neurochemistry, 2018-01, Vol.144 (2), p.201-217

2018

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Pursuing the Molecular Nexus Connecting Diabetes and the Associated Cognitive Impairments

The Journal of neuroscience, 2019-10, Vol.39 (44), p.8614-8616

2019

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Impact of Sustained Exposure to β-Amyloid on Calcium Homeostasis and Neuronal Integrity in Model Nerve Cell System Expressing α4β2 Nicotinic Acetylcholine Receptors

The Journal of biological chemistry, 2013-04, Vol.288 (16), p.11175-11190

2013

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Neuroprotective Potential of the N-Terminal Beta Amyloid Peptide Fragment in the Neurodegeneration, Synaptic Dysfunction and Memory Deficits in Models of Alzheimer's Disease

Alfulaij, Naghum

2017

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ProQuest

Protection against [beta]-amyloid neurotoxicity by a non-toxic endogenous N-terminal [beta]-amyloid fragment and its active hexapeptide core sequence

Journal of neurochemistry, 2018-01, Vol.144 (2), p.201

2018

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P4‐004: The presence of beta‐amyloid 1‐42 nicotinic acetylcholine receptors in an in vitro presynaptic model causes dysregulated calcium signaling, mitochondrial dysfunction and altered ERK signaling on sustained exposure to beta‐amyloid

Alzheimer's & dementia, 2012-07, Vol.8 (4S_Part_17), p.P639-P639

2012

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The presence of beta-amyloid 1-42 nicotinic acetylcholine receptors in an in vitro presynaptic model causes dysregulated calcium signaling, mitochondrial dysfunction and altered ERK signaling on sustained exposure to beta-amyloid

Alzheimer's & dementia, 2012-07, Vol.8 (4), p.P639-P639

2012

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Regulation of Presynaptic Ca super(2+), Synaptic Plasticity and Contextual Fear Conditioning by a N-terminal beta -Amyloid Fragment

The Journal of neuroscience, 2014-10, Vol.34 (43), p.14210-14218

2014

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The Impact of Selenium Deficiency on Cardiovascular Function

From Selenium Absorption to Selenoprotein Degradation

From Selenium Absorption to Selenoprotein Degradation

Stress and the Brain: An Emerging Role for Selenium

Cannabinoids, the Heart of the Matter

TRPV1 is a component of the atrial natriuretic signaling complex, and using orally delivered antagonists, presents a valid therapeutic target in the longitudinal reversal and treatment of cardiac hypertrophy and heart failure

High-fat, Selenium Deficient Diet Reduces Glutathione Peroxidase in the Hearts of Selenocysteine Lyase Knockout Mice

New insights on selenoproteins and neuronal function

Thyroid Hormone Status in Mice Lacking Selenium Recycling

P31-053-23 Selenium Deficiency and Loss of Selenocysteine Lyase Activity Exacerbates Diet-Induced Obesity in Female Mice

Regulation of presynaptic Ca2+, synaptic plasticity and contextual fear conditioning by a N-terminal β-amyloid fragment

Effect of statin treatment in obese selenium-supplemented mice lacking selenocysteine lyase

JIP1-Mediated JNK Activation Negatively Regulates Synaptic Plasticity and Spatial Memory

Protection against β‐amyloid neurotoxicity by a non‐toxic endogenous N‐terminal β‐amyloid fragment and its active hexapeptide core sequence

Pursuing the Molecular Nexus Connecting Diabetes and the Associated Cognitive Impairments

Impact of Sustained Exposure to β-Amyloid on Calcium Homeostasis and Neuronal Integrity in Model Nerve Cell System Expressing α4β2 Nicotinic Acetylcholine Receptors

Neuroprotective Potential of the N-Terminal Beta Amyloid Peptide Fragment in the Neurodegeneration, Synaptic Dysfunction and Memory Deficits in Models of Alzheimer's Disease

Protection against [beta]-amyloid neurotoxicity by a non-toxic endogenous N-terminal [beta]-amyloid fragment and its active hexapeptide core sequence

P4‐004: The presence of beta‐amyloid 1‐42 nicotinic acetylcholine receptors in an in vitro presynaptic model causes dysregulated calcium signaling, mitochondrial dysfunction and altered ERK signaling on sustained exposure to beta‐amyloid

The presence of beta-amyloid 1-42 nicotinic acetylcholine receptors in an in vitro presynaptic model causes dysregulated calcium signaling, mitochondrial dysfunction and altered ERK signaling on sustained exposure to beta-amyloid

Regulation of Presynaptic Ca super(2+), Synaptic Plasticity and Contextual Fear Conditioning by a N-terminal beta -Amyloid Fragment

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