LIVIVO - Search results -

Search results

Result 1 - 10 of total 22

Search options

Article ; Online: Antibody-Mediated Depletion of Autoreactive T Lymphocytes through PD-1 Improves Disease Outcomes and Visualizes T Cell Activation in Experimental Autoimmune Encephalomyelitis.

Frank, Connor / Salapa, Hannah E / Allen, Kevin J H / Levin, Michael C / Dawicki, Wojciech / Dadachova, Ekaterina

Journal of immunology (Baltimore, Md. : 1950)

2024

Abstract: Long-term therapeutic outcomes of multiple sclerosis (MS) remain hindered by the chronic nature of immune cell stimulation toward self-antigens. Development of novel methods to target and deplete autoreactive T lymphocytes remains an attractive target ... ...

Abstract	Long-term therapeutic outcomes of multiple sclerosis (MS) remain hindered by the chronic nature of immune cell stimulation toward self-antigens. Development of novel methods to target and deplete autoreactive T lymphocytes remains an attractive target for therapeutics for MS. We developed a programmed cell death 1 (PD-1)-targeted radiolabeled mAb and assessed its ability to deplete activated PD-1+ T lymphocytes in vitro and its ability to reduce disease burden of the myelin oligodendrocyte glycoprotein 35-55 experimental autoimmune encephalomyelitis (EAE) model in C57BL/6 mice. We also investigated the upregulation of PD-1 on infiltrating lymphocytes in an animal model of MS. Finally, we demonstrate the (to our knowledge) first reported positron-emission tomography/computed tomography imaging of activated PD-1+ cells in the EAE animal model of MS. We found that the 177Lu radioisotope-labeled anti-PD-1 mAb demonstrated significant in vitro cytotoxicity toward activated CD4+PD-1+ T lymphocytes and led to significant reduction in overall disease progression in the EAE animal model. Our results show high expression of PD-1 on infiltrating lymphocytes in the spinal cords of EAE diseased animals. Positron-emission tomography/computed tomography imaging of the anti-PD-1 mAb demonstrated significant uptake in the cervical draining lymph nodes highlighting accumulation of activated lymphocytes. Targeted depletion of T lymphocytes using T cell activation markers such as PD-1 may present a novel method to reduce autoimmune attack and inflammation in autoimmune diseases such as MS. Development of multimodal nuclear theranostic agents may present the opportunity to monitor T cell activation via imaging radioisotopes and simultaneously treat MS using therapeutic radioisotopes.
Language	English
Publishing date	2024-04-05
Publishing country	United States
Document type	Journal Article
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2300751
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 28: Show issues

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: The Potential Contribution of Dysfunctional RNA-Binding Proteins to the Pathogenesis of Neurodegeneration in Multiple Sclerosis and Relevant Models.

Libner, Cole D / Salapa, Hannah E / Levin, Michael C

International journal of molecular sciences

2020 Volume 21, Issue 13

Abstract: Neurodegeneration in multiple sclerosis (MS) is believed to underlie disease progression and permanent disability. Many mechanisms of neurodegeneration in MS have been proposed, such as mitochondrial dysfunction, oxidative stress, neuroinflammation, and ... ...

Abstract	Neurodegeneration in multiple sclerosis (MS) is believed to underlie disease progression and permanent disability. Many mechanisms of neurodegeneration in MS have been proposed, such as mitochondrial dysfunction, oxidative stress, neuroinflammation, and RNA-binding protein dysfunction. The purpose of this review is to highlight mechanisms of neurodegeneration in MS and its models, with a focus on RNA-binding protein dysfunction. Studying RNA-binding protein dysfunction addresses a gap in our understanding of the pathogenesis of MS, which will allow for novel therapies to be generated to attenuate neurodegeneration before irreversible central nervous system damage occurs.
MeSH term(s)	Animals ; Disease Progression ; Humans ; Multiple Sclerosis/complications ; Neurodegenerative Diseases/etiology ; Neurodegenerative Diseases/metabolism ; Neurodegenerative Diseases/pathology ; Oxidative Stress ; RNA-Binding Proteins/metabolism
Chemical Substances	RNA-Binding Proteins
Language	English
Publishing date	2020-06-27
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21134571
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: A Comprehensive Analysis of the Role of hnRNP A1 Function and Dysfunction in the Pathogenesis of Neurodegenerative Disease.

Clarke, Joseph P / Thibault, Patricia A / Salapa, Hannah E / Levin, Michael C

Frontiers in molecular biosciences

2021 Volume 8, Page(s) 659610

Abstract: Heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) is a member of the hnRNP family of conserved proteins that is involved in RNA transcription, pre-mRNA splicing, mRNA transport, protein translation, microRNA processing, telomere maintenance and the ... ...

Abstract	Heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) is a member of the hnRNP family of conserved proteins that is involved in RNA transcription, pre-mRNA splicing, mRNA transport, protein translation, microRNA processing, telomere maintenance and the regulation of transcription factor activity. HnRNP A1 is ubiquitously, yet differentially, expressed in many cell types, and due to post-translational modifications, can vary in its molecular function. While a plethora of knowledge is known about the function and dysfunction of hnRNP A1 in diseases other than neurodegenerative disease (e.g., cancer), numerous studies in amyotrophic lateral sclerosis, frontotemporal lobar degeneration, multiple sclerosis, spinal muscular atrophy, Alzheimer's disease, and Huntington's disease have found that the dysregulation of hnRNP A1 may contribute to disease pathogenesis. How hnRNP A1 mechanistically contributes to these diseases, and whether mutations and/or altered post-translational modifications contribute to pathogenesis, however, is currently under investigation. The aim of this comprehensive review is to first describe the background of hnRNP A1, including its structure, biological functions in RNA metabolism and the post-translational modifications known to modify its function. With this knowledge, the review then describes the influence of hnRNP A1 in neurodegenerative disease, and how its dysfunction may contribute the pathogenesis.
Language	English
Publishing date	2021-04-12
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2021.659610
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article: Pro-Inflammatory Cytokines and Antibodies Induce hnRNP A1 Dysfunction in Mouse Primary Cortical Neurons.

Li, Muxue / Hamilton, Rachel / Salapa, Hannah E / Levin, Michael C

Brain sciences

2021 Volume 11, Issue 10

Abstract: Multiple sclerosis (MS) is an inflammatory disease of the central nervous system with a significant neurodegenerative component. Dysfunctional RNA-binding proteins (RBPs) are causally linked to neuronal damage and are a feature of MS, including the ... ...

Abstract	Multiple sclerosis (MS) is an inflammatory disease of the central nervous system with a significant neurodegenerative component. Dysfunctional RNA-binding proteins (RBPs) are causally linked to neuronal damage and are a feature of MS, including the mislocalization of the RBP heterogeneous nuclear ribonucleoprotein A1 (A1). Here, we show that primary neurons exposed to pro-inflammatory cytokines and anti-A1 antibodies, both characteristic of an MS autoimmune response, displayed increased A1 mislocalization, stress granule formation, and decreased neurite length, a marker of neurodegeneration. These findings illustrate a significant relationship between secreted immune factors, A1 dysfunction, and neuronal damage in a disease-relevant model system.
Language	English
Publishing date	2021-09-28
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2651993-8
ISSN	2076-3425
ISSN	2076-3425
DOI	10.3390/brainsci11101282
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: hnRNP A1 dysfunction in oligodendrocytes contributes to the pathogenesis of multiple sclerosis.

Jahanbazi Jahan-Abad, Ali / Salapa, Hannah E / Libner, Cole D / Thibault, Patricia A / Levin, Michael C

Glia

2022 Volume 71, Issue 3, Page(s) 633–647

Abstract: Oligodendrocyte (OL) damage and death are prominent features of multiple sclerosis (MS) pathology, yet mechanisms contributing to OL loss are incompletely understood. Dysfunctional RNA binding proteins (RBPs), hallmarked by nucleocytoplasmic ... ...

Abstract	Oligodendrocyte (OL) damage and death are prominent features of multiple sclerosis (MS) pathology, yet mechanisms contributing to OL loss are incompletely understood. Dysfunctional RNA binding proteins (RBPs), hallmarked by nucleocytoplasmic mislocalization and altered expression, have been shown to result in cell loss in neurologic diseases, including in MS. Since we previously observed that the RBP heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) was dysfunctional in neurons in MS, we hypothesized that it might also contribute to OL pathology in MS and relevant models. We discovered that hnRNP A1 dysfunction is characteristic of OLs in MS brains. These findings were recapitulated in the experimental autoimmune encephalomyelitis (EAE) mouse model of MS, where hnRNP A1 dysfunction was characteristic of OLs, including oligodendrocyte precursor cells and mature OLs in which hnRNP A1 dysfunction correlated with demyelination. We also found that hnRNP A1 dysfunction was induced by IFNγ, indicating that inflammation influences hnRNP A1 function. To fully understand the effects of hnRNP A1 dysfunction on OLs, we performed siRNA knockdown of hnRNP A1, followed by RNA sequencing. RNA sequencing detected over 4000 differentially expressed transcripts revealing alterations to RNA metabolism, cell morphology, and programmed cell death pathways. We confirmed that hnRNP A1 knockdown was detrimental to OLs and induced apoptosis and necroptosis. Together, these data demonstrate a critical role for hnRNP A1 in proper OL functioning and survival and suggest a potential mechanism of OL damage and death in MS that involves hnRNP A1 dysfunction.
MeSH term(s)	Animals ; Mice ; Heterogeneous Nuclear Ribonucleoprotein A1/genetics ; Heterogeneous Nuclear Ribonucleoprotein A1/metabolism ; Multiple Sclerosis/pathology ; RNA-Binding Proteins/metabolism ; Encephalomyelitis, Autoimmune, Experimental ; RNA, Small Interfering
Chemical Substances	Heterogeneous Nuclear Ribonucleoprotein A1 ; RNA-Binding Proteins ; RNA, Small Interfering
Language	English
Publishing date	2022-11-16
Publishing country	United States
Document type	Journal Article
ZDB-ID	639414-0
ISSN	1098-1136 ; 0894-1491
ISSN (online)	1098-1136
ISSN	0894-1491
DOI	10.1002/glia.24300
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2345: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article: Sequence- and structure-specific RNA oligonucleotide binding attenuates heterogeneous nuclear ribonucleoprotein A1 dysfunction.

Clarke, Joseph P / Thibault, Patricia A / Fatima, Sakina / Salapa, Hannah E / Kalyaanamoorthy, Subha / Ganesan, Aravindhan / Levin, Michael C

Frontiers in molecular biosciences

2023 Volume 10, Page(s) 1178439

Abstract: The RNA binding protein heterogeneous nuclear ribonucleoprotein A1 (A1) regulates RNA metabolism, which is crucial to maintaining cellular homeostasis. A1 dysfunction mechanistically contributes to reduced cell viability and loss, but molecular ... ...

Abstract	The RNA binding protein heterogeneous nuclear ribonucleoprotein A1 (A1) regulates RNA metabolism, which is crucial to maintaining cellular homeostasis. A1 dysfunction mechanistically contributes to reduced cell viability and loss, but molecular mechanisms of how A1 dysfunction affects cell viability and loss, and methodologies to attenuate its dysfunction, are lacking. Utilizing
Language	English
Publishing date	2023-06-22
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2814330-9
ISSN	2296-889X
ISSN	2296-889X
DOI	10.3389/fmolb.2023.1178439
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: hnRNP A1 dysfunction alters RNA splicing and drives neurodegeneration in multiple sclerosis (MS).

Salapa, Hannah E / Thibault, Patricia A / Libner, Cole D / Ding, Yulian / Clarke, Joseph-Patrick W E / Denomy, Connor / Hutchinson, Catherine / Abidullah, Hashim M / Austin Hammond, S / Pastushok, Landon / Vizeacoumar, Frederick S / Levin, Michael C

Nature communications

2024 Volume 15, Issue 1, Page(s) 356

Abstract: Neurodegeneration is the primary driver of disease progression in multiple sclerosis (MS) resulting in permanent disability, creating an urgent need to discover its underlying mechanisms. Herein, we establish that dysfunction of the RNA binding protein ... ...

Abstract	Neurodegeneration is the primary driver of disease progression in multiple sclerosis (MS) resulting in permanent disability, creating an urgent need to discover its underlying mechanisms. Herein, we establish that dysfunction of the RNA binding protein heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) results in differential of binding to RNA targets causing alternative RNA splicing, which contributes to neurodegeneration in MS and its models. Using RNAseq of MS brains, we discovered differential expression and aberrant splicing of hnRNP A1 target RNAs involved in neuronal function and RNA homeostasis. We confirmed this in vivo in experimental autoimmune encephalomyelitis employing CLIPseq specific for hnRNP A1, where hnRNP A1 differentially binds and regulates RNA, including aberrantly spliced targets identified in human samples. Additionally, dysfunctional hnRNP A1 expression in neurons caused neurite loss and identical changes in splicing, corroborating hnRNP A1 dysfunction as a cause of neurodegeneration. Collectively, these data indicate hnRNP A1 dysfunction causes altered neuronal RNA splicing, resulting in neurodegeneration in MS.
MeSH term(s)	Humans ; Alternative Splicing ; Heterogeneous Nuclear Ribonucleoprotein A1/genetics ; Multiple Sclerosis/genetics ; RNA ; RNA Splicing/genetics
Chemical Substances	Heterogeneous Nuclear Ribonucleoprotein A1 ; RNA (63231-63-0) ; hnRNPA1 protein, human
Language	English
Publishing date	2024-01-08
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-44658-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Localization of near-infrared labeled antibodies to the central nervous system in experimental autoimmune encephalomyelitis.

Lee, Sangmin / Salapa, Hannah E / Levin, Michael C

PloS one

2019 Volume 14, Issue 2, Page(s) e0212357

Abstract: Antibodies, including antibodies to the RNA binding protein heterogeneous nuclear ribonucleoprotein A1, have been shown to contribute to the pathogenesis of multiple sclerosis, thus it is important to assess their biological activity using animal models ... ...

Abstract	Antibodies, including antibodies to the RNA binding protein heterogeneous nuclear ribonucleoprotein A1, have been shown to contribute to the pathogenesis of multiple sclerosis, thus it is important to assess their biological activity using animal models of disease. Near-infrared optical imaging of fluorescently labeled antibodies and matrix metalloproteinase activity were measured and quantified in an animal model of multiple sclerosis, experimental autoimmune encephalomyelitis. We successfully labeled, imaged and quantified the fluorescence signal of antibodies that localized to the central nervous system of mice with experimental autoimmune encephalomyelitis. Fluorescently labeled anti-heterogeneous nuclear ribonucleoprotein A1 antibodies persisted in the central nervous system of mice with experimental autoimmune encephalomyelitis, colocalized with matrix metalloproteinase activity, correlated with clinical disease and shifted rostrally within the spinal cord, consistent with experimental autoimmune encephalomyelitis being an ascending paralysis. The fluorescent antibody signal also colocalized with matrix metalloproteinase activity in brain. Previous imaging studies in experimental autoimmune encephalomyelitis analyzed inflammatory markers such as cellular immune responses, dendritic cell activity, blood brain barrier integrity and myelination, but none assessed fluorescently labeled antibodies within the central nervous system. This data suggests a strong association between autoantibody localization and disease. This system can be used to detect other antibodies that might contribute to the pathogenesis of autoimmune diseases of the central nervous system including multiple sclerosis.
MeSH term(s)	Animals ; Antibodies, Monoclonal/chemistry ; Antibodies, Monoclonal/immunology ; Blood-Brain Barrier/metabolism ; Brain/diagnostic imaging ; Central Nervous System/diagnostic imaging ; Central Nervous System/metabolism ; Disease Models, Animal ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Female ; Fluorescent Dyes/chemistry ; Heterogeneous Nuclear Ribonucleoprotein A1/immunology ; Matrix Metalloproteinases/metabolism ; Mice ; Mice, Inbred C57BL ; Spectroscopy, Near-Infrared ; Spinal Cord/diagnostic imaging
Chemical Substances	Antibodies, Monoclonal ; Fluorescent Dyes ; Heterogeneous Nuclear Ribonucleoprotein A1 ; Matrix Metalloproteinases (EC 3.4.24.-)
Language	English
Publishing date	2019-02-15
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0212357
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Dysfunctional RNA-binding protein biology and neurodegeneration in experimental autoimmune encephalomyelitis in female mice.

Salapa, Hannah E / Libner, Cole D / Levin, Michael C

Journal of neuroscience research

2019 Volume 98, Issue 4, Page(s) 704–717

Abstract: Altered stress granule (SG) and RNA-binding protein (RBP) biology have been shown to contribute to the pathogenesis of several neurodegenerative diseases, yet little is known about their role in multiple sclerosis (MS). Pathological features associated ... ...

Abstract	Altered stress granule (SG) and RNA-binding protein (RBP) biology have been shown to contribute to the pathogenesis of several neurodegenerative diseases, yet little is known about their role in multiple sclerosis (MS). Pathological features associated with dysfunctional RBPs include RBP mislocalization from its normal nuclear location to the cytoplasm and the formation of chronic SGs. We tested the hypothesis that altered SG and RBP biology might contribute to the neurodegeneration in experimental autoimmune encephalomyelitis (EAE). C57BL/6 female mice were actively immunized with MOG
MeSH term(s)	Animals ; DNA-Binding Proteins/metabolism ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Encephalomyelitis, Autoimmune, Experimental/pathology ; Female ; Gray Matter/metabolism ; Gray Matter/pathology ; Heterogeneous Nuclear Ribonucleoprotein A1/metabolism ; Mice, Inbred C57BL ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/pathology ; Neurons/metabolism ; Neurons/pathology ; RNA-Binding Proteins/metabolism ; Spinal Cord/metabolism ; Spinal Cord/pathology ; Stress, Physiological
Chemical Substances	DNA-Binding Proteins ; Heterogeneous Nuclear Ribonucleoprotein A1 ; Hnrnpa1 protein, mouse ; RNA-Binding Proteins ; TDP-43 protein, mouse
Language	English
Publishing date	2019-11-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	195324-2
ISSN	1097-4547 ; 0360-4012
ISSN (online)	1097-4547
ISSN	0360-4012
DOI	10.1002/jnr.24554
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 1232: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Neuronal RNA-binding protein dysfunction in multiple sclerosis cortex.

Salapa, Hannah E / Hutchinson, Catherine / Popescu, Bogdan F / Levin, Michael C

Annals of clinical and translational neurology

2020 Volume 7, Issue 7, Page(s) 1214–1224

Abstract: Objective: Neurodegeneration is thought to be the primary cause of neurological disability in multiple sclerosis (MS). Dysfunctional RNA-binding proteins (RBPs) including their mislocalization from nucleus to cytoplasm, stress granule formation, and ... ...

Abstract	Objective: Neurodegeneration is thought to be the primary cause of neurological disability in multiple sclerosis (MS). Dysfunctional RNA-binding proteins (RBPs) including their mislocalization from nucleus to cytoplasm, stress granule formation, and altered RNA metabolism have been found to underlie neurodegeneration in amyotrophic lateral sclerosis and frontotemporal dementia. Yet, little is known about the role of dysfunctional RBPs in the pathogenesis of neurodegeneration in MS. As a follow-up to our seminal finding of altered RBP function in a single case of MS, we posited that there would be evidence of RBP dysfunction in cortical neurons in MS. Methods: Cortical neurons from 12 MS and six control cases were analyzed by immunohistochemistry for heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) and TAR-DNA-binding protein-43 (TDP-43). Seven distinct neuronal phenotypes were identified based on the nucleocytoplasmic staining of these RBPs. Statistical analyses were performed by analyzing each phenotype in relation to MS versus controls. Results: Analyses revealed a continuum of hnRNP A1 and TDP-43 nucleocytoplasmic staining was found in cortical neurons, from neurons with entirely nuclear staining with little cytoplasmic staining in contrast to those with complete nuclear depletion of RBPs concurrent with robust cytoplasmic staining. The neuronal phenotypes that showed the most nucleocytoplasmic mislocalization of hnRNP A1 and TDP-43 statistically distinguished MS from control cases (P < 0.01, P < 0.001, respectively). Interpretation: The discovery of hnRNP A1 and TDP-43 nucleocytoplasmic mislocalization in neurons in MS brain demonstrate that dysfunctional RBPs may play a role in neurodegeneration in MS, as they do in other neurological diseases.
MeSH term(s)	Adult ; Aged ; Cerebral Cortex/metabolism ; DNA-Binding Proteins/metabolism ; Female ; Heterogeneous Nuclear Ribonucleoprotein A1/metabolism ; Humans ; Male ; Middle Aged ; Multiple Sclerosis/metabolism ; Multiple Sclerosis/pathology ; Neurons/classification ; Neurons/metabolism ; RNA-Binding Proteins/metabolism
Chemical Substances	DNA-Binding Proteins ; Heterogeneous Nuclear Ribonucleoprotein A1 ; RNA-Binding Proteins ; TARDBP protein, human ; hnRNPA1 protein, human
Language	English
Publishing date	2020-07-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2740696-9
ISSN	2328-9503 ; 2328-9503
ISSN (online)	2328-9503
ISSN	2328-9503
DOI	10.1002/acn3.51103
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito