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Article: Gadd45 in Neuronal Development, Function, and Injury.

Sultan, Faraz A / Sawaya, Bassel E

Advances in experimental medicine and biology

2022 Volume 1360, Page(s) 117–148

Abstract: The growth arrest and DNA damage-inducible (Gadd) 45 proteins have been associated with numerous cellular mechanisms including cell cycle control, DNA damage sensation and repair, genotoxic stress, neoplasia, and molecular epigenetics. The genes were ... ...

Abstract	The growth arrest and DNA damage-inducible (Gadd) 45 proteins have been associated with numerous cellular mechanisms including cell cycle control, DNA damage sensation and repair, genotoxic stress, neoplasia, and molecular epigenetics. The genes were originally identified in in vitro screens of irradiation- and interleukin-induced transcription and have since been implicated in a host of normal and aberrant central nervous system processes. These include early and postnatal development, injury, cancer, memory, aging, and neurodegenerative and psychiatric disease states. The proteins act through a variety of molecular signaling cascades including the MAPK cascade, cell cycle control mechanisms, histone regulation, and epigenetic DNA demethylation. In this review, we provide a comprehensive discussion of the literature implicating each of the three members of the Gadd45 family in these processes.
MeSH term(s)	Cell Cycle Checkpoints ; Cell Cycle Proteins/metabolism ; Epigenesis, Genetic ; Neurogenesis/genetics ; Nuclear Proteins/metabolism
Chemical Substances	Cell Cycle Proteins ; Nuclear Proteins
Language	English
Publishing date	2022-05-03
Publishing country	United States
Document type	Journal Article ; Review
ISSN	2214-8019 ; 0065-2598
ISSN (online)	2214-8019
ISSN	0065-2598
DOI	10.1007/978-3-030-94804-7_9
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis.

Allen, Charles N S / Arjona, Sterling P / Santerre, Maryline / Sawaya, Bassel E

Viruses

2022 Volume 14, Issue 3

Abstract: Metabolic reprogramming is a hallmark of cancer and has proven to be critical in viral infections. Metabolic reprogramming provides the cell with energy and biomass for large-scale biosynthesis. Based on studies of the cellular changes that contribute to ...

Abstract	Metabolic reprogramming is a hallmark of cancer and has proven to be critical in viral infections. Metabolic reprogramming provides the cell with energy and biomass for large-scale biosynthesis. Based on studies of the cellular changes that contribute to metabolic reprogramming, seven main hallmarks can be identified: (1) increased glycolysis and lactic acid, (2) increased glutaminolysis, (3) increased pentose phosphate pathway, (4) mitochondrial changes, (5) increased lipid metabolism, (6) changes in amino acid metabolism, and (7) changes in other biosynthetic and bioenergetic pathways. Viruses depend on metabolic reprogramming to increase biomass to fuel viral genome replication and production of new virions. Viruses take advantage of the non-metabolic effects of metabolic reprogramming, creating an anti-apoptotic environment and evading the immune system. Other non-metabolic effects can negatively affect cellular function. Understanding the role metabolic reprogramming plays in viral pathogenesis may provide better therapeutic targets for antivirals.
MeSH term(s)	Energy Metabolism ; Glycolysis ; Humans ; Mitochondria/metabolism ; Neoplasms/metabolism ; Virus Replication ; Viruses/genetics
Language	English
Publishing date	2022-03-14
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14030602
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Article: Hallmarks of Metabolic Reprogramming and Their Role in Viral Pathogenesis

Allen, Charles N. S. / Arjona, Sterling P. / Santerre, Maryline / Sawaya, Bassel E.

Viruses. 2022 Mar. 14, v. 14, no. 3

2022

Abstract	Metabolic reprogramming is a hallmark of cancer and has proven to be critical in viral infections. Metabolic reprogramming provides the cell with energy and biomass for large-scale biosynthesis. Based on studies of the cellular changes that contribute to metabolic reprogramming, seven main hallmarks can be identified: (1) increased glycolysis and lactic acid, (2) increased glutaminolysis, (3) increased pentose phosphate pathway, (4) mitochondrial changes, (5) increased lipid metabolism, (6) changes in amino acid metabolism, and (7) changes in other biosynthetic and bioenergetic pathways. Viruses depend on metabolic reprogramming to increase biomass to fuel viral genome replication and production of new virions. Viruses take advantage of the non-metabolic effects of metabolic reprogramming, creating an anti-apoptotic environment and evading the immune system. Other non-metabolic effects can negatively affect cellular function. Understanding the role metabolic reprogramming plays in viral pathogenesis may provide better therapeutic targets for antivirals.
Keywords	amino acid metabolism ; antiviral agents ; biomass ; biosynthesis ; energy ; glycolysis ; immune system ; lactic acid ; lipid metabolism ; mitochondria ; pathogenesis ; pentose phosphate cycle ; therapeutics ; viral genome
Language	English
Dates of publication	2022-0314
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2516098-9
ISSN	1999-4915
ISSN	1999-4915
DOI	10.3390/v14030602
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Article ; Online: HIV-1 Vpr protein impairs lysosome clearance causing SNCA/alpha-synuclein accumulation in neurons.

Santerre, Maryline / Arjona, Sterling P / Allen, Charles Ns / Callen, Shannon / Buch, Shilpa / Sawaya, Bassel E

Autophagy

2021 Volume 17, Issue 7, Page(s) 1768–1782

Abstract: Despite the promising therapeutic effects of combinatory antiretroviral therapy (cART), 20% to 30% of HIV/AIDS patients living with long term infection still exhibit related cognitive and motor disorders. Clinical studies in HIV-infected patients ... ...

Abstract	Despite the promising therapeutic effects of combinatory antiretroviral therapy (cART), 20% to 30% of HIV/AIDS patients living with long term infection still exhibit related cognitive and motor disorders. Clinical studies in HIV-infected patients revealed evidence of basal ganglia dysfunction, tremors, fine motor movement deficits, gait, balance, and increased risk of falls. Among older HIV
MeSH term(s)	AIDS Dementia Complex/etiology ; AIDS Dementia Complex/metabolism ; AIDS Dementia Complex/pathology ; Animals ; Autophagosomes/virology ; Blotting, Western ; Brain/pathology ; Brain/virology ; Fluorescent Antibody Technique ; HIV-1 ; Humans ; Lysosomes/physiology ; Lysosomes/virology ; Macaca mulatta ; Mice ; Mice, Inbred C57BL ; Microscopy, Electron, Transmission ; Neurons/metabolism ; Neurons/physiology ; Neurons/virology ; alpha-Synuclein/metabolism ; vpr Gene Products, Human Immunodeficiency Virus/metabolism
Chemical Substances	SNCA protein, human ; alpha-Synuclein ; vpr Gene Products, Human Immunodeficiency Virus ; vpr protein, Human immunodeficiency virus 1
Language	English
Publishing date	2021-04-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2021.1915641
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Article ; Online: SARS-CoV-2 Causes Lung Inflammation through Metabolic Reprogramming and RAGE.

Allen, Charles N S / Santerre, Maryline / Arjona, Sterling P / Ghaleb, Lea J / Herzi, Muna / Llewellyn, Megan D / Shcherbik, Natalia / Sawaya, Bassel E

Viruses

2022 Volume 14, Issue 5

Abstract: Clinical studies indicate that patients infected with SARS-CoV-2 develop hyperinflammation, which correlates with increased mortality. The SARS-CoV-2/COVID-19-dependent inflammation is thought to occur via increased cytokine production and hyperactivity ... ...

Abstract	Clinical studies indicate that patients infected with SARS-CoV-2 develop hyperinflammation, which correlates with increased mortality. The SARS-CoV-2/COVID-19-dependent inflammation is thought to occur via increased cytokine production and hyperactivity of RAGE in several cell types, a phenomenon observed for other disorders and diseases. Metabolic reprogramming has been shown to contribute to inflammation and is considered a hallmark of cancer, neurodegenerative diseases, and viral infections. Malfunctioning glycolysis, which normally aims to convert glucose into pyruvate, leads to the accumulation of advanced glycation end products (AGEs). Being aberrantly generated, AGEs then bind to their receptor, RAGE, and activate several pro-inflammatory genes, such as IL-1b and IL-6, thus, increasing hypoxia and inducing senescence. Using the lung epithelial cell (BEAS-2B) line, we demonstrated that SARS-CoV-2 proteins reprogram the cellular metabolism and increase pyruvate kinase muscle isoform 2 (PKM2). This deregulation promotes the accumulation of AGEs and senescence induction. We showed the ability of the PKM2 stabilizer, Tepp-46, to reverse the observed glycolysis changes/alterations and restore this essential metabolic process.
MeSH term(s)	COVID-19 ; Humans ; Inflammation ; Pneumonia ; Pyridazines ; Pyrroles ; SARS-CoV-2
Chemical Substances	ML-265 ; Pyridazines ; Pyrroles
Language	English
Publishing date	2022-05-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v14050983
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Article: Metabolic Reprogramming in HIV-Associated Neurocognitive Disorders.

Allen, Charles N S / Arjona, Sterling P / Santerre, Maryline / De Lucia, Claudio / Koch, Walter J / Sawaya, Bassel E

Frontiers in cellular neuroscience

2022 Volume 16, Page(s) 812887

Abstract: A significant number of patients infected with HIV-1 suffer from HIV-associated neurocognitive disorders (HAND) such as spatial memory impairments and learning disabilities (SMI-LD). SMI-LD is also observed in patients using combination antiretroviral ... ...

Abstract	A significant number of patients infected with HIV-1 suffer from HIV-associated neurocognitive disorders (HAND) such as spatial memory impairments and learning disabilities (SMI-LD). SMI-LD is also observed in patients using combination antiretroviral therapy (cART). Our lab has demonstrated that the HIV-1 protein, gp120, promotes SMI-LD by altering mitochondrial functions and energy production. We have investigated cellular processes upstream of the mitochondrial functions and discovered that gp120 causes metabolic reprogramming. Effectively, the addition of gp120 protein to neuronal cells disrupted the glycolysis pathway at the pyruvate level. Looking for the players involved, we found that gp120 promotes increased expression of polypyrimidine tract binding protein 1 (PTBP1), causing the splicing of pyruvate kinase M (PKM) into PKM1 and PKM2. We have also shown that these events lead to the accumulation of advanced glycation end products (AGEs) and prevent the cleavage of pro-brain-derived neurotrophic factor (pro-BDNF) protein into mature brain-derived neurotrophic factor (BDNF). The accumulation of proBDNF results in signaling that increases the expression of the inducible cAMP early repressor (ICER) protein which then occupies the cAMP response element (CRE)-binding sites within the BDNF promoters II and IV, thus altering normal synaptic plasticity. We reversed these events by adding Tepp-46, which stabilizes the tetrameric form of PKM2. Therefore, we concluded that gp120 reprograms cellular metabolism, causing changes linked to disrupted memory in HIV-infected patients and that preventing the disruption of the metabolism presents a potential cure against HAND progression.
Language	English
Publishing date	2022-03-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2022.812887
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Article ; Online: Disruption of Mitochondrial-associated ER membranes by HIV-1 tat protein contributes to premature brain aging.

Arjona, Sterling P / Allen, Charles N S / Santerre, Maryline / Gross, Scott / Soboloff, Jonathan / Booze, Rosemarie / Sawaya, Bassel E

CNS neuroscience & therapeutics

2022 Volume 29, Issue 1, Page(s) 365–377

Abstract: Introduction: Mitochondrial-associated ER membranes (MAMs) control many cellular functions, including calcium and lipid exchange, intracellular trafficking, and mitochondrial biogenesis. The disruption of these functions contributes to neurocognitive ... ...

Abstract	Introduction: Mitochondrial-associated ER membranes (MAMs) control many cellular functions, including calcium and lipid exchange, intracellular trafficking, and mitochondrial biogenesis. The disruption of these functions contributes to neurocognitive disorders, such as spatial memory impairment and premature brain aging. Using neuronal cells, we demonstrated that HIV-1 Tat protein deregulates the mitochondria. Methods& results: To determine the mechanisms, we used a neuronal cell line and showed that Tat-induced changes in expression and interactions of both MAM-associated proteins and MAM tethering proteins. The addition of HIV-1 Tat protein alters expression levels of PTPIP51 and VAPB proteins in the MAM fraction but not the whole cell. Phosphorylation of PTPIP51 protein regulates its subcellular localization and function. We demonstrated that the Tat protein promotes PTPIP51 phosphorylation on tyrosine residues and prevents its binding to VAPB. Treatment of the cells with a kinase inhibitor restores the PTPIP51-VAPB interaction and overcomes the effect of Tat. Conclusion: These results suggest that Tat disrupts the MAM, through the induction of PTPIP51 phosphorylation, leading to ROS accumulation, mitochondrial stress, and altered movement. Hence, we concluded that interfering in the MAM-associated cellular pathways contributes to spatial memory impairment and premature brain aging often observed in HIV-1-infected patients.
MeSH term(s)	Humans ; Brain/metabolism ; Gene Products, tat/metabolism ; Gene Products, tat/pharmacology ; HIV-1/metabolism ; Mitochondria/metabolism ; Protein Tyrosine Phosphatases/metabolism ; Protein Tyrosine Phosphatases/pharmacology ; Endoplasmic Reticulum/metabolism
Chemical Substances	Gene Products, tat ; Protein Tyrosine Phosphatases (EC 3.1.3.48)
Language	English
Publishing date	2022-11-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2423461-8
ISSN	1755-5949 ; 1755-5930
ISSN (online)	1755-5949
ISSN	1755-5930
DOI	10.1111/cns.14011
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Article ; Online: Why do SARS-CoV-2 NSPs rush to the ER?

Santerre, Maryline / Arjona, Sterling P / Allen, Charles Ns / Shcherbik, Natalia / Sawaya, Bassel E

Journal of neurology

2020 Volume 268, Issue 6, Page(s) 2013–2022

Abstract: SARS-CoV-2, which led to the 2020 global pandemic, is responsible for the Coronavirus Disease 2019 (COVID-19), a respiratory illness, and presents a tropism for the central nervous system. Like most members of this family, the virus is composed of ... ...

Abstract	SARS-CoV-2, which led to the 2020 global pandemic, is responsible for the Coronavirus Disease 2019 (COVID-19), a respiratory illness, and presents a tropism for the central nervous system. Like most members of this family, the virus is composed of structural and non-structural proteins (NSPs). The non-structural proteins are critical elements of the replication and transcription complex (RTC), as well as immune system evasion. Through hijacking the endoplasmic reticulum (ER) membrane, NSPs help the virus establish the RTC, inducing ER stress after membrane rearrangement and causing severe neuronal disturbance. In this review, we focus on the role of Nsp3, 4, and 6 in intracellular membrane rearrangement and evaluate the potential disruption of the central nervous system and the neurodegeneration which it could trigger. Studies of these NSPs will not only bring to light their specific role in viral infection but also facilitate the discovery of novel targeted drugs.
MeSH term(s)	COVID-19 ; Humans ; Pandemics ; Proteins ; SARS-CoV-2 ; Virus Replication
Chemical Substances	Proteins
Keywords	covid19
Language	English
Publishing date	2020-09-01
Publishing country	Germany
Document type	Journal Article ; Review
ZDB-ID	187050-6
ISSN	1432-1459 ; 0340-5354 ; 0012-1037 ; 0939-1517 ; 1619-800X
ISSN (online)	1432-1459
ISSN	0340-5354 ; 0012-1037 ; 0939-1517 ; 1619-800X
DOI	10.1007/s00415-020-10197-8
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Article ; Online: HIV-1 gp120 protein promotes HAND through the calcineurin pathway activation.

Shrestha, Jenny / Santerre, Maryline / Allen, Charles N / Arjona, Sterling P / Hooper, Robert / Mukerjee, Ruma / Kaul, Marcus / Shcherbik, Natalia / Soboloff, Jonathan / Sawaya, Bassel E

Mitochondrion

2023 Volume 70, Page(s) 31–40

Abstract: For over two decades, highly active antiretroviral therapy (HAART) was able to help prolong the life expectancy of people living with HIV-1 (PLWH) and eliminate the virus to an undetectable level. However, an increased prevalence of HIV- associated ... ...

Abstract	For over two decades, highly active antiretroviral therapy (HAART) was able to help prolong the life expectancy of people living with HIV-1 (PLWH) and eliminate the virus to an undetectable level. However, an increased prevalence of HIV- associated neurocognitive disorders (HAND) was observed. These symptoms range from neuronal dysfunction to cell death. Among the markers of neuronal deregulation, we cite the alteration of synaptic plasticity and neuronal communications. Clinically, these dysfunctions led to neurocognitive disorders such as learning alteration and loss of spatial memory, which promote premature brain aging even in HAART-treated patients. In support of these observations, we showed that the gp120 protein deregulates miR-499-5p and its downstream target, the calcineurin (CaN) protein. The gp120 protein also promotes the accumulation of calcium (Ca
MeSH term(s)	Humans ; HIV-1/metabolism ; Calcineurin/metabolism ; Calcineurin/pharmacology ; Brain/metabolism ; Cell Death ; HIV Infections ; MicroRNAs/genetics ; MicroRNAs/metabolism
Chemical Substances	Calcineurin (EC 3.1.3.16) ; MicroRNAs
Language	English
Publishing date	2023-03-15
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2056923-3
ISSN	1872-8278 ; 1567-7249
ISSN (online)	1872-8278
ISSN	1567-7249
DOI	10.1016/j.mito.2023.03.003
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Book ; Online: Potential use of RNA-dependent RNA polymerase (RdRp) inhibitor against SARS-CoV2 infection

Allen, Charles / Arjona, Sterling / Santerre, Maryline / Sawaya, Bassel E

2020

Abstract: Favipiravir, an inhibitor of RNA-dependent RNA polymerase used against the Japanese flu, was recently suggested as a potential COVID-19 inhibitor. Since Favipiravir targets a critical and a viral specific process, using it as a treatment could be ... ...

Abstract	Favipiravir, an inhibitor of RNA-dependent RNA polymerase used against the Japanese flu, was recently suggested as a potential COVID-19 inhibitor. Since Favipiravir targets a critical and a viral specific process, using it as a treatment could be beneficial in slowing the outbreak. Though there have been many suggested antivirals to treat SARS-CoV-2 infection, most treatments target host-associated pathways that may cause adverse effects, Favipiravir or similar combination may be the best remedy against COVID-19 pandemic.
Keywords	covid19
Publisher	Center for Open Science
Publishing country	us
Document type	Book ; Online
DOI	10.31219/osf.io/cgb25
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