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Article ; Online: Negative Regulation of Autophagy during Macrophage Infection by

Maldonado-Bravo, Rafael / Villaseñor, Tomás / Pedraza-Escalona, Martha / Pérez-Martínez, Leonor / Hernández-Pando, Rogelio / Pedraza-Alva, Gustavo

International journal of molecular sciences

2024 Volume 25, Issue 6

Abstract: Mycobacterium ... ...

Abstract	Mycobacterium tuberculosis
MeSH term(s)	Humans ; Mycobacterium bovis/physiology ; Chromatography, Liquid ; Tandem Mass Spectrometry ; Macrophages/metabolism ; Autophagy ; Mycobacterium Infections/metabolism ; Mycobacterium tuberculosis ; Protein Kinase C/metabolism
Chemical Substances	Protein Kinase C (EC 2.7.11.13)
Language	English
Publishing date	2024-03-09
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/ijms25063145
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Article ; Online: Adipose tissue IL-18 production is independent of caspase-1 and caspase-11.

Román-Domínguez, Luis / Salazar-León, Jonathan / Meza-Sosa, Karla F / Pérez-Martínez, Leonor / Pedraza-Alva, Gustavo

Immunity, inflammation and disease

2024 Volume 12, Issue 4, Page(s) e1241

Abstract: Background: Inflammation in adipose tissue, resulting from imbalanced caloric intake and energy expenditure, contributes to the metabolic dysregulation observed in obesity. The production of inflammatory cytokines, such as IL-1β and IL-18, plays a key ... ...

Abstract	Background: Inflammation in adipose tissue, resulting from imbalanced caloric intake and energy expenditure, contributes to the metabolic dysregulation observed in obesity. The production of inflammatory cytokines, such as IL-1β and IL-18, plays a key role in this process. While IL-1β promotes insulin resistance and diabetes, IL-18 regulates energy expenditure and food intake. Previous studies have suggested that caspase-1, activated by the Nlrp3 inflammasome in response to lipid excess, mediates IL-1β production, whereas activated by the Nlrp1b inflammasome in response to energy excess, mediates IL-18 production. However, this has not been formally tested. Methods: Wild-type and caspase-1-deficient Balb/c mice, carrying the Nlrp1b1 allele, were fed with regular chow or a high-fat diet for twelve weeks. Food intake and mass gain were recorded weekly. At the end of the twelve weeks, glucose tolerance and insulin resistance were evaluated. Mature IL-18 protein levels and the inflammatory process in the adipose tissue were determined. Fasting lipid and cytokine levels were quantified in the sera of the different experimental groups. Results: We found that IL-18 production in adipose tissue is independent of caspase-1 activity, regardless of the metabolic state, while Nlrp3-mediated IL-1β production remains caspase-1 dependent. Additionally, caspase-1 null Balb/c mice did not develop metabolic abnormalities in response to energy excess from the high-fat diet. Conclusion: Our findings suggest that IL-18 production in the adipose tissue is independent of Nlrp3 inflammasome and caspase-1 activation, regardless of caloric food intake. In contrast, Nlrp3-mediated IL-1β production is caspase-1 dependent. These results provide new insights into the mechanisms underlying cytokine production in the adipose tissue during both homeostatic conditions and metabolic stress, highlighting the distinct roles of caspase-1 and the Nlrp inflammasomes in regulating inflammatory responses.
MeSH term(s)	Animals ; Mice ; Adipose Tissue/metabolism ; Caspase 1/metabolism ; Caspases/metabolism ; Cytokines/metabolism ; Inflammasomes/metabolism ; Insulin Resistance ; Interleukin-18/metabolism ; Lipids ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Caspases, Initiator/metabolism
Chemical Substances	Caspase 1 (EC 3.4.22.36) ; Caspases (EC 3.4.22.-) ; Cytokines ; Inflammasomes ; Interleukin-18 ; Lipids ; NLR Family, Pyrin Domain-Containing 3 Protein ; Casp4 protein, mouse (EC 3.4.22.-) ; Caspases, Initiator (EC 3.4.22.-)
Language	English
Publishing date	2024-04-17
Publishing country	England
Document type	Journal Article
ZDB-ID	2740382-8
ISSN	2050-4527 ; 2050-4527
ISSN (online)	2050-4527
ISSN	2050-4527
DOI	10.1002/iid3.1241
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Article: Insights into Zika Virus Pathogenesis and Potential Therapeutic Strategies.

Camacho-Concha, Nohemi / Santana-Román, María E / Sánchez, Nilda C / Velasco, Iván / Pando-Robles, Victoria / Pedraza-Alva, Gustavo / Pérez-Martínez, Leonor

Biomedicines

2023 Volume 11, Issue 12

Abstract: Zika virus (ZIKV) has emerged as a significant public health threat, reaching pandemic levels in 2016. Human infection with ZIKV can manifest as either asymptomatic or as an acute illness characterized by symptoms such as fever and headache. Moreover, it ...

Abstract	Zika virus (ZIKV) has emerged as a significant public health threat, reaching pandemic levels in 2016. Human infection with ZIKV can manifest as either asymptomatic or as an acute illness characterized by symptoms such as fever and headache. Moreover, it has been associated with severe neurological complications in adults, including Guillain-Barre syndrome, and devastating fetal abnormalities, like microcephaly. The primary mode of transmission is through
Language	English
Publishing date	2023-12-15
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2720867-9
ISSN	2227-9059
ISSN	2227-9059
DOI	10.3390/biomedicines11123316
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Article ; Online: Microglial activation in Alzheimer's disease: The role of flavonoids and microRNAs.

Medrano-Jiménez, Elisa / Meza-Sosa, Karla F / Urbán-Aragón, José A / Secundino, Ismael / Pedraza-Alva, Gustavo / Pérez-Martínez, Leonor

Journal of leukocyte biology

2022 Volume 112, Issue 1, Page(s) 47–77

Abstract: Alzheimer's disease (AD) is the most common form of senile dementia and is characterized by progressive cognitive impairment and neuronal degeneration. Microglial activation is an important pathologic hallmark of AD. During disease progression, ... ...

Abstract	Alzheimer's disease (AD) is the most common form of senile dementia and is characterized by progressive cognitive impairment and neuronal degeneration. Microglial activation is an important pathologic hallmark of AD. During disease progression, microglial cells switch from an alternative or anti-inflammatory and neuroprotective profile (M2) to a classic or proinflammatory and neurotoxic profile (M1). Phenotypically, M1 microglia is characterized by the activation of inflammatory signaling pathways that cause increased expression of proinflammatory genes, including those coding for cytokines and chemokines. This microglia-mediated neuroinflammation contributes to neuronal cell death. Recent studies in microglial cells have shown that a group of plant-derived compounds, known as flavonoids, possess anti-inflammatory properties and therefore exert a neuroprotective effect through regulating microglia activation. Here, we discuss how flavonoids can promote the switch from an inflammatory M1 phenotype to an anti-inflammatory M2 phenotype in microglia and how this represents a valuable opportunity for the development of novel therapeutic strategies to blunt neuroinflammation and boost neuronal recovery in AD. We also review how certain flavonoids can inhibit neuroinflammation through their action on the expression of microglia-specific microRNAs (miRNAs), which also constitute a key therapeutic approach in different neuropathologies involving an inflammatory component, including AD. Finally, we propose novel targets of microglia-specific miRNAs that may be considered for AD treatment.
MeSH term(s)	Alzheimer Disease/drug therapy ; Alzheimer Disease/genetics ; Alzheimer Disease/metabolism ; Anti-Inflammatory Agents/pharmacology ; Flavonoids/pharmacology ; Flavonoids/therapeutic use ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Microglia/pathology
Chemical Substances	Anti-Inflammatory Agents ; Flavonoids ; MicroRNAs
Language	English
Publishing date	2022-03-16
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	605722-6
ISSN	1938-3673 ; 0741-5400
ISSN (online)	1938-3673
ISSN	0741-5400
DOI	10.1002/JLB.3MR1021-531R
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Article: Mycobacterium bovis BCG promotes IL-10 expression by establishing a SYK/PKCα/β positive autoregulatory loop that sustains STAT3 activation

Villaseñor, Tomás / Madrid-Paulino, Edgardo / Maldonado-Bravo, Rafael / Pérez-Martínez, Leonor / Pedraza-Alva, Gustavo

Pathogens and disease. 2019 June 07, v. 77, no. 3

2019

Abstract: Mycobacterium ensures its survival inside macrophages and long-term infection by subverting the innate and adaptive immune response through the modulation of cytokine gene expression profiles. Different Mycobacterium species promote the expression of ... ...

Abstract	Mycobacterium ensures its survival inside macrophages and long-term infection by subverting the innate and adaptive immune response through the modulation of cytokine gene expression profiles. Different Mycobacterium species promote the expression of TGFβ and IL-10, which, at the early stages of infection, block the formation of the phagolysosome, thereby securing mycobacterial survival upon phagocytosis, and at later stages, antagonize IFNγ production and functions. Despite the key role of IL-10 in mycobacterium infection, the signal transduction pathways leading to IL-10 expression in infected macrophages are poorly understood. Here, we report that Mycobacterium bovis BCG promotes IL-10 expression and cytokine production by establishing a SYK/PKCα/β positive feedback loop that leads to STAT3 activation.
Keywords	Mycobacterium bovis BCG ; adaptive immunity ; gene expression ; interleukin-10 ; macrophages ; mycobacterial diseases ; phagocytosis ; protein kinase C ; signal transduction ; transforming growth factor beta
Language	English
Dates of publication	2019-0607
Publishing place	Oxford University Press
Document type	Article
ISSN	2049-632X
DOI	10.1093/femspd/ftz032
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Article ; Online: Mycobacterium bovis BCG promotes IL-10 expression by establishing a SYK/PKCα/β positive autoregulatory loop that sustains STAT3 activation.

Villaseñor, Tomás / Madrid-Paulino, Edgardo / Maldonado-Bravo, Rafael / Pérez-Martínez, Leonor / Pedraza-Alva, Gustavo

Pathogens and disease

2019 Volume 77, Issue 3

Abstract	Mycobacterium ensures its survival inside macrophages and long-term infection by subverting the innate and adaptive immune response through the modulation of cytokine gene expression profiles. Different Mycobacterium species promote the expression of TGFβ and IL-10, which, at the early stages of infection, block the formation of the phagolysosome, thereby securing mycobacterial survival upon phagocytosis, and at later stages, antagonize IFNγ production and functions. Despite the key role of IL-10 in mycobacterium infection, the signal transduction pathways leading to IL-10 expression in infected macrophages are poorly understood. Here, we report that Mycobacterium bovis BCG promotes IL-10 expression and cytokine production by establishing a SYK/PKCα/β positive feedback loop that leads to STAT3 activation.
MeSH term(s)	Gene Expression ; Gene Expression Regulation ; Gene Regulatory Networks ; Humans ; Interleukin-10/biosynthesis ; Monocytes/immunology ; Mycobacterium bovis/immunology ; Protein Kinase C beta/metabolism ; Protein Kinase C-alpha/metabolism ; STAT3 Transcription Factor/metabolism ; Syk Kinase/metabolism ; THP-1 Cells
Chemical Substances	IL10 protein, human ; STAT3 Transcription Factor ; Interleukin-10 (130068-27-8) ; SYK protein, human (EC 2.7.10.2) ; Syk Kinase (EC 2.7.10.2) ; PRKCA protein, human (EC 2.7.11.13) ; Protein Kinase C beta (EC 2.7.11.13) ; Protein Kinase C-alpha (EC 2.7.11.13)
Language	English
Publishing date	2019-06-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	2049-632X
ISSN (online)	2049-632X
DOI	10.1093/femspd/ftz032
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Article ; Online: An enriched environment re-establishes metabolic homeostasis by reducing obesity-induced inflammation.

Díaz de León-Guerrero, Sol / Salazar-León, Jonathan / Meza-Sosa, Karla F / Valle-Garcia, David / Aguilar-León, Diana / Pedraza-Alva, Gustavo / Pérez-Martínez, Leonor

Disease models & mechanisms

2022 Volume 15, Issue 6

Abstract: Obesity can lead to chronic inflammation in different tissues, generating insulin and leptin resistance and alterations in glucose and lipid metabolism, favoring the development of degenerative diseases, including type II diabetes. Congruently, the ... ...

Abstract	Obesity can lead to chronic inflammation in different tissues, generating insulin and leptin resistance and alterations in glucose and lipid metabolism, favoring the development of degenerative diseases, including type II diabetes. Congruently, the inflammatory signaling inhibition prevents the development of obesity and restores insulin sensitivity. Via the enhancement of central nervous system activity, an enriched environment (EE) has beneficial effects on learning and memory as well as on immune cell functions and inflammation in different disease models. Here, we explored whether an EE can restore energy balance in obese mice that previously presented metabolic alterations. We discovered that an EE improved glucose metabolism, increased insulin signaling in liver, and reduced hepatic steatosis and inflammation, and increased lipolysis and browning in the white adipose tissue of high-fat diet (HFD)-fed mice. Finally, we found reduced inflammatory signaling and increased anorexigenic signaling in the hypothalamus of HFD-fed mice exposed to an EE. These data indicate that an EE is able to restore the metabolic imbalance caused by HFD feeding. Thus, we propose EE as a novel therapeutic approach for treating obesity-related metabolic alterations. This article has an associated First Person interview with the first author of the paper.
MeSH term(s)	Adipose Tissue/metabolism ; Animals ; Diabetes Mellitus, Type 2/metabolism ; Diet, High-Fat ; Homeostasis ; Humans ; Inflammation/complications ; Insulin Resistance ; Insulins/metabolism ; Insulins/pharmacology ; Liver/metabolism ; Mice ; Mice, Inbred C57BL ; Obesity/complications ; Obesity/metabolism
Chemical Substances	Insulins
Language	English
Publishing date	2022-06-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2451104-3
ISSN	1754-8411 ; 1754-8403
ISSN (online)	1754-8411
ISSN	1754-8403
DOI	10.1242/dmm.048936
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Article ; Online: SPARCLE, a p53-induced lncRNA, controls apoptosis after genotoxic stress by promoting PARP-1 cleavage.

Meza-Sosa, Karla F / Miao, Rui / Navarro, Francisco / Zhang, Zhibin / Zhang, Ying / Hu, Jun Jacob / Hartford, Corrine Corrina R / Li, Xiao Ling / Pedraza-Alva, Gustavo / Pérez-Martínez, Leonor / Lal, Ashish / Wu, Hao / Lieberman, Judy

Molecular cell

2022 Volume 82, Issue 4, Page(s) 785–802.e10

Abstract: p53, master transcriptional regulator of the genotoxic stress response, controls cell-cycle arrest and apoptosis following DNA damage. Here, we identify a p53-induced lncRNA suicidal PARP-1 cleavage enhancer (SPARCLE) adjacent to miR-34b/c required for ... ...

Abstract	p53, master transcriptional regulator of the genotoxic stress response, controls cell-cycle arrest and apoptosis following DNA damage. Here, we identify a p53-induced lncRNA suicidal PARP-1 cleavage enhancer (SPARCLE) adjacent to miR-34b/c required for p53-mediated apoptosis. SPARCLE is a ∼770-nt, nuclear lncRNA induced 1 day after DNA damage. Despite low expression (<16 copies/cell), SPARCLE deletion increases DNA repair and reduces DNA-damage-induced apoptosis as much as p53 deficiency, while its overexpression restores apoptosis in p53-deficient cells. SPARCLE does not alter gene expression. SPARCLE binds to PARP-1 with nanomolar affinity and causes apoptosis by acting as a caspase-3 cofactor for PARP-1 cleavage, which separates PARP-1's N-terminal (NT) DNA-binding domain from its catalytic domains. NT-PARP-1 inhibits DNA repair. Expressing NT-PARP-1 in SPARCLE-deficient cells increases unrepaired DNA damage and restores apoptosis after DNA damage. Thus, SPARCLE enhances p53-induced apoptosis by promoting PARP-1 cleavage, which interferes with DNA-damage repair.
MeSH term(s)	A549 Cells ; Animals ; Apoptosis ; Caspase 3/metabolism ; Colorectal Neoplasms/enzymology ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; DNA Breaks, Double-Stranded ; DNA Breaks, Single-Stranded ; DNA Repair ; Gene Expression Regulation, Neoplastic ; HCT116 Cells ; HEK293 Cells ; Hep G2 Cells ; Humans ; Male ; Mice, Nude ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Poly (ADP-Ribose) Polymerase-1/genetics ; Poly (ADP-Ribose) Polymerase-1/metabolism ; RNA, Long Noncoding/genetics ; RNA, Long Noncoding/metabolism ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Mice
Chemical Substances	MIRN34 microRNA, human ; MicroRNAs ; RNA, Long Noncoding ; TP53 protein, human ; Tumor Suppressor Protein p53 ; PARP1 protein, human (EC 2.4.2.30) ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30) ; CASP3 protein, human (EC 3.4.22.-) ; Caspase 3 (EC 3.4.22.-)
Language	English
Publishing date	2022-01-31
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2022.01.001
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Article: SPARCLE, a p53-induced lncRNA, controls apoptosis after genotoxic stress by promoting PARP-1 cleavage

Meza-Sosa, Karla F. / Miao, Rui / Navarro, Francisco / Zhang, Zhibin / Zhang, Ying / Hu, Jun Jacob / Hartford, Corrine Corrina R. / Li, Xiao Ling / Pedraza-Alva, Gustavo / Pérez-Martínez, Leonor / Lal, Ashish / Wu, Hao / Lieberman, Judy

Molecular cell. 2022 Feb. 17, v. 82, no. 4

2022

Abstract	p53, master transcriptional regulator of the genotoxic stress response, controls cell-cycle arrest and apoptosis following DNA damage. Here, we identify a p53-induced lncRNA suicidal PARP-1 cleavage enhancer (SPARCLE) adjacent to miR-34b/c required for p53-mediated apoptosis. SPARCLE is a ∼770-nt, nuclear lncRNA induced 1 day after DNA damage. Despite low expression (<16 copies/cell), SPARCLE deletion increases DNA repair and reduces DNA-damage-induced apoptosis as much as p53 deficiency, while its overexpression restores apoptosis in p53-deficient cells. SPARCLE does not alter gene expression. SPARCLE binds to PARP-1 with nanomolar affinity and causes apoptosis by acting as a caspase-3 cofactor for PARP-1 cleavage, which separates PARP-1’s N-terminal (NT) DNA-binding domain from its catalytic domains. NT-PARP-1 inhibits DNA repair. Expressing NT-PARP-1 in SPARCLE-deficient cells increases unrepaired DNA damage and restores apoptosis after DNA damage. Thus, SPARCLE enhances p53-induced apoptosis by promoting PARP-1 cleavage, which interferes with DNA-damage repair.
Keywords	DNA damage ; DNA repair ; DNA-binding domains ; apoptosis ; caspase-3 ; cell cycle checkpoints ; stress response ; transcription factors
Language	English
Dates of publication	2022-0217
Size	p. 785-802.e10.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	1415236-8
ISSN	1097-4164 ; 1097-2765
ISSN (online)	1097-4164
ISSN	1097-2765
DOI	10.1016/j.molcel.2022.01.001
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Article ; Online: Tumor Necrosis Factor-Induced miR-146a Upregulation Promotes Human Lung Adenocarcinoma Metastasis by Targeting Merlin.

Sánchez, Nilda C / Medrano-Jiménez, Elisa / Aguilar-León, Diana / Pérez-Martínez, Leonor / Pedraza-Alva, Gustavo

DNA and cell biology

2020 Volume 39, Issue 3, Page(s) 484–497

Abstract: Inflammation plays a key role in carcinogenesis and metastasis. This process involves the inactivation of tumor suppressor molecules, yet the molecular mechanisms by which inflammation impairs tumor suppressors are not completely understood. In this ... ...

Abstract	Inflammation plays a key role in carcinogenesis and metastasis. This process involves the inactivation of tumor suppressor molecules, yet the molecular mechanisms by which inflammation impairs tumor suppressors are not completely understood. In this study, we show that proinflammatory signals such as tumor necrosis factor (TNF) support lung cancer metastasis by reducing the levels of the tumor suppressor Merlin through regulation of miR-146a. Immunodeficient mice inoculated with A549 cells expressing high miR-146a levels and low Merlin protein levels exhibited reduced survival, which correlated with the number of metastatic nodes formed. Accordingly, restoring Merlin protein levels inhibited metastasis and increased survival of the mice. Consistent with these results, we found that elevated miR-146a expression levels correlated with low Merlin protein levels in human lung adenocarcinoma. Furthermore, human invasive and metastatic tumors showed higher TNF and miR-146a levels, but lower Merlin protein levels than noninvasive tumors. These findings indicate that upregulation of miR-146a by TNF in lung adenocarcinoma promotes Merlin protein inhibition and metastasis. Thus, we suggest that the ratio between miR-146a and Merlin protein levels could be a relevant molecular biomarker that can predict lung cancer progression and that the TNF/miR-146a/Merlin pathway is a promising new therapeutic target to inhibit lung adenocarcinoma progression.
MeSH term(s)	Adenocarcinoma of Lung/genetics ; Adenocarcinoma of Lung/metabolism ; Adenocarcinoma of Lung/pathology ; Aged ; Aged, 80 and over ; Animals ; Cell Line, Tumor ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Male ; Mice ; Mice, Inbred NOD ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Middle Aged ; Neoplasm Metastasis ; Neurofibromin 2/genetics ; Neurofibromin 2/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Up-Regulation
Chemical Substances	MIRN146 microRNA, human ; MicroRNAs ; Neurofibromin 2 ; Tumor Necrosis Factor-alpha
Language	English
Publishing date	2020-01-30
Publishing country	United States
Document type	Journal Article
ZDB-ID	1024454-2
ISSN	1557-7430 ; 0198-0238 ; 1044-5498
ISSN (online)	1557-7430
ISSN	0198-0238 ; 1044-5498
DOI	10.1089/dna.2019.4620
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