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Article: CXCL8 - The First Chemokine.

Baggiolini, Marco

2015 Volume 6, Page(s) 285

Language	English
Publishing date	2015
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2015.00285
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Article: Glucocorticoids downregulate gene expression of GM-CSF, NAP-1/IL-8, and IL-6, but not of M-CSF in human fibroblasts.

Tobler, A / Meier, R / Seitz, M / Dewald, B / Baggiolini, M / Fey, M F

Blood

1992 Volume 79, Issue 1, Page(s) 45–51

Abstract: Cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage-CSF (M-CSF ... in the range of 1 hour. In contrast, dexamethasone (1 mumol/L) did not decrease M-CSF RNA levels and protein ... release. M-CSF RNA and protein levels were maintained even when dexamethasone (1 mumol/L) was present ...

Abstract	Cytokines such as granulocyte-macrophage colony-stimulating factor (GM-CSF), macrophage-CSF (M-CSF), neutrophil-activating peptide-1/interleukin-8 (NAP-1/IL-8), and interleukin-6 (IL-6) are pivotal in the regulation of hematopoiesis and immune responses. In mesenchymal cells, their expression is induced by tumor necrosis factor alpha (TNF) and other agents. We now show that, while induction of cytokine expression by TNF in human lung fibroblasts was parallel, glucocorticoid hormones differentially affected their production. Dexamethasone (1 mumol/L) concordantly repressed expression of GM-CSF, NAP-1/IL-8 and IL-6. RNA and protein levels were reduced to approximately 5%, 20%, and 30% of control cells, respectively, as determined by Northern blot analyses and immunoassays. A 50% reduction of RNA levels for all three cytokines occurred in the range of 1 hour. In contrast, dexamethasone (1 mumol/L) did not decrease M-CSF RNA levels and protein release. M-CSF RNA and protein levels were maintained even when dexamethasone (1 mumol/L) was present for the whole duration of a 48-hour TNF stimulation. Further experiments showed that dexamethasone downregulates expression of GM-CSF, NAP-1/IL-8, and IL-6 mainly by decreasing the mRNA stability of these cytokines, and that the dexamethasone-mediated repression of cytokine expression depends on ongoing protein and RNA syntheses. Our study suggests that glucocorticoid hormones repress expression of a set of cytokine genes important in conditions of stress. However, they seem not to affect M-CSF expression, which is likely to be more crucial in maintaining long-term functions of myeloid cells.
MeSH term(s)	Blotting, Northern ; Cells, Cultured ; Cycloheximide/pharmacology ; Dactinomycin/pharmacology ; Dexamethasone/pharmacology ; Embryo, Mammalian ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Gene Expression Regulation/drug effects ; Granulocyte-Macrophage Colony-Stimulating Factor/genetics ; Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Humans ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Interleukin-8/genetics ; Interleukin-8/metabolism ; Macrophage Colony-Stimulating Factor/genetics ; Macrophage Colony-Stimulating Factor/metabolism ; RNA/metabolism ; RNA, Messenger/metabolism ; Tumor Necrosis Factor-alpha/pharmacology
Chemical Substances	Interleukin-6 ; Interleukin-8 ; RNA, Messenger ; Tumor Necrosis Factor-alpha ; Dactinomycin (1CC1JFE158) ; RNA (63231-63-0) ; Dexamethasone (7S5I7G3JQL) ; Macrophage Colony-Stimulating Factor (81627-83-0) ; Granulocyte-Macrophage Colony-Stimulating Factor (83869-56-1) ; Cycloheximide (98600C0908)
Language	English
Publishing date	1992-01-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
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Zs.MO 364: Show issues

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Article ; Online: Combined small-molecule treatment accelerates maturation of human pluripotent stem cell-derived neurons.

Hergenreder, Emiliano / Minotti, Andrew P / Zorina, Yana / Oberst, Polina / Zhao, Zeping / Munguba, Hermany / Calder, Elizabeth L / Baggiolini, Arianna / Walsh, Ryan M / Liston, Conor / Levitz, Joshua / Garippa, Ralph / Chen, Shuibing / Ciceri, Gabriele / Studer, Lorenz

Nature biotechnology

2024

Abstract: The maturation of human pluripotent stem cell (hPSC)-derived neurons mimics the protracted timing of human brain development, extending over months to years for reaching adult-like function. Prolonged in vitro maturation presents a major challenge to ... ...

Abstract	The maturation of human pluripotent stem cell (hPSC)-derived neurons mimics the protracted timing of human brain development, extending over months to years for reaching adult-like function. Prolonged in vitro maturation presents a major challenge to stem cell-based applications in modeling and treating neurological disease. Therefore, we designed a high-content imaging assay based on morphological and functional readouts in hPSC-derived cortical neurons which identified multiple compounds that drive neuronal maturation including inhibitors of lysine-specific demethylase 1 and disruptor of telomerase-like 1 and activators of calcium-dependent transcription. A cocktail of four factors, GSK2879552, EPZ-5676, N-methyl-D-aspartate and Bay K 8644, collectively termed GENtoniK, triggered maturation across all parameters tested, including synaptic density, electrophysiology and transcriptomics. Maturation effects were further validated in cortical organoids, spinal motoneurons and non-neural lineages including melanocytes and pancreatic β-cells. The effects on maturation observed across a broad range of hPSC-derived cell types indicate that some of the mechanisms controlling the timing of human maturation might be shared across lineages.
Language	English
Publishing date	2024-01-02
Publishing country	United States
Document type	Journal Article
ZDB-ID	1311932-1
ISSN	1546-1696 ; 1087-0156
ISSN (online)	1546-1696
ISSN	1087-0156
DOI	10.1038/s41587-023-02031-z
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Article ; Online: Neutrophil Activation and the Role of Interleukin-8 and Related Cytokines.

Baggiolini, Marco

International archives of allergy and immunology

2009 Volume 99, Issue 2-4, Page(s) 196–199

Abstract: Neutrophils are usually the first blood cells to enter inflammatory lesions. They accumulate in high numbers, and perform defence functions that often lead to tissue damage as a consequence of release of lytic enzymes and oxygen-derived radicals. Like ... ...

Abstract	Neutrophils are usually the first blood cells to enter inflammatory lesions. They accumulate in high numbers, and perform defence functions that often lead to tissue damage as a consequence of release of lytic enzymes and oxygen-derived radicals. Like other leukocytes, the circulating neutrophils are in a resting state and are recruited into inflamed tissues by chemotactic stimuli. Several types of chemotactic agonists are known. Their formation in the tissues depends on the type of inflammatory injury. A single type of agonist may act initially, but the recruitment process usually depends on several agonists, which can act in concert since they bind to distinct receptors. Once the neutrophils have migrated into a diseased tissue, phagocytosis usually concurs in the triggering of product release.
Language	English
Publishing date	2009-09-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	1108932-5
ISSN	1423-0097 ; 1018-2438
ISSN (online)	1423-0097
ISSN	1018-2438
DOI	10.1159/000236247
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Article ; Online: DNA damage remodels the MITF interactome to increase melanoma genomic instability.

Binet, Romuald / Lambert, Jean-Philippe / Tomkova, Marketa / Tischfield, Samuel / Baggiolini, Arianna / Picaud, Sarah / Sarkar, Sovan / Louphrasitthiphol, Pakavarin / Dias, Diogo / Carreira, Suzanne / Humphrey, Timothy C / Fillipakopoulos, Panagis / White, Richard / Goding, Colin R

Genes & development

2024 Volume 38, Issue 1-2, Page(s) 70–94

Abstract: Since genome instability can drive cancer initiation and progression, cells have evolved highly effective and ubiquitous DNA damage response (DDR) programs. However, some cells (for example, in skin) are normally exposed to high levels of DNA-damaging ... ...

Abstract	Since genome instability can drive cancer initiation and progression, cells have evolved highly effective and ubiquitous DNA damage response (DDR) programs. However, some cells (for example, in skin) are normally exposed to high levels of DNA-damaging agents. Whether such high-risk cells possess lineage-specific mechanisms that tailor DNA repair to the tissue remains largely unknown. Using melanoma as a model, we show here that the microphthalmia-associated transcription factor MITF, a lineage addition oncogene that coordinates many aspects of melanocyte and melanoma biology, plays a nontranscriptional role in shaping the DDR. On exposure to DNA-damaging agents, MITF is phosphorylated at S325, and its interactome is dramatically remodeled; most transcription cofactors dissociate, and instead MITF interacts with the MRE11-RAD50-NBS1 (MRN) complex. Consequently, cells with high MITF levels accumulate stalled replication forks and display defects in homologous recombination-mediated repair associated with impaired MRN recruitment to DNA damage. In agreement with this, high MITF levels are associated with increased single-nucleotide and copy number variant burdens in melanoma. Significantly, the SUMOylation-defective MITF-E318K melanoma predisposition mutation recapitulates the effects of DNA-PKcs-phosphorylated MITF. Our data suggest that a nontranscriptional function of a lineage-restricted transcription factor contributes to a tissue-specialized modulation of the DDR that can impact cancer initiation.
MeSH term(s)	Humans ; Melanoma/genetics ; Microphthalmia-Associated Transcription Factor/genetics ; DNA Damage ; Genomic Instability/genetics ; DNA
Chemical Substances	Microphthalmia-Associated Transcription Factor ; DNA (9007-49-2) ; MITF protein, human
Language	English
Publishing date	2024-02-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	806684-x
ISSN	1549-5477 ; 0890-9369
ISSN (online)	1549-5477
ISSN	0890-9369
DOI	10.1101/gad.350740.123
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Article ; Online: An epigenetic barrier sets the timing of human neuronal maturation.

Ciceri, Gabriele / Baggiolini, Arianna / Cho, Hyein S / Kshirsagar, Meghana / Benito-Kwiecinski, Silvia / Walsh, Ryan M / Aromolaran, Kelly A / Gonzalez-Hernandez, Alberto J / Munguba, Hermany / Koo, So Yeon / Xu, Nan / Sevilla, Kaylin J / Goldstein, Peter A / Levitz, Joshua / Leslie, Christina S / Koche, Richard P / Studer, Lorenz

Nature

2024 Volume 626, Issue 8000, Page(s) 881–890

Abstract: The pace of human brain development is highly protracted compared with most other ... ...

Abstract	The pace of human brain development is highly protracted compared with most other species
MeSH term(s)	Adult ; Animals ; Humans ; Mice ; Epigenesis, Genetic ; Gene Expression Regulation, Developmental ; Histocompatibility Antigens/metabolism ; Histone-Lysine N-Methyltransferase/antagonists & inhibitors ; Histone-Lysine N-Methyltransferase/metabolism ; Human Embryonic Stem Cells/cytology ; Human Embryonic Stem Cells/metabolism ; Neural Stem Cells/cytology ; Neural Stem Cells/metabolism ; Neurogenesis/genetics ; Neurons/cytology ; Neurons/metabolism ; Time Factors ; Transcription, Genetic
Chemical Substances	DOT1L protein, human (EC 2.1.1.-) ; EHMT1 protein, human (EC 2.1.1.-) ; EHMT2 protein, human (EC 2.1.1.43) ; EZH2 protein, human (EC 2.1.1.43) ; Histocompatibility Antigens ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
Language	English
Publishing date	2024-01-31
Publishing country	England
Document type	Journal Article
ZDB-ID	120714-3
ISSN	1476-4687 ; 0028-0836
ISSN (online)	1476-4687
ISSN	0028-0836
DOI	10.1038/s41586-023-06984-8
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Zs.MG 9: Show issues
Zs.MO 244: Show issues

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Article ; Online: Generation of human cerebral organoids with a structured outer subventricular zone.

Walsh, Ryan M / Luongo, Raffaele / Giacomelli, Elisa / Ciceri, Gabriele / Rittenhouse, Chelsea / Verrillo, Antonietta / Galimberti, Maura / Bocchi, Vittoria Dickinson / Wu, Youjun / Xu, Nan / Mosole, Simone / Muller, James / Vezzoli, Elena / Jungverdorben, Johannes / Zhou, Ting / Barker, Roger A / Cattaneo, Elena / Studer, Lorenz / Baggiolini, Arianna

Cell reports

2024 Volume 43, Issue 4, Page(s) 114031

Abstract: Outer radial glia (oRG) emerge as cortical progenitor cells that support the development of an enlarged outer subventricular zone (oSVZ) and the expansion of the neocortex. The in vitro generation of oRG is essential to investigate the underlying ... ...

Abstract	Outer radial glia (oRG) emerge as cortical progenitor cells that support the development of an enlarged outer subventricular zone (oSVZ) and the expansion of the neocortex. The in vitro generation of oRG is essential to investigate the underlying mechanisms of human neocortical development and expansion. By activating the STAT3 signaling pathway using leukemia inhibitory factor (LIF), which is not expressed in guided cortical organoids, we define a cortical organoid differentiation method from human pluripotent stem cells (hPSCs) that recapitulates the expansion of a progenitor pool into the oSVZ. The oSVZ comprises progenitor cells expressing specific oRG markers such as GFAP, LIFR, and HOPX, closely matching human fetal oRG. Finally, incorporating neural crest-derived LIF-producing cortical pericytes into cortical organoids recapitulates the effects of LIF treatment. These data indicate that increasing the cellular complexity of the organoid microenvironment promotes the emergence of oRG and supports a platform to study oRG in hPSC-derived brain organoids routinely.
MeSH term(s)	Humans ; Organoids/metabolism ; Organoids/cytology ; Leukemia Inhibitory Factor/metabolism ; Leukemia Inhibitory Factor/pharmacology ; Cell Differentiation ; Pluripotent Stem Cells/metabolism ; Pluripotent Stem Cells/cytology ; Lateral Ventricles/cytology ; Lateral Ventricles/metabolism ; STAT3 Transcription Factor/metabolism ; Neuroglia/metabolism ; Neuroglia/cytology ; Signal Transduction
Chemical Substances	Leukemia Inhibitory Factor ; STAT3 Transcription Factor
Language	English
Publishing date	2024-04-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2024.114031
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Article ; Online: Lipid droplets are a metabolic vulnerability in melanoma.

Lumaquin-Yin, Dianne / Montal, Emily / Johns, Eleanor / Baggiolini, Arianna / Huang, Ting-Hsiang / Ma, Yilun / LaPlante, Charlotte / Suresh, Shruthy / Studer, Lorenz / White, Richard M

Nature communications

2023 Volume 14, Issue 1, Page(s) 3192

Abstract: Melanoma exhibits numerous transcriptional cell states including neural crest-like cells as well as pigmented melanocytic cells. How these different cell states relate to distinct tumorigenic phenotypes remains unclear. Here, we use a zebrafish melanoma ... ...

Abstract	Melanoma exhibits numerous transcriptional cell states including neural crest-like cells as well as pigmented melanocytic cells. How these different cell states relate to distinct tumorigenic phenotypes remains unclear. Here, we use a zebrafish melanoma model to identify a transcriptional program linking the melanocytic cell state to a dependence on lipid droplets, the specialized organelle responsible for lipid storage. Single-cell RNA-sequencing of these tumors show a concordance between genes regulating pigmentation and those involved in lipid and oxidative metabolism. This state is conserved across human melanoma cell lines and patient tumors. This melanocytic state demonstrates increased fatty acid uptake, an increased number of lipid droplets, and dependence upon fatty acid oxidative metabolism. Genetic and pharmacologic suppression of lipid droplet production is sufficient to disrupt cell cycle progression and slow melanoma growth in vivo. Because the melanocytic cell state is linked to poor outcomes in patients, these data indicate a metabolic vulnerability in melanoma that depends on the lipid droplet organelle.
MeSH term(s)	Animals ; Humans ; Lipid Droplets/metabolism ; Zebrafish/genetics ; Melanoma/pathology ; Melanocytes/metabolism ; Fatty Acids/metabolism ; Lipid Metabolism/genetics
Chemical Substances	Fatty Acids
Language	English
Publishing date	2023-06-02
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-38831-9
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Article ; Online: Synergistic Pharmacological Therapy to Modulate Glial Cells in Spinal Cord Injury.

Veneruso, Valeria / Petillo, Emilia / Pizzetti, Fabio / Orro, Alessandro / Comolli, Davide / De Paola, Massimiliano / Verrillo, Antonietta / Baggiolini, Arianna / Votano, Simona / Castiglione, Franca / Sponchioni, Mattia / Forloni, Gianluigi / Rossi, Filippo / Veglianese, Pietro

Advanced materials (Deerfield Beach, Fla.)

2023 Volume 36, Issue 3, Page(s) e2307747

Abstract: Current treatments for modulating the glial-mediated inflammatory response after spinal cord injury (SCI) have limited ability to improve recovery. This is quite likely due to the lack of a selective therapeutic approach acting on microgliosis and ... ...

Abstract	Current treatments for modulating the glial-mediated inflammatory response after spinal cord injury (SCI) have limited ability to improve recovery. This is quite likely due to the lack of a selective therapeutic approach acting on microgliosis and astrocytosis, the glia components most involved after trauma, while maximizing efficacy and minimizing side effects. A new nanogel that can selectively release active compounds in microglial cells and astrocytes is developed and characterized. The degree of selectivity and subcellular distribution of the nanogel is evaluated by applying an innovative super-resolution microscopy technique, expansion microscopy. Two different administration schemes are then tested in a SCI mouse model: in an early phase, the nanogel loaded with Rolipram, an anti-inflammatory drug, achieves significant improvement in the animal's motor performance due to the increased recruitment of microglia and macrophages that are able to localize the lesion. Treatment in the late phase, however, gives opposite results, with worse motor recovery because of the widespread degeneration. These findings demonstrate that the nanovector can be selective and functional in the treatment of the glial component in different phases of SCI. They also open a new therapeutic scenario for tackling glia-mediated inflammation after neurodegenerative events in the central nervous system.
MeSH term(s)	Mice ; Animals ; Nanogels/therapeutic use ; Spinal Cord Injuries/pathology ; Neuroglia/pathology ; Microglia ; Polyethylene Glycols ; Polyethyleneimine
Chemical Substances	polyethylene glycol polyethyleneimine nanogel ; Nanogels ; Polyethylene Glycols (3WJQ0SDW1A) ; Polyethyleneimine (9002-98-6)
Language	English
Publishing date	2023-12-02
Publishing country	Germany
Document type	Journal Article
ZDB-ID	1474949-X
ISSN	1521-4095 ; 0935-9648
ISSN (online)	1521-4095
ISSN	0935-9648
DOI	10.1002/adma.202307747
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Article: DNA damage-induced interaction between a lineage addiction oncogenic transcription factor and the MRN complex shapes a tissue-specific DNA Damage Response and cancer predisposition.

Binet, Romuald / Lambert, Jean-Philippe / Tomkova, Marketa / Tischfield, Samuel / Baggiolini, Arianna / Picaud, Sarah / Sarkar, Sovan / Louphrasitthiphol, Pakavarin / Dias, Diogo / Carreira, Suzanne / Humphrey, Timothy / Fillipakopoulos, Panagis / White, Richard / Goding, Colin R

bioRxiv : the preprint server for biology

2023

Abstract: Since genome instability can drive cancer initiation and progression, cells have evolved highly effective and ubiquitous DNA Damage Response (DDR) programs. However, some cells, in skin for example, are normally exposed to high levels of DNA damaging ... ...

Abstract	Since genome instability can drive cancer initiation and progression, cells have evolved highly effective and ubiquitous DNA Damage Response (DDR) programs. However, some cells, in skin for example, are normally exposed to high levels of DNA damaging agents. Whether such high-risk cells possess lineage-specific mechanisms that tailor DNA repair to the tissue remains largely unknown. Here we show, using melanoma as a model, that the microphthalmia-associated transcription factor MITF, a lineage addition oncogene that coordinates many aspects of melanocyte and melanoma biology, plays a non-transcriptional role in shaping the DDR. On exposure to DNA damaging agents, MITF is phosphorylated by ATM/DNA-PKcs, and unexpectedly its interactome is dramatically remodelled; most transcription (co)factors dissociate, and instead MITF interacts with the MRE11-RAD50-NBS1 (MRN) complex. Consequently, cells with high MITF levels accumulate stalled replication forks, and display defects in homologous recombination-mediated repair associated with impaired MRN recruitment to DNA damage. In agreement, high MITF levels are associated with increased SNV burden in melanoma. Significantly, the SUMOylation-defective MITF-E318K melanoma predisposition mutation recapitulates the effects of ATM/DNA-PKcs-phosphorylated MITF. Our data suggest that a non-transcriptional function of a lineage-restricted transcription factor contributes to a tissue-specialised modulation of the DDR that can impact cancer initiation.
Language	English
Publishing date	2023-04-21
Publishing country	United States
Document type	Preprint
DOI	10.1101/2023.04.21.537819
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