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Article ; Online: SARS-CoV-2 Spike Targets USP33-IRF9 Axis

Mishra, Ritu / Banerjea, Akhil C

2021 Volume 12, Page(s) 656700

Abstract: SARS-CoV-2, the novel coronavirus infection has consistently shown an association with neurological anomalies in patients, in addition to its usual respiratory distress syndrome. Multi-organ dysfunctions including neurological sequelae during COVID-19 ... ...

Abstract	SARS-CoV-2, the novel coronavirus infection has consistently shown an association with neurological anomalies in patients, in addition to its usual respiratory distress syndrome. Multi-organ dysfunctions including neurological sequelae during COVID-19 persist even after declining viral load. We propose that SARS-CoV-2 gene product, Spike, is able to modify the host exosomal cargo, which gets transported to distant uninfected tissues and organs and can initiate a catastrophic immune cascade within Central Nervous System (CNS). SARS-CoV-2 Spike transfected cells release a significant amount of exosomes loaded with microRNAs such as miR-148a and miR-590. microRNAs gets internalized by human microglia and suppress target gene expression of USP33 (Ubiquitin Specific peptidase 33) and downstream IRF9 levels. Cellular levels of USP33 regulate the turnover time of IRF9
MeSH term(s)	COVID-19/genetics ; COVID-19/metabolism ; COVID-19/physiopathology ; COVID-19/virology ; Cell Line ; Central Nervous System/immunology ; Central Nervous System/physiopathology ; Central Nervous System/virology ; Endopeptidases/metabolism ; Exosomes/genetics ; Exosomes/metabolism ; Exosomes/pathology ; Humans ; Inflammation/immunology ; Inflammation/virology ; Interferon-Stimulated Gene Factor 3, gamma Subunit/metabolism ; Interferon-beta/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Microglia/metabolism ; Microglia/pathology ; NF-kappa B/metabolism ; Protein Stability ; SARS-CoV-2/metabolism ; Spike Glycoprotein, Coronavirus/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Ubiquitin Thiolesterase/metabolism
Chemical Substances	IRF9 protein, human ; Interferon-Stimulated Gene Factor 3, gamma Subunit ; MIRN148 microRNA, human ; MIRN590 microRNA, human ; MicroRNAs ; NF-kappa B ; Spike Glycoprotein, Coronavirus ; Tumor Necrosis Factor-alpha ; spike protein, SARS-CoV-2 ; Interferon-beta (77238-31-4) ; Endopeptidases (EC 3.4.-) ; USP33 protein, human (EC 3.4.19.12) ; Ubiquitin Thiolesterase (EC 3.4.19.12) ; ubiquitin isopeptidase (EC 3.4.99.-)
Language	English
Publishing date	2021-04-14
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.656700
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Article: Human Immunodeficiency Virus Type 1 Vif Up-Regulates the Expression of Tat

Lata, Sneh / Sood, Vikas / Banerjea, Akhil C

Frontiers in microbiology

2022 Volume 13, Page(s) 828430

Abstract: Human immunodeficiency virus type 1 (HIV-1) has RNA genome and depends on host cellular machinery for most of its activities. Host cellular proteins modulate the expression and activity of viral proteins to combat the virus. HIV-1 proteins are known to ... ...

Abstract	Human immunodeficiency virus type 1 (HIV-1) has RNA genome and depends on host cellular machinery for most of its activities. Host cellular proteins modulate the expression and activity of viral proteins to combat the virus. HIV-1 proteins are known to regulate each other for the benefit of virus by exploiting these modulations. Here, we report that HIV-1 Vif increases the levels of Tat
Language	English
Publishing date	2022-03-21
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2587354-4
ISSN	1664-302X
ISSN	1664-302X
DOI	10.3389/fmicb.2022.828430
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Article ; Online: Neurological Damage by Coronaviruses: A Catastrophe in the Queue!

Mishra, Ritu / Banerjea, Akhil C

Frontiers in immunology

2020 Volume 11, Page(s) 565521

Abstract: Neurological disorders caused by neuroviral infections are an obvious pathogenic manifestation. However, non-neurotropic viruses or peripheral viral infections pose a considerable challenge as their neuropathological manifestations do not emerge because ... ...

Abstract	Neurological disorders caused by neuroviral infections are an obvious pathogenic manifestation. However, non-neurotropic viruses or peripheral viral infections pose a considerable challenge as their neuropathological manifestations do not emerge because of primary infection. Their secondary or bystander pathologies develop much later, like a syndrome, during and after the recovery of patients from the primary disease. Massive inflammation caused by peripheral viral infections can trigger multiple neurological anomalies. These neurological damages may range from a general cognitive and motor dysfunction up to a wide spectrum of CNS anomalies, such as Acute Necrotizing Hemorrhagic Encephalopathy, Guillain-Barré syndrome, Encephalitis, Meningitis, anxiety, and other audio-visual disabilities. Peripheral viruses like Measles virus, Enteroviruses, Influenza viruses (HIN1 series), SARS-CoV-1, MERS-CoV, and, recently, SARS-CoV-2 are reported to cause various neurological manifestations in patients and are proven to be neuropathogenic even in cellular and animal model systems. This review presents a comprehensive picture of CNS susceptibilities toward these peripheral viral infections and explains some common underlying themes of their neuropathology in the human brain.
MeSH term(s)	Animals ; Betacoronavirus/immunology ; Blood-Brain Barrier/immunology ; Blood-Brain Barrier/virology ; COVID-19 ; Coronavirus Infections/complications ; Coronavirus Infections/immunology ; Coronavirus Infections/virology ; Cytokines/blood ; Disease Models, Animal ; Humans ; Microglia/immunology ; Microglia/virology ; Middle East Respiratory Syndrome Coronavirus/immunology ; Neurogenic Inflammation/complications ; Neurogenic Inflammation/immunology ; Neurogenic Inflammation/virology ; Pandemics ; Pneumonia, Viral/complications ; Pneumonia, Viral/immunology ; Pneumonia, Viral/virology ; Severe acute respiratory syndrome-related coronavirus/immunology ; SARS-CoV-2 ; Severe Acute Respiratory Syndrome/complications ; Severe Acute Respiratory Syndrome/immunology ; Severe Acute Respiratory Syndrome/virology
Chemical Substances	Cytokines
Keywords	covid19
Language	English
Publishing date	2020-09-10
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.565521
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Article: STUB1/CHIP promotes ubiquitination and degradation of HIV-1 Vif to restore the cellular level of APOBEC3G protein

Ali, Amjad / Kumar, Vivek / Banerjea, Akhil C.

Biochemical and biophysical research communications. 2021 Oct. 15, v. 574

2021

Abstract: HIV-1 accessory protein Vif is required for neutralization of cellular restriction factor APOBEC3G through its ubiquitination and proteasomal degradation which allows replication of HIV-1 in non-permissive cells. This function of Vif is required for ... ...

Abstract	HIV-1 accessory protein Vif is required for neutralization of cellular restriction factor APOBEC3G through its ubiquitination and proteasomal degradation which allows replication of HIV-1 in non-permissive cells. This function of Vif is required for maintaining the genomic integrity of HIV-1. We here report that the Vif interacts with the cellular E3 ubiquitin ligase CHIP and the level of Vif protein gets reduced by the expression of CHIP. Reduction of Vif by CHIP expression is due to its increased rate of degradation as shown by cycloheximide (CHX) chase assay. CHIP expression also resulted in the ubiquitination of Vif protein in a dose dependent manner. The role of CHIP in the ubiquitination and degradation was confirmed by the endogenous knockdown of CHIP using CRISPR Cas9 method. Loss of endogenous CHIP protein showed the stabilization of Vif with concomitant destabilization of APOBEC3G. As expected Vif mediated ubiquitination of APOBEC3G was also reduced in CHIP knockdown cells. These results established that CHIP functions as a negative regulator of Vif protein which in-turn stabilizes APOBEC3G.
Keywords	cycloheximide ; dose response ; genomics ; neutralization ; research ; ubiquitin-protein ligase ; ubiquitination
Language	English
Dates of publication	2021-1015
Size	p. 27-32.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2021.08.031
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Article ; Online: Dengue Virus Dysregulates Master Transcription Factors and PI3K/AKT/mTOR Signaling Pathway in Megakaryocytes.

Lahon, Anismrita / Arya, Ravi P / Banerjea, Akhil C

Frontiers in cellular and infection microbiology

2021 Volume 11, Page(s) 715208

Abstract: Dengue virus (DENV) infection can cause either self-limited dengue fever or hemorrhagic complications. Low platelet count is one of the manifestations of dengue fever. Megakaryocytes are the sole producers of platelets. However, the role of both host and ...

Abstract	Dengue virus (DENV) infection can cause either self-limited dengue fever or hemorrhagic complications. Low platelet count is one of the manifestations of dengue fever. Megakaryocytes are the sole producers of platelets. However, the role of both host and viral factors in megakaryocyte development, maturation, and platelet production is largely unknown in DENV infection. PI3K/AKT/mTOR pathway plays a significant role in cell survival, maturation, and megakaryocyte development. We were interested to check whether pathogenic insult can impact this pathway. We observed decreased expression of most of the major key molecules associated with the PI3K/AKT/mTOR pathway in DENV infected MEG-01 cells. In this study, the involvement of PI3K/AKT/mTOR pathway in megakaryocyte development and maturation was confirmed with the use of specific inhibitors in infected MEG-01 cells. Our results showed that direct pharmacologic inhibition of this pathway greatly impacted megakaryopoiesis associated molecule CD61 and some essential transcription factors (GATA-1, GATA-2, and NF-E2). Additionally, we observed apoptosis in megakaryocytes due to DENV infection. Our results may suggest that DENV impairs PI3K/AKT/mTOR axis and molecules involved in the development and maturation of megakaryocytes. It is imperative to investigate the role of these molecules in the context of megakaryopoiesis during DENV infection to better understand the pathways and mechanisms, which in turn might provide insights into the development of antiviral strategies.
MeSH term(s)	Cell Line ; Dengue Virus ; Humans ; Megakaryocytes/metabolism ; Megakaryocytes/virology ; Phosphatidylinositol 3-Kinases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism ; Transcription Factors/metabolism
Chemical Substances	Transcription Factors ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2021-08-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2619676-1
ISSN	2235-2988 ; 2235-2988
ISSN (online)	2235-2988
ISSN	2235-2988
DOI	10.3389/fcimb.2021.715208
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Article ; Online: STUB1/CHIP promotes ubiquitination and degradation of HIV-1 Vif to restore the cellular level of APOBEC3G protein.

Ali, Amjad / Kumar, Vivek / Banerjea, Akhil C

Biochemical and biophysical research communications

2021 Volume 574, Page(s) 27–32

Abstract	HIV-1 accessory protein Vif is required for neutralization of cellular restriction factor APOBEC3G through its ubiquitination and proteasomal degradation which allows replication of HIV-1 in non-permissive cells. This function of Vif is required for maintaining the genomic integrity of HIV-1. We here report that the Vif interacts with the cellular E3 ubiquitin ligase CHIP and the level of Vif protein gets reduced by the expression of CHIP. Reduction of Vif by CHIP expression is due to its increased rate of degradation as shown by cycloheximide (CHX) chase assay. CHIP expression also resulted in the ubiquitination of Vif protein in a dose dependent manner. The role of CHIP in the ubiquitination and degradation was confirmed by the endogenous knockdown of CHIP using CRISPR Cas9 method. Loss of endogenous CHIP protein showed the stabilization of Vif with concomitant destabilization of APOBEC3G. As expected Vif mediated ubiquitination of APOBEC3G was also reduced in CHIP knockdown cells. These results established that CHIP functions as a negative regulator of Vif protein which in-turn stabilizes APOBEC3G.
MeSH term(s)	APOBEC-3G Deaminase/metabolism ; Cells, Cultured ; Humans ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination ; vif Gene Products, Human Immunodeficiency Virus/metabolism
Chemical Substances	vif Gene Products, Human Immunodeficiency Virus ; vif protein, Human immunodeficiency virus 1 ; STUB1 protein, human (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; APOBEC-3G Deaminase (EC 3.5.4.5) ; APOBEC3G protein, human (EC 3.5.4.5)
Language	English
Publishing date	2021-08-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2021.08.031
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Article ; Online: Japanese Encephalitis Virus infection increases USP42 to stabilize TRIM21 and OAS1 for neuroinflammatory and anti-viral response in human microglia.

Mishra, Ritu / Kumawat, Kanhaiya Lal / Basu, Anirban / Banerjea, Akhil C

Virology

2022 Volume 573, Page(s) 131–140

Abstract: Japanese Encephalitis Virus (JEV), a member virus of Flaviviridae family causes Japanese encephalitis (JE). JE is a mosquito-borne disease, spread mainly by Culex spp. During JE, dysregulated inflammatory responses play a central role in neuronal death ... ...

Abstract	Japanese Encephalitis Virus (JEV), a member virus of Flaviviridae family causes Japanese encephalitis (JE). JE is a mosquito-borne disease, spread mainly by Culex spp. During JE, dysregulated inflammatory responses play a central role in neuronal death and damage leading to Neuroinflammation. In this study, we show that JEV infection in human microglial cells (CHME3) reduces the cellular miR-590-3p levels. miR-590-3p could directly target the expression levels of USP42 (Ubiquitin Specific Peptidase 42) resulting in increased cellular levels of USP42 upon JEV infection. Our results suggest that USP42 stabilizes cellular TRIM21 via deubiquitinating them. We also established through various in vitro and in vivo experiments that increased USP42 can maintain a higher cellular level of both TRIM21 as well as OAS1. This study also suggests that TRIM21, independently of its RING domain, can increase USP42 level in a positive feedback loop and induces the cellular OAS1 levels in human microglial cells.
MeSH term(s)	2',5'-Oligoadenylate Synthetase/metabolism ; Animals ; Encephalitis Virus, Japanese ; Encephalitis, Japanese ; Humans ; MicroRNAs/metabolism ; Microglia/metabolism ; Ribonucleoproteins/metabolism ; Thiolester Hydrolases/metabolism
Chemical Substances	MIRN590 microRNA, human ; MicroRNAs ; Ribonucleoproteins ; SS-A antigen ; USP42 protein, human ; OAS1 protein, human (EC 2.7.7.-) ; 2',5'-Oligoadenylate Synthetase (EC 2.7.7.84) ; Thiolester Hydrolases (EC 3.1.2.-)
Language	English
Publishing date	2022-06-25
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2022.06.012
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Article: JEV infection increases USP42 to stabilize TRIM21 and OAS1 for neuroinflammatory and anti-viral response in human microglia

Mishra, Ritu / Kumawat, Kanhaiya Lal / Basu, Anirban / Banerjea, Akhil C.

Virology. 2022 June 22,

2022

Abstract: Japanese Encephalitis Virus (JEV), a member virus of Flaviviridae family causes Japanese encephalitis (JE). JE is a mosquito-borne disease, spread mainly by Culexspp. During JE, dysregulated inflammatory responses play a central role in neuronal death ... ...

Abstract	Japanese Encephalitis Virus (JEV), a member virus of Flaviviridae family causes Japanese encephalitis (JE). JE is a mosquito-borne disease, spread mainly by Culexspp. During JE, dysregulated inflammatory responses play a central role in neuronal death and damage leading to Neuroinflammation. In this study, we show that JEV infection in human microglial cells (CHME3) reduces the cellular miR-590-3p levels. miR-590-3p could directly target the expression levels of USP42 (Ubiquitin Specific Peptidase 42) resulting in increased cellular levels of USP42 upon JEV infection. Our results suggest that USP42 stabilizes cellular TRIM21 via deubiquitinating them. We also established through various in vitro and in vivo experiments that increased USP42 can maintain a higher cellular level of both TRIM21 as well as OAS1. This study also suggests that TRIM21, independently of its RING domain, can increase USP42 level in a positive feedback loop and induces the cellular OAS1 levels in human microglial cells.
Keywords	Japanese encephalitis virus ; death ; encephalitis ; humans ; mosquito-borne diseases ; neuroglia ; neurons ; ubiquitin ; virology ; viruses
Language	English
Dates of publication	2022-0622
Publishing place	Elsevier Inc.
Document type	Article
Note	Pre-press version
ZDB-ID	200425-2
ISSN	1096-0341 ; 0042-6822
ISSN (online)	1096-0341
ISSN	0042-6822
DOI	10.1016/j.virol.2022.06.012
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Article: Neurological Damage by Coronaviruses: A Catastrophe in the Queue!

Mishra, Ritu / Banerjea, Akhil C

Front Immunol

Abstract	Neurological disorders caused by neuroviral infections are an obvious pathogenic manifestation. However, non-neurotropic viruses or peripheral viral infections pose a considerable challenge as their neuropathological manifestations do not emerge because of primary infection. Their secondary or bystander pathologies develop much later, like a syndrome, during and after the recovery of patients from the primary disease. Massive inflammation caused by peripheral viral infections can trigger multiple neurological anomalies. These neurological damages may range from a general cognitive and motor dysfunction up to a wide spectrum of CNS anomalies, such as Acute Necrotizing Hemorrhagic Encephalopathy, Guillain-Barré syndrome, Encephalitis, Meningitis, anxiety, and other audio-visual disabilities. Peripheral viruses like Measles virus, Enteroviruses, Influenza viruses (HIN1 series), SARS-CoV-1, MERS-CoV, and, recently, SARS-CoV-2 are reported to cause various neurological manifestations in patients and are proven to be neuropathogenic even in cellular and animal model systems. This review presents a comprehensive picture of CNS susceptibilities toward these peripheral viral infections and explains some common underlying themes of their neuropathology in the human brain.
Keywords	covid19
Publisher	WHO
Document type	Article
Note	WHO #Covidence: #805569
Database	COVID19

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Article ; Online: Dengue Virus Degrades USP33-ATF3 Axis via Extracellular Vesicles to Activate Human Microglial Cells.

Mishra, Ritu / Lahon, Anismrita / Banerjea, Akhil C

Journal of immunology (Baltimore, Md. : 1950)

2020 Volume 205, Issue 7, Page(s) 1787–1798

Abstract: Dengue virus (DENV) infection disrupts host innate immune signaling at various checkpoints. Cellular levels and stability of intermediate signaling molecules are a crucial hijacking point for a successful viral pathogenesis. Stability and turnover of all ...

Abstract	Dengue virus (DENV) infection disrupts host innate immune signaling at various checkpoints. Cellular levels and stability of intermediate signaling molecules are a crucial hijacking point for a successful viral pathogenesis. Stability and turnover of all the cellular proteins including intermediate signaling molecules are principally regulated by proteasomal degradation pathway. In this study, we show that how DENV infection and particularly DENV-NS1 can modulate the host extracellular vesicle (EV) cargo to manipulate the deubiquitination machinery of the human microglial cell (CHME3). We have performed EV harvesting, size analysis by nanoparticle tracking analysis, identification of cargo microRNA via quantitative PCR, microRNA target validation by overexpression, and knockdown via mimics and anti-miRs, immunoblotting, dual luciferase reporter assay, in vivo ubiquitination assay, chase assay, and promoter activity assay to reach the conclusion. In this study, we show that DENV-infected monocytes and DENV-NS1-transfected cells release high amounts of EVs loaded with miR-148a. These EVs get internalized by human microglial cells, and miR-148a suppresses the ubiquitin-specific peptidase 33 (USP33) protein expression levels via binding to its 3' untranslated region. Reduced USP33 in turn decreases the stability of cellular ATF3 protein via deubiquitylation. ATF3 acts as a suppressor of major proinflammatory gene expression pathways of TNF-α, NF-κB, and IFN-β. Our mechanistic model explains how DENV uses the EV pathway to transfer miR-148a for modulating USP33 and downstream ATF3 levels in human microglial cells and contributes in neuroinflammation within the CNS.
MeSH term(s)	Activating Transcription Factor 3/metabolism ; Animals ; Cell Line ; Cells, Cultured ; Culicidae ; Cytokines/metabolism ; Dengue/immunology ; Dengue/virology ; Dengue Virus/physiology ; Extracellular Vesicles/metabolism ; Gene Expression Regulation ; Host-Pathogen Interactions ; Humans ; Inflammation Mediators/metabolism ; MicroRNAs/genetics ; Microglia/physiology ; Neurogenic Inflammation/immunology ; Neurogenic Inflammation/virology ; Signal Transduction ; Ubiquitin Thiolesterase/metabolism ; Ubiquitination/genetics ; Virus Replication
Chemical Substances	ATF3 protein, human ; Activating Transcription Factor 3 ; Cytokines ; Inflammation Mediators ; MIRN148 microRNA, human ; MicroRNAs ; USP33 protein, human (EC 3.4.19.12) ; Ubiquitin Thiolesterase (EC 3.4.19.12)
Language	English
Publishing date	2020-08-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
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.2000411
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