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Article ; Online: Accelerated brain aging with opioid misuse and HIV: New insights on the role of glially derived pro-inflammation mediators and neuronal chloride homeostasis.

Hauser, Kurt F / Ohene-Nyako, Michael / Knapp, Pamela E

2022 Volume 78, Page(s) 102653

Abstract: Opioid use disorder (OUD) has become a national crisis and contributes to the spread of human immunodeficiency virus (HIV) infection. Emerging evidence and advances in experimental models, methodology, and our understanding of disease processes at the ... ...

Abstract	Opioid use disorder (OUD) has become a national crisis and contributes to the spread of human immunodeficiency virus (HIV) infection. Emerging evidence and advances in experimental models, methodology, and our understanding of disease processes at the molecular and cellular levels reveal that opioids per se can directly exacerbate the pathophysiology of neuroHIV. Despite substantial inroads, the impact of OUD on the severity, development, and prognosis of neuroHIV and HIV-associated neurocognitive disorders is not fully understood. In this review, we explore current evidence that OUD and neuroHIV interact to accelerate cognitive deficits and enhance the neurodegenerative changes typically seen with aging, through their effects on neuroinflammation. We suggest new thoughts on the processes that may underlie accelerated brain aging, including dysregulation of neuronal inhibition, and highlight findings suggesting that opioids, through actions at the μ-opioid receptor, interact with HIV in the central nervous system to promote unique structural and functional comorbid deficits not seen in either OUD or neuroHIV alone.
MeSH term(s)	Humans ; Chlorides ; Inflammation Mediators ; Opioid-Related Disorders ; HIV Infections/complications ; Brain ; Analgesics, Opioid/pharmacology
Chemical Substances	Chlorides ; Inflammation Mediators ; Analgesics, Opioid
Language	English
Publishing date	2022-12-28
Publishing country	England
Document type	Journal Article ; Review ; Research Support, N.I.H., Extramural
ZDB-ID	1078046-4
ISSN	1873-6882 ; 0959-4388
ISSN (online)	1873-6882
ISSN	0959-4388
DOI	10.1016/j.conb.2022.102653
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Article ; Online: HIV-1 Tat and morphine interactions dynamically shift striatal monoamine levels and exploratory behaviors over time.

Lark, Arianna R S / Nass, Sara R / Hahn, Yun K / Gao, Benlian / Milne, Ginger L / Knapp, Pamela E / Hauser, Kurt F

Journal of neurochemistry

2024 Volume 168, Issue 3, Page(s) 185–204

Abstract: Despite the advent of combination anti-retroviral therapy (cART), nearly half of people infected with HIV treated with cART still exhibit HIV-associated neurocognitive disorders (HAND). HAND can be worsened by co-morbid opioid use disorder. The basal ... ...

Abstract	Despite the advent of combination anti-retroviral therapy (cART), nearly half of people infected with HIV treated with cART still exhibit HIV-associated neurocognitive disorders (HAND). HAND can be worsened by co-morbid opioid use disorder. The basal ganglia are particularly vulnerable to HIV-1 and exhibit higher viral loads and more severe pathology, which can be exacerbated by co-exposure to opioids. Evidence suggests that dopaminergic neurotransmission is disrupted by HIV exposure, however, little is known about whether co-exposure to opioids may alter neurotransmitter levels in the striatum and if this in turn influences behavior. Therefore, we assayed motor, anxiety-like, novelty-seeking, exploratory, and social behaviors, and levels of monoamines and their metabolites following 2 weeks and 2 months of Tat and/or morphine exposure in transgenic mice. Morphine decreased dopamine levels, but significantly elevated norepinephrine, the dopamine metabolites dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA), and the serotonin metabolite 5-hydroxyindoleacetic acid, which typically correlated with increased locomotor behavior. The combination of Tat and morphine altered dopamine, DOPAC, and HVA concentrations differently depending on the neurotransmitter/metabolite and duration of exposure but did not affect the numbers of tyrosine hydroxylase-positive neurons in the mesencephalon. Tat exposure increased the latency to interact with novel conspecifics, but not other novel objects, suggesting the viral protein inhibits exploratory behavior initiation in a context-dependent manner. By contrast, and consistent with prior findings that opioid misuse can increase novelty-seeking behavior, morphine exposure increased the time spent exploring a novel environment. Finally, Tat and morphine interacted to affect locomotor activity in a time-dependent manner, while grip strength and rotarod performance were unaffected. Together, our results provide novel insight into the unique effects of HIV-1 Tat and morphine on monoamine neurochemistry that may underlie their divergent effects on motor and exploratory behavior.
MeSH term(s)	Humans ; Mice ; Animals ; Morphine/pharmacology ; Exploratory Behavior ; HIV-1/metabolism ; Dopamine/metabolism ; 3,4-Dihydroxyphenylacetic Acid/metabolism ; Mice, Transgenic ; Analgesics, Opioid/pharmacology ; Homovanillic Acid ; HIV Infections ; Neurotransmitter Agents ; tat Gene Products, Human Immunodeficiency Virus/metabolism
Chemical Substances	Morphine (76I7G6D29C) ; Dopamine (VTD58H1Z2X) ; 3,4-Dihydroxyphenylacetic Acid (102-32-9) ; Analgesics, Opioid ; Homovanillic Acid (X77S6GMS36) ; Neurotransmitter Agents ; tat Gene Products, Human Immunodeficiency Virus
Language	English
Publishing date	2024-02-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.16057
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Article ; Online: Fentanyl dysregulates neuroinflammation and disrupts blood-brain barrier integrity in HIV-1 Tat transgenic mice.

Rademeyer, Kara M / R Nass, Sara / Jones, Austin M / Ohene-Nyako, Michael / Hauser, Kurt F / McRae, MaryPeace

Journal of neurovirology

2024 Volume 30, Issue 1, Page(s) 1–21

Abstract: Opioid overdose deaths have dramatically increased by 781% from 1999 to 2021. In the setting of HIV, opioid drug abuse exacerbates neurotoxic effects of HIV in the brain, as opioids enhance viral replication, promote neuronal dysfunction and injury, and ... ...

Abstract	Opioid overdose deaths have dramatically increased by 781% from 1999 to 2021. In the setting of HIV, opioid drug abuse exacerbates neurotoxic effects of HIV in the brain, as opioids enhance viral replication, promote neuronal dysfunction and injury, and dysregulate an already compromised inflammatory response. Despite the rise in fentanyl abuse and the close association between opioid abuse and HIV infection, the interactive comorbidity between fentanyl abuse and HIV has yet to be examined in vivo. The HIV-1 Tat-transgenic mouse model was used to understand the interactive effects between fentanyl and HIV. Tat is an essential protein produced during HIV that drives the transcription of new virions and exerts neurotoxic effects within the brain. The Tat-transgenic mouse model uses a glial fibrillary acidic protein (GFAP)-driven tetracycline promoter which limits Tat production to the brain and this model is well used for examining mechanisms related to neuroHIV. After 7 days of fentanyl exposure, brains were harvested. Tight junction proteins, the vascular cell adhesion molecule, and platelet-derived growth factor receptor-β were measured to examine the integrity of the blood brain barrier. The immune response was assessed using a mouse-specific multiplex chemokine assay. For the first time in vivo, we demonstrate that fentanyl by itself can severely disrupt the blood-brain barrier and dysregulate the immune response. In addition, we reveal associations between inflammatory markers and tight junction proteins at the blood-brain barrier.
MeSH term(s)	Animals ; Blood-Brain Barrier/drug effects ; Blood-Brain Barrier/metabolism ; Blood-Brain Barrier/pathology ; Blood-Brain Barrier/virology ; Mice, Transgenic ; Mice ; Fentanyl/pharmacology ; HIV-1/drug effects ; HIV-1/genetics ; tat Gene Products, Human Immunodeficiency Virus/genetics ; tat Gene Products, Human Immunodeficiency Virus/metabolism ; Neuroinflammatory Diseases/genetics ; Neuroinflammatory Diseases/pathology ; Neuroinflammatory Diseases/virology ; HIV Infections/virology ; HIV Infections/genetics ; HIV Infections/pathology ; HIV Infections/drug therapy ; Disease Models, Animal ; Analgesics, Opioid/pharmacology ; Analgesics, Opioid/adverse effects ; Glial Fibrillary Acidic Protein/genetics ; Glial Fibrillary Acidic Protein/metabolism ; Tight Junction Proteins/metabolism ; Tight Junction Proteins/genetics ; Humans ; Brain/drug effects ; Brain/virology ; Brain/metabolism ; Brain/pathology ; Opioid-Related Disorders/genetics ; Opioid-Related Disorders/pathology ; Opioid-Related Disorders/metabolism
Chemical Substances	Fentanyl (UF599785JZ) ; tat Gene Products, Human Immunodeficiency Virus ; Analgesics, Opioid ; Glial Fibrillary Acidic Protein ; Tight Junction Proteins
Language	English
Publishing date	2024-01-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1283265-0
ISSN	1538-2443 ; 1355-0284
ISSN (online)	1538-2443
ISSN	1355-0284
DOI	10.1007/s13365-023-01186-4
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Zs.A 4426: Show issues

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Article: Opiate Drugs with Abuse Liability Hijack the Endogenous Opioid System to Disrupt Neuronal and Glial Maturation in the Central Nervous System.

Hauser, Kurt F / Knapp, Pamela E

Frontiers in pediatrics

2018 Volume 5, Page(s) 294

Abstract: The endogenous opioid system, comprised of multiple opioid neuropeptide and receptor gene families, is highly expressed by developing neural cells and can significantly influence neuronal and glial maturation. In many central nervous system (CNS) regions, ...

Abstract	The endogenous opioid system, comprised of multiple opioid neuropeptide and receptor gene families, is highly expressed by developing neural cells and can significantly influence neuronal and glial maturation. In many central nervous system (CNS) regions, the expression of opioid peptides and receptors occurs only transiently during development, effectively disappearing with subsequent maturation only to reemerge under pathologic conditions, such as with inflammation or injury. Opiate drugs with abuse liability act to modify growth and development by mimicking the actions of endogenous opioids. Although typically mediated by μ-opioid receptors, opiate drugs can also act through δ- and κ-opioid receptors to modulate growth in a cell-type, region-specific, and developmentally regulated manner. Opioids act as biological response modifiers and their actions are highly contextual, plastic, modifiable, and influenced by other physiological processes or pathophysiological conditions, such as neuro-acquired immunodeficiency syndrome. To date, most studies have considered the acute effects of opiates on cellular maturation. For example, activating opioid receptors typically results in acute growth inhibition in both neurons and glia. However, with sustained opioid exposure, compensatory factors become operative, a concept that has been largely overlooked during CNS maturation. Accordingly, this article surveys prior studies on the effects of opiates on CNS maturation, and also suggests new directions for future research in this area. Identifying the cellular and molecular mechanisms underlying the adaptive responses to chronic opiate exposure (e.g., tolerance) during maturation is crucial toward understanding the consequences of perinatal opiate exposure on the CNS.
Language	English
Publishing date	2018-01-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2711999-3
ISSN	2296-2360
ISSN	2296-2360
DOI	10.3389/fped.2017.00294
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Article ; Online: Opioid and neuroHIV Comorbidity - Current and Future Perspectives.

Fitting, Sylvia / McRae, MaryPeace / Hauser, Kurt F

Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology

2020 Volume 15, Issue 4, Page(s) 584–627

Abstract: With the current national opioid crisis, it is critical to examine the mechanisms underlying pathophysiologic interactions between human immunodeficiency virus (HIV) and opioids in the central nervous system (CNS). Recent advances in experimental models, ...

Abstract	With the current national opioid crisis, it is critical to examine the mechanisms underlying pathophysiologic interactions between human immunodeficiency virus (HIV) and opioids in the central nervous system (CNS). Recent advances in experimental models, methodology, and our understanding of disease processes at the molecular and cellular levels reveal opioid-HIV interactions with increasing clarity. However, despite the substantial new insight, the unique impact of opioids on the severity, progression, and prognosis of neuroHIV and HIV-associated neurocognitive disorders (HAND) are not fully understood. In this review, we explore, in detail, what is currently known about mechanisms underlying opioid interactions with HIV, with emphasis on individual HIV-1-expressed gene products at the molecular, cellular and systems levels. Furthermore, we review preclinical and clinical studies with a focus on key considerations when addressing questions of whether opioid-HIV interactive pathogenesis results in unique structural or functional deficits not seen with either disease alone. These considerations include, understanding the combined consequences of HIV-1 genetic variants, host variants, and μ-opioid receptor (MOR) and HIV chemokine co-receptor interactions on the comorbidity. Lastly, we present topics that need to be considered in the future to better understand the unique contributions of opioids to the pathophysiology of neuroHIV. Graphical Abstract Blood-brain barrier and the neurovascular unit. With HIV and opiate co-exposure (represented below the dotted line), there is breakdown of tight junction proteins and increased leakage of paracellular compounds into the brain. Despite this, opiate exposure selectively increases the expression of some efflux transporters, thereby restricting brain penetration of specific drugs.
MeSH term(s)	AIDS Dementia Complex/complications ; COVID-19 ; HIV Infections/complications ; HIV-1/immunology ; Humans ; Opioid Epidemic ; Opioid-Related Disorders/epidemiology
Keywords	covid19
Language	English
Publishing date	2020-09-02
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2227405-4
ISSN	1557-1904 ; 1557-1890
ISSN (online)	1557-1904
ISSN	1557-1890
DOI	10.1007/s11481-020-09941-8
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Article: Neurodegeneration Within the Amygdala Is Differentially Induced by Opioid and HIV-1 Tat Exposure.

Nass, Sara R / Ohene-Nyako, Michael / Hahn, Yun K / Knapp, Pamela E / Hauser, Kurt F

Frontiers in neuroscience

2022 Volume 16, Page(s) 804774

Abstract: Opioid use disorder (OUD) is a critical problem that contributes to the spread of HIV and may intrinsically worsen neuroHIV. Despite the advent of combined antiretroviral therapies (cART), about half of persons infected with HIV (PWH) experience ... ...

Abstract	Opioid use disorder (OUD) is a critical problem that contributes to the spread of HIV and may intrinsically worsen neuroHIV. Despite the advent of combined antiretroviral therapies (cART), about half of persons infected with HIV (PWH) experience cognitive and emotional deficits that can be exacerbated by opioid abuse. HIV-1 Tat is expressed in the central nervous system (CNS) of PWH on cART and is thought to contribute to neuroHIV. The amygdala regulates emotion and memories associated with fear and stress and is important in addiction behavior. Notwithstanding its importance in emotional saliency, the effects of HIV and opioids in the amygdala are underexplored. To assess Tat- and morphine-induced neuropathology within the amygdala, male Tat transgenic mice were exposed to Tat for 8 weeks and administered saline and/or escalating doses of morphine twice daily (s.c.) during the last 2 weeks of Tat exposure. Eight weeks of Tat exposure decreased the acoustic startle response and the dendritic spine density in the basolateral amygdala, but not the central nucleus of the amygdala. In contrast, repeated exposure to morphine alone, but not Tat, increased the acoustic startle response and whole amygdalar levels of amyloid-β (Aβ) monomers and oligomers and tau phosphorylation at Ser396, but not neurofilament light chain levels. Co-exposure to Tat and morphine decreased habituation and prepulse inhibition to the acoustic startle response and potentiated the morphine-induced increase in Aβ monomers. Together, our findings indicate that sustained Tat and morphine exposure differentially promote synaptodendritic degeneration within the amygdala and alter sensorimotor processing.
Language	English
Publishing date	2022-05-04
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2411902-7
ISSN	1662-453X ; 1662-4548
ISSN (online)	1662-453X
ISSN	1662-4548
DOI	10.3389/fnins.2022.804774
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Article ; Online: HIV-1 Tat reduces apical dendritic spine density throughout the trisynaptic pathway in the hippocampus of male transgenic mice.

McLane, Virginia D / Lark, Arianna R S / Nass, Sara R / Knapp, Pamela E / Hauser, Kurt F

Neuroscience letters

2022 Volume 782, Page(s) 136688

Abstract: Nearly one-third of persons infected with HIV-1 (PWH) develop HIV-associated neurocognitive disorders (HAND), which can be exacerbated by exposure to opioids. The impact of opioids on HIV-induced alterations in neuronal plasticity is less well understood. ...

Abstract	Nearly one-third of persons infected with HIV-1 (PWH) develop HIV-associated neurocognitive disorders (HAND), which can be exacerbated by exposure to opioids. The impact of opioids on HIV-induced alterations in neuronal plasticity is less well understood. Both morphine exposure and HIV have been shown to disrupt synaptic growth and stability in the hippocampus suggesting a potential site of convergence for their deleterious effects. In the present study, we examined the density of dendritic spines in CA1 and CA3 pyramidal neurons, and granule neurons within the dentate gyrus representing the hippocampal trisynaptic pathway after short-term exposure to the HIV transactivator of transcription (Tat) protein and morphine. We exposed inducible male, HIV-1 Tat transgenic mice to escalating doses of morphine (10-40 mg/kg, b.i.d.) and examined synaptodendritic structure in Golgi-impregnated hippocampal neurons. HIV-1 Tat, but not morphine, systematically reduced the density of apical, but not basilar, dendrites of CA1 and CA3 pyramidal neurons, and granule neuronal apical dendrites, suggesting the coordinated loss of specific synaptic interconnections throughout the hippocampal trisynaptic pathway.
MeSH term(s)	Analgesics, Opioid/pharmacology ; Animals ; Dendrites/metabolism ; Dendritic Spines ; HIV-1 ; Hippocampus ; Male ; Mice ; Mice, Transgenic ; Morphine/metabolism ; Morphine/pharmacology
Chemical Substances	Analgesics, Opioid ; Morphine (76I7G6D29C)
Language	English
Publishing date	2022-05-17
Publishing country	Ireland
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	194929-9
ISSN	1872-7972 ; 0304-3940
ISSN (online)	1872-7972
ISSN	0304-3940
DOI	10.1016/j.neulet.2022.136688
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Zs.A 1166: Show issues

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Article ; Online: Myelin regulatory factor is a target of individual and interactive effects of HIV-1 Tat and morphine in the striatum and pre-frontal cortex.

Flounlacker, Kelly M / Hahn, Yun Kyung / Xu, Ruqiang / Simons, Chloe A / Tian, Tao / Hauser, Kurt F / Knapp, Pamela E

Journal of neurovirology

2023 Volume 29, Issue 1, Page(s) 15–26

Abstract: HIV-associated neurocognitive disorders (HAND) remain pervasive even with increased efficacy/use of antiretroviral therapies. Opioid use/abuse among HIV + individuals is documented to exacerbate CNS deficits. White matter (WM) alterations, including ... ...

Abstract	HIV-associated neurocognitive disorders (HAND) remain pervasive even with increased efficacy/use of antiretroviral therapies. Opioid use/abuse among HIV + individuals is documented to exacerbate CNS deficits. White matter (WM) alterations, including myelin pallor, and volume/structural alterations detected by diffusion tensor imaging are common observations in HIV + individuals, and studies in non-human primates suggest that WM may harbor virus. Using transgenic mice that express the HIV-1 Tat protein, we examined in vivo effects of 2-6 weeks of Tat and morphine exposure on WM using genomic and biochemical methods. RNA sequencing of striatal tissue at 2 weeks revealed robust changes in mRNAs associated with oligodendrocyte precursor populations and myelin integrity, including those for transferrin, the atypical oligodendrocyte marker N-myc downstream regulated 1 (Ndrg1), and myelin regulatory factor (Myrf/Mrf), an oligodendrocyte-specific transcription factor with a significant role in oligodendrocyte differentiation/maturation. Western blots conducted after 6-weeks exposure in 3 brain regions (striatum, corpus callosum, pre-frontal cortex) revealed regional differences in the effect of Tat and morphine on Myrf levels, and on levels of myelin basic protein (MBP), whose transcription is regulated by Myrf. Responses included individual and interactive effects. Although baseline and post-treatment levels of Myrf and MBP differed between brain regions, post-treatment MBP levels in striatum and pre-frontal cortex were compatible with changes in Myrf activity. Additionally, the Myrf regulatory ubiquitin ligase Fbxw7 was identified as a novel target in our model. These results suggest that Myrf and Fbxw7 contribute to altered myelin gene regulation in HIV.
MeSH term(s)	Animals ; Mice ; Diffusion Tensor Imaging ; F-Box-WD Repeat-Containing Protein 7/metabolism ; Frontal Lobe/metabolism ; HIV Infections ; HIV-1/metabolism ; Mice, Transgenic ; Morphine ; Transcription Factors/genetics ; tat Gene Products, Human Immunodeficiency Virus/metabolism
Chemical Substances	F-Box-WD Repeat-Containing Protein 7 ; Morphine (76I7G6D29C) ; Transcription Factors ; tat Gene Products, Human Immunodeficiency Virus
Language	English
Publishing date	2023-02-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	1283265-0
ISSN	1538-2443 ; 1355-0284
ISSN (online)	1538-2443
ISSN	1355-0284
DOI	10.1007/s13365-022-01107-x
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Zs.A 4426: Show issues

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Article ; Online: Restoration of KCC2 Membrane Localization in Striatal Dopamine D2 Receptor-Expressing Medium Spiny Neurons Rescues Locomotor Deficits in HIV Tat-Transgenic Mice.

Barbour, Aaron J / Nass, Sara R / Hahn, Yun K / Hauser, Kurt F / Knapp, Pamela E

ASN neuro

2021 Volume 13, Page(s) 17590914211022089

Abstract: People infected with HIV (PWH) are highly susceptible to striatal and hippocampal damage. Motor and memory impairments are common among these patients, likely as behavioral manifestations of damage to these brain regions. GABAergic dysfunction from HIV ... ...

Abstract	People infected with HIV (PWH) are highly susceptible to striatal and hippocampal damage. Motor and memory impairments are common among these patients, likely as behavioral manifestations of damage to these brain regions. GABAergic dysfunction from HIV infection and viral proteins such as transactivator of transcription (Tat) have been well documented. We recently demonstrated that the neuron specific Cl
MeSH term(s)	Animals ; Corpus Striatum/metabolism ; HIV Infections ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Neurons/metabolism ; Receptors, Dopamine D1/genetics ; Receptors, Dopamine D1/metabolism ; Receptors, Dopamine D2/genetics ; Receptors, Dopamine D2/metabolism ; Symporters/genetics ; Symporters/metabolism ; Trans-Activators ; tat Gene Products, Human Immunodeficiency Virus ; K Cl- Cotransporters
Chemical Substances	DRD2 protein, mouse ; Receptors, Dopamine D1 ; Receptors, Dopamine D2 ; Symporters ; Trans-Activators ; tat Gene Products, Human Immunodeficiency Virus
Language	English
Publishing date	2021-08-18
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2485467-0
ISSN	1759-0914 ; 1759-0914
ISSN (online)	1759-0914
ISSN	1759-0914
DOI	10.1177/17590914211022089
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Article ; Online: Casein Kinase 2 Mediates HIV- and Opioid-Induced Pathologic Phosphorylation of TAR DNA Binding Protein 43 in the Basal Ganglia.

Ohene-Nyako, Michael / Nass, Sara R / Richard, Hope T / Lukande, Robert / Nicol, Melanie R / McRae, MaryPeace / Knapp, Pamela E / Hauser, Kurt F

ASN neuro

2023 Volume 15, Page(s) 17590914231158218

Abstract: Summary statement: HIV/HIV-1 Tat and morphine independently increase pathologic phosphorylation of TAR DNA binding protein 43 in the striatum. HIV- and opioid-induced pathologic phosphorylation of TAR DNA binding protein 43 may involve enhanced CK2 ... ...

Abstract	Summary statement: HIV/HIV-1 Tat and morphine independently increase pathologic phosphorylation of TAR DNA binding protein 43 in the striatum. HIV- and opioid-induced pathologic phosphorylation of TAR DNA binding protein 43 may involve enhanced CK2 activity and protein levels.
MeSH term(s)	Humans ; Phosphorylation ; Casein Kinase II/metabolism ; Analgesics, Opioid/pharmacology ; Analgesics, Opioid/metabolism ; tat Gene Products, Human Immunodeficiency Virus/metabolism ; DNA-Binding Proteins ; HIV-1/metabolism ; Basal Ganglia/metabolism ; HIV Infections ; Protein Binding
Chemical Substances	Casein Kinase II (EC 2.7.11.1) ; Analgesics, Opioid ; tat Gene Products, Human Immunodeficiency Virus ; DNA-Binding Proteins
Language	English
Publishing date	2023-03-08
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2485467-0
ISSN	1759-0914 ; 1759-0914
ISSN (online)	1759-0914
ISSN	1759-0914
DOI	10.1177/17590914231158218
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