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Article ; Online: Mesenchymal Stem Cells from Familial Alzheimer's Patients Express MicroRNA Differently.

Rochín-Hernández, Lory J / Rochín-Hernández, Lory S / Padilla-Cristerna, Mayte L / Duarte-García, Andrea / Jiménez-Acosta, Miguel A / Figueroa-Corona, María P / Meraz-Ríos, Marco A

International journal of molecular sciences

2024 Volume 25, Issue 3

Abstract: Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the predominant form of dementia globally. No reliable diagnostic, predictive techniques, or curative interventions are available. MicroRNAs (miRNAs) are vital to controlling gene ... ...

Abstract	Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the predominant form of dementia globally. No reliable diagnostic, predictive techniques, or curative interventions are available. MicroRNAs (miRNAs) are vital to controlling gene expression, making them valuable biomarkers for diagnosis and prognosis. This study examines the transcriptome of olfactory ecto-mesenchymal stem cells (MSCs) derived from individuals with the PSEN1(A431E) mutation (Jalisco mutation). The aim is to determine whether this mutation affects the transcriptome and expression profile of miRNAs and their target genes at different stages of asymptomatic, presymptomatic, and symptomatic conditions. Expression microarrays compare the MSCs from mutation carriers with those from healthy donors. The results indicate a distinct variation in the expression of miRNAs and mRNAs among different symptomatologic groups and between individuals with the mutation. Using bioinformatics tools allows us to identify target genes for miRNAs, which in turn affect various biological processes and pathways. These include the cell cycle, senescence, transcription, and pathways involved in regulating the pluripotency of stem cells. These processes are closely linked to inter- and intracellular communication, vital for cellular functioning. These findings can enhance our comprehension and monitoring of the disease's physiological processes, identify new disorder indicators, and develop innovative treatments and diagnostic tools for preventing or treating AD.
MeSH term(s)	Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Alzheimer Disease/metabolism ; Mutation ; Biomarkers/metabolism ; Mesenchymal Stem Cells/metabolism
Chemical Substances	MicroRNAs ; Biomarkers
Language	English
Publishing date	2024-01-27
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms25031580
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Article ; Online: Mesenchymal Stem Cells: New Alternatives for Nervous System Disorders.

Jiménez-Acosta, Miguel Antonio / Hernández, Lory Jhenifer Rochin / Cristerna, Mayte Lizeth Padilla / Meraz-Ríos, Marco Alejandro

Current stem cell research & therapy

2022 Volume 18, Issue 3, Page(s) 299–321

Abstract: Mesenchymal stem cells (MSCs) are self-renewing cells found in almost all postnatal organs and tissues in the perivascular region. These cells have a high capacity for mesodermal differentiation; however, numerous studies have shown that MSCs can also ... ...

Abstract	Mesenchymal stem cells (MSCs) are self-renewing cells found in almost all postnatal organs and tissues in the perivascular region. These cells have a high capacity for mesodermal differentiation; however, numerous studies have shown that MSCs can also differentiate into cells of endodermal and ectodermal lineages. Due to this multilineage differentiation capacity, these cells could function as restoratives of various cell populations after transplantation. However, not only their differentiation potential makes them ideal candidates for this, but also a series of trophic properties that promote regeneration in the surrounding tissue, such as their migratory capacity, secretory and immunomodulatory actions. This review analyzes several MSC transplantation trials to treat neurological diseases, such as demyelinating injury, spinal cord injury, paraplegia, Parkinson's disease, cochlear injury, and Alzheimer's disease. These cells could facilitate functional recovery in multiple models of neurodegenerative diseases and nervous system injuries by using their trophic capacities, reducing inflammation in the injured area, reducing apoptosis, and enhancing endogenous neurogenesis through the secretion of bioactive factors. Furthermore, since cells derived from patients have demonstrated disease-associated differences in various brain diseases, these cells represent an excellent candidate for the study of these diseases, functioning as "a window to the brain."
MeSH term(s)	Humans ; Mesenchymal Stem Cells ; Neurodegenerative Diseases/therapy ; Cell Differentiation/physiology ; Neurogenesis/physiology ; Parkinson Disease ; Mesenchymal Stem Cell Transplantation
Language	English
Publishing date	2022-05-13
Publishing country	United Arab Emirates
Document type	Review ; Journal Article
ZDB-ID	2251937-3
ISSN	2212-3946 ; 1574-888X
ISSN (online)	2212-3946
ISSN	1574-888X
DOI	10.2174/1574888X17666220511153133
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Book ; Online: Neurodegeneration: From Genetics to Molecules

Guevara-Guzman, Rosalinda / Meraz-Rios, Marco Antonio / Campos-Pena, Victoria / Carvajal, Karla Guadalupe

2016

Abstract: Chronic degenerative diseases are one of the major public health problems, particularly those affecting the nervous system. They are characterized by the degeneration of specific cell populations that include several pathologies which contribute ... ...

Abstract	Chronic degenerative diseases are one of the major public health problems, particularly those affecting the nervous system. They are characterized by the degeneration of specific cell populations that include several pathologies which contribute significantly to morbidity and mortality in the elderly population. Therefore, in recent years, the study of neuroscience has gained significant importance. Most of these neurodegenerative disorders are the result of a complex interaction between genetic and environmental factors that generate progression and can even determine its severity. The presence of mutations in genes as LRRK2, SNCA, PARK7, PARK2 or PINK1 is associated with Parkinsons disease. Mutations in genes such as APP, PS1 and PS2 are associated with familial Alzheimers disease; while HTT gene mutations are the cause of Huntingtons disease.- In most cases, this condition is inherited in an autosomal dominant pattern, which means one copy of the altered gene in each cell is sufficient to cause the disorder. It is known that these mutations can also alter the proteins function; however, it has not yet been possible to fully understand how some genetic changes cause the disease or influence the risk of developing these disorders. Most symptoms seen in these conditions occurs when specific nerve cells are damaged or die generating a loss in brain communication. Also many of these mutations generate aggregation of intracellular or extracellular proteins affecting cell function and eventually causing neuronal death. It is unclear whether the presence of these aggregates play an important role in nerve cell death during the development of neurodegenerative diseases, or if they are simply part of the response of cells to the disease.- Other mutations affect the mitochondrial function generating alterations in energy production and promoting the formation of unstable molecules such as free radicals. Under normal conditions, the harmful effects caused by free radicals, are offset within the cell. However, in pathological conditions, the presence of mutations can alter this process by allowing the accumulation of radicals and damaging or killing cells. On the other hand, we also know that these diseases may not have a direct genetic component, thus, the study of sporadic type neurodegenerative diseases is much more complex. Histopathological lesions as well as the cellular and molecular alterations are generally indistinguishable from familial cases. For this reason, it is important to understand the genetic and molecular mechanisms associated with this type of pathologies.-
Keywords	Science (General) ; Neurosciences. Biological psychiatry. Neuropsychiatry
Size	1 electronic resource (264 p.)
Publisher	Frontiers Media SA
Document type	Book ; Online
Note	English ; Open Access
HBZ-ID	HT020097371
ISBN	9782889450206 ; 2889450201
Database	ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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Article: Antineoplastic effect of compounds C14 and P8 on TNBC and radioresistant TNBC cells by stabilizing the K-Ras4B

Carrión-Estrada, Dayan A / Aguilar-Rojas, Arturo / Huerta-Yepez, Sara / Montecillo-Aguado, Mayra / Bello, Martiniano / Rojo-Domínguez, Arturo / Arechaga-Ocampo, Elena / Briseño-Díaz, Paola / Meraz-Ríos, Marco Antonio / Thompson-Bonilla, María Del Rocío / Hernández-Rivas, Rosaura / Vargas, Miguel

Frontiers in oncology

2024 Volume 14, Page(s) 1341766

Abstract: Introduction: Breast cancer (BC) is the leading cause of cancer-related deaths among women, with triple-negative breast cancer (TNBC) representing one of the most aggressive and treatment-resistant subtypes. In this study, we aimed to evaluate the ... ...

Abstract	Introduction: Breast cancer (BC) is the leading cause of cancer-related deaths among women, with triple-negative breast cancer (TNBC) representing one of the most aggressive and treatment-resistant subtypes. In this study, we aimed to evaluate the antitumor potential of C14 and P8 molecules in both TNBC and radioresistant TNBC cells. These compounds were chosen for their ability to stabilize the complex formed by the overactivated form of K-Ras4B Methods: The antitumor potential of C14 and P8 was assessed using TNBC cell lines, MDA-MB-231, and the radioresistant derivative MDA-MB-231RR, both carrying the K-Ras4B> Results: Western blotting analysis determined the negative impact of C14 and P8 on the activation of mutant K-Ras signaling pathways in MDA-MB-231 and MDA-MB-231RR cells. Proliferation assays demonstrated their efficacy as cytotoxic agents against K-Ras Discussion: These findings suggest that C14 and P8 could serve as promising adjuvant treatments for TNBC, particularly for non-responders to standard therapies. By targeting overactivated K-Ras and its membrane transporter, these compounds offer potential therapeutic benefits against TNBC, including its radioresistant form. Further research and clinical trials are warranted to validate their efficacy and safety as novel TNBC treatments.
Language	English
Publishing date	2024-03-20
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2649216-7
ISSN	2234-943X
ISSN	2234-943X
DOI	10.3389/fonc.2024.1341766
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Article ; Online: Distinct Transcriptional Profile of PDZ Genes after Activation of Human Macrophages and Dendritic Cells.

Rosas-García, Jorge / Ramón-Luing, Lucero A / Bobadilla, Karen / Meraz-Ríos, Marco Antonio / Sevilla-Reyes, Edgar E / Santos-Mendoza, Teresa

International journal of molecular sciences

2022 Volume 23, Issue 13

Abstract: The PDZ (PSD95, Dlg and ZO-1) genes encode proteins that primarily function as scaffolds of diverse signaling pathways. To date, 153 PDZ genes have been identified in the human genome, most of which have multiple protein isoforms widely studied in ... ...

Abstract	The PDZ (PSD95, Dlg and ZO-1) genes encode proteins that primarily function as scaffolds of diverse signaling pathways. To date, 153 PDZ genes have been identified in the human genome, most of which have multiple protein isoforms widely studied in epithelial and neural cells. However, their expression and function in immune cells have been poorly studied. Herein, we aimed to assess the transcriptional profiles of 83 PDZ genes in human macrophages (Mɸ) and dendritic cells (DCs) and changes in their relative expression during cell PRR stimulation. Significantly distinct PDZ gene transcriptional profiles were identified under different stimulation conditions. Furthermore, a distinct PDZ gene transcriptional signature was found in Mɸ and DCs under the same phagocytic stimuli. Notably, more than 40 PDZ genes had significant changes in expression, with potentially relevant functions in antigen-presenting cells (APCs). Given that several PDZ proteins are targeted by viral products, our results support that many of these proteins might be viral targets in APCs as part of evasion mechanisms. Our results suggest a distinct requirement for PDZ scaffolds in Mɸ and DCs signaling pathways activation. More assessments on the functions of PDZ proteins in APCs and their role in immune evasion mechanisms are needed.
MeSH term(s)	Dendritic Cells ; Humans ; Immune Evasion ; Macrophages/metabolism ; Signal Transduction
Language	English
Publishing date	2022-06-24
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23137010
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Article ; Online: Factorial design in the optimization and study 'in combo' of derivatives of imidazo[1,2-a]azines in the COX´s isoforms inhibition.

Guerrero-González, Miguel / Aldrete, María-Elena Campos / Meraz-Rios, Marco Antonio

Future medicinal chemistry

2022 Volume 14, Issue 11, Page(s) 771–784

Abstract: Background: ...

Abstract	Background:
MeSH term(s)	Animals ; Cyclooxygenase 2/metabolism ; Ibuprofen/pharmacology ; Indomethacin ; Mice ; Molecular Docking Simulation ; Protein Isoforms ; Pyrimidines/chemistry ; Structure-Activity Relationship
Chemical Substances	Protein Isoforms ; Pyrimidines ; Cyclooxygenase 2 (EC 1.14.99.1) ; Ibuprofen (WK2XYI10QM) ; Indomethacin (XXE1CET956)
Language	English
Publishing date	2022-05-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1756-8927
ISSN (online)	1756-8927
DOI	10.4155/fmc-2022-0017
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Article ; Online: The Proteome Profile of Olfactory Ecto-Mesenchymal Stem Cells-Derived from Patients with Familial Alzheimer's Disease Reveals New Insights for AD Study.

Rochín-Hernández, Lory J / Jiménez-Acosta, Miguel A / Ramírez-Reyes, Lorena / Figueroa-Corona, María Del Pilar / Sánchez-González, Víctor J / Orozco-Barajas, Maribel / Meraz-Ríos, Marco A

International journal of molecular sciences

2023 Volume 24, Issue 16

Abstract: Alzheimer's disease (AD), the most common neurodegenerative disease and the first cause of dementia worldwide, has no effective treatment, and its pathological mechanisms are not yet fully understood. We conducted this study to explore the proteomic ... ...

Abstract	Alzheimer's disease (AD), the most common neurodegenerative disease and the first cause of dementia worldwide, has no effective treatment, and its pathological mechanisms are not yet fully understood. We conducted this study to explore the proteomic differences associated with Familial Alzheimer's Disease (FAD) in olfactory ecto-mesenchymal stem cells (MSCs) derived from PSEN1 (A431E) mutation carriers compared with healthy donors paired by age and gender through two label-free liquid chromatography-mass spectrometry approaches. The first analysis compared carrier 1 (patient with symptoms, P1) and its control (healthy donor, C1), and the second compared carrier 2 (patient with pre-symptoms, P2) with its respective control cells (C2) to evaluate whether the protein alterations presented in the symptomatic carrier were also present in the pre-symptom stages. Finally, we analyzed the differentially expressed proteins (DEPs) for biological and functional enrichment. These proteins showed impaired expression in a stage-dependent manner and are involved in energy metabolism, vesicle transport, actin cytoskeleton, cell proliferation, and proteostasis pathways, in line with previous AD reports. Our study is the first to conduct a proteomic analysis of MSCs from the Jalisco FAD patients in two stages of the disease (symptomatic and presymptomatic), showing these cells as a new and excellent in vitro model for future AD studies.
MeSH term(s)	Humans ; Alzheimer Disease/genetics ; Neurodegenerative Diseases ; Proteome ; Proteomics ; Mesenchymal Stem Cells
Chemical Substances	Proteome
Language	English
Publishing date	2023-08-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241612606
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Article ; Online: NAT2 global landscape: Genetic diversity and acetylation statuses from a systematic review.

Gutiérrez-Virgen, Jorge E / Piña-Pozas, Maricela / Hernández-Tobías, Esther A / Taja-Chayeb, Lucia / López-González, Ma de Lourdes / Meraz-Ríos, Marco A / Gómez, Rocío

PloS one

2023 Volume 18, Issue 4, Page(s) e0283726

Abstract: Arylamine N-acetyltransferase 2 has been related to drug side effects and cancer susceptibility; its protein structure and acetylation capacity results from the polymorphism's arrays on the NAT2 gene. Absorption, distribution, metabolism, and excretion, ... ...

Abstract	Arylamine N-acetyltransferase 2 has been related to drug side effects and cancer susceptibility; its protein structure and acetylation capacity results from the polymorphism's arrays on the NAT2 gene. Absorption, distribution, metabolism, and excretion, cornerstones of the pharmacological effects, have shown diversity patterns across populations, ethnic groups, and even interethnic variation. Although the 1000 Genomes Project database has portrayed the global diversity of the NAT2 polymorphisms, several populations and ethnicities remain underrepresented, limiting the comprehensive picture of its variation. The NAT2 clinical entails require a detailed landscape of its striking diversity. This systematic review spans the genetic and acetylation patterns from 164 articles from October 1992 to October 2020. Descriptive studies and controls from observational studies expanded the NAT2 diversity landscape. Our study included 243 different populations and 101 ethnic minorities, and, for the first time, we presented the global patterns in the Middle Eastern populations. Europeans, including its derived populations, and East Asians have been the most studied genetic backgrounds. Contrary to the popular perception, Africans, Latinos and Native Americans have been significantly represented in recent years. NAT24, 5B, and 6A were the most frequent haplotypes globally. Nonetheless, the distribution of 5B and *7B were less and more frequent in Asians, respectively. Regarding the acetylator status, East Asians and Native Americans harboured the highest frequencies of the fast phenotype, followed by South Europeans. Central Asia, the Middle East, and West European populations were the major carriers of the slow acetylator status. The detailed panorama presented herein, expands the knowledge about the diversity patterns to genetic and acetylation levels. These data could help clarify the controversial findings between acetylator states and the susceptibility to diseases and reinforce the utility of NAT2 in precision medicine.
MeSH term(s)	Arylamine N-Acetyltransferase/genetics ; Arylamine N-Acetyltransferase/metabolism ; Acetylation ; Polymorphism, Genetic ; Haplotypes ; Phenotype ; Genotype
Chemical Substances	Arylamine N-Acetyltransferase (EC 2.3.1.5)
Language	English
Publishing date	2023-04-06
Publishing country	United States
Document type	Systematic Review ; Journal Article
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0283726
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Article ; Online: The nuclear receptor Nurr1 is preferentially expressed in human pro-inflammatory macrophages and limits their inflammatory profile.

Solís-Barbosa, Miguel A / Santana, Eduardo / Muñoz-Torres, José R / Segovia-Gamboa, Norma C / Patiño-Martínez, Eduardo / Meraz-Ríos, Marco A / Samaniego, Rafael / Sánchez-Mateos, Paloma / Sánchez-Torres, Carmen

International immunology

2023 Volume 36, Issue 3, Page(s) 111–128

Abstract: Nurr1 is a member of the orphan nuclear receptor family NR4A (nuclear receptor subfamily 4 group A) that modulates inflammation in several cell lineages, both positively and negatively. Macrophages are key regulators of inflammatory responses, yet ... ...

Abstract	Nurr1 is a member of the orphan nuclear receptor family NR4A (nuclear receptor subfamily 4 group A) that modulates inflammation in several cell lineages, both positively and negatively. Macrophages are key regulators of inflammatory responses, yet information about the role of Nurr1 in human macrophages is scarce. Here we examined Nurr1 expression and activity in steady state and activated human macrophages. Pro- and anti-inflammatory macrophages were generated in vitro by culture of blood monocytes with granulocyte/macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF), respectively. Nurr1 expression was predominant in macrophages with the pro-inflammatory phenotype. Nurr1 activation with the agonists 1,1-bis(3'-indolyl)-1-(p-chlorophenyl) methane (C-DIM12) or isoxazolo-pyridinone 7e (IP7e) did not globally modify the polarization status of pro-inflammatory macrophages, but they decreased their production of TNF, IL-1β, IL-6, IL-8, IL-12 p40, CCL2, IFN-β, and reactive oxygen species, with variable potencies. Conversely, Nurr1 deficient macrophages increased the expression of transcripts encoding inflammatory mediators, particularly that of IL6, IFNB1, and CCL2. Mechanistically, endogenous Nurr1 interacted with NF-κB p65 in basal conditions and upon lipopolysaccharide (LPS)-mediated activation. C-DIM12 stabilized those complexes in cells exposed to LPS and concurrently decreased NF-κB transcriptional activity and p65 nuclear translocation. Expression of high levels of Nurr1 was associated with a subset of dermal macrophages that display enhanced levels of TNF and lower expression of the anti-inflammatory marker CD163L1 in skin lesions from patients with bullous pemphigoid (BP), a chronic inflammatory autoimmune blistering disorder. These results suggest that Nurr1 expression is linked with the pro-inflammatory phenotype of human macrophages, both in vivo and in vitro, where it may constitute a brake to attenuate the synthesis of inflammatory mediators.
MeSH term(s)	Humans ; NF-kappa B/metabolism ; Macrophage Colony-Stimulating Factor/metabolism ; Lipopolysaccharides/pharmacology ; Macrophages ; Nuclear Receptor Subfamily 4, Group A, Member 2/genetics ; Nuclear Receptor Subfamily 4, Group A, Member 2/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism ; Inflammation/metabolism ; Inflammation Mediators/metabolism ; Anti-Inflammatory Agents/metabolism
Chemical Substances	NF-kappa B ; Macrophage Colony-Stimulating Factor (81627-83-0) ; Lipopolysaccharides ; Nuclear Receptor Subfamily 4, Group A, Member 2 ; Receptors, Cytoplasmic and Nuclear ; Inflammation Mediators ; Anti-Inflammatory Agents
Language	English
Publishing date	2023-12-09
Publishing country	England
Document type	Journal Article
ZDB-ID	1013745-2
ISSN	1460-2377 ; 0953-8178
ISSN (online)	1460-2377
ISSN	0953-8178
DOI	10.1093/intimm/dxad048
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Article ; Online: An ivermectin - atorvastatin combination impairs nuclear transport inhibiting dengue infection

Palacios-Rápalo, Selvin Noé / Farfan-Morales, Carlos Noe / Cordero-Rivera, Carlos Daniel / De Jesús-González, Luis Adrián / Reyes-Ruiz, José Manuel / Meraz-Ríos, Marco Antonio / Del Ángel, Rosa María

iScience

2023 Volume 26, Issue 12, Page(s) 108294

Abstract: Dengue virus (DENV) uses cellular nuclear transport machinery to import some proteins into the nucleus. Recently, the non-structural protein 3 (NS3) of DENV was localized in the nucleus of infected cells; however, its nuclear import mechanism is still ... ...

Abstract	Dengue virus (DENV) uses cellular nuclear transport machinery to import some proteins into the nucleus. Recently, the non-structural protein 3 (NS3) of DENV was localized in the nucleus of infected cells; however, its nuclear import mechanism is still unknown. In this study, we demonstrate that Ivermectin (IVM) inhibits the nuclear localization of NS3 through the inhibition of the Importin α/β1 pathway. We also report that Atorvastatin (ATV) can modulate the nuclear transport of NS3 protease and NS5 polymerase of DENV-2. On the other hand, we found that IVM and ATV treatments reduce the alteration of nuclear pore complex (NPC) proteins, and an IVM+ATV combination reduced DENV infection both
Language	English
Publishing date	2023-10-27
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.108294
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