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Article ; Online: A BAX door to venetoclax resistance.

Izzo, Franco / Landau, Dan A

2022 Volume 139, Issue 8, Page(s) 1124–1126

MeSH term(s)	Bridged Bicyclo Compounds, Heterocyclic/pharmacology ; Bridged Bicyclo Compounds, Heterocyclic/therapeutic use ; Sulfonamides/pharmacology ; Sulfonamides/therapeutic use ; bcl-2-Associated X Protein
Chemical Substances	Bridged Bicyclo Compounds, Heterocyclic ; Sulfonamides ; bcl-2-Associated X Protein ; venetoclax (N54AIC43PW)
Language	English
Publishing date	2022-02-24
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	80069-7
ISSN	1528-0020 ; 0006-4971
ISSN (online)	1528-0020
ISSN	0006-4971
DOI	10.1182/blood.2021013788
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Zs.MO 364: Show issues

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Article ; Online: Genetic and epigenetic determinants of B-cell lymphoma evolution.

Izzo, Franco / Landau, Dan A

Current opinion in hematology

2016 Volume 23, Issue 4, Page(s) 392–401

Abstract: Purpose of review: The success of targeted therapies fostered the development of increasingly specific and effective therapeutics for B-cell malignancies. However, cancer plasticity facilitates disease relapse, whereby intratumoral heterogeneity fuels ... ...

Abstract	Purpose of review: The success of targeted therapies fostered the development of increasingly specific and effective therapeutics for B-cell malignancies. However, cancer plasticity facilitates disease relapse, whereby intratumoral heterogeneity fuels tumor evolution into a more aggressive and resistant form. Understanding cancer heterogeneity and the evolutionary processes underlying disease relapse is key for overcoming this limitation of current treatment strategies. In the present review, we delineate the current understanding of cancer evolution and the advances in both genetic and epigenetic fields, with a focus on non-Hodgkin B-cell lymphomas. Recent findings: The use of massively parallel sequencing has provided insights into tumor heterogeneity, allowing determination of intratumoral genetic and epigenetic variability and identification of cancer driver mutations and (epi-)mutations. Increased heterogeneity prior to treatment results in faster disease relapse, and in many cases studying pretreatment clonal admixtures predicts the future evolutionary trajectory of relapsed disease. Summary: Understanding the mechanisms underlying tumor heterogeneity and evolution provides valuable tools for the design of therapy within an evolutionary framework. This framework will ultimately aid in accurately predicting the evolutionary paths of B-cell malignancies, thereby guiding therapeutic strategies geared at directly anticipating and addressing cancer evolution.
MeSH term(s)	Clonal Evolution ; Disease Progression ; Epigenesis, Genetic ; Gene Expression Regulation, Neoplastic ; Genetic Heterogeneity ; Genetic Predisposition to Disease ; Humans ; Lymphoma, B-Cell/genetics ; Lymphoma, B-Cell/pathology ; Lymphoma, B-Cell/therapy ; Molecular Targeted Therapy ; Mutation ; Recurrence
Language	English
Publishing date	2016-07
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0000000000000258
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Article ; Online: MAVS signaling is required for preventing persistent chikungunya heart infection and chronic vascular tissue inflammation.

Noval, Maria G / Spector, Sophie N / Bartnicki, Eric / Izzo, Franco / Narula, Navneet / Yeung, Stephen T / Damani-Yokota, Payal / Dewan, M Zahidunnabi / Mezzano, Valeria / Rodriguez-Rodriguez, Bruno A / Loomis, Cynthia / Khanna, Kamal M / Stapleford, Kenneth A

Nature communications

2023 Volume 14, Issue 1, Page(s) 4668

Abstract: Chikungunya virus (CHIKV) infection has been associated with severe cardiac manifestations, yet, how CHIKV infection leads to heart disease remains unknown. Here, we leveraged both mouse models and human primary cardiac cells to define the mechanisms of ... ...

Abstract	Chikungunya virus (CHIKV) infection has been associated with severe cardiac manifestations, yet, how CHIKV infection leads to heart disease remains unknown. Here, we leveraged both mouse models and human primary cardiac cells to define the mechanisms of CHIKV heart infection. Using an immunocompetent mouse model of CHIKV infection as well as human primary cardiac cells, we demonstrate that CHIKV directly infects and actively replicates in cardiac fibroblasts. In immunocompetent mice, CHIKV is cleared from cardiac tissue without significant damage through the induction of a local type I interferon response from both infected and non-infected cardiac cells. Using mice deficient in major innate immunity signaling components, we found that signaling through the mitochondrial antiviral-signaling protein (MAVS) is required for viral clearance from the heart. In the absence of MAVS signaling, persistent infection leads to focal myocarditis and vasculitis of the large vessels attached to the base of the heart. Large vessel vasculitis was observed for up to 60 days post infection, suggesting CHIKV can lead to vascular inflammation and potential long-lasting cardiovascular complications. This study provides a model of CHIKV cardiac infection and mechanistic insight into CHIKV-induced heart disease, underscoring the importance of monitoring cardiac function in patients with CHIKV infections.
MeSH term(s)	Animals ; Humans ; Mice ; Chikungunya Fever ; Chikungunya virus ; Communicable Diseases ; Disease Models, Animal ; Heart Diseases ; Inflammation ; Persistent Infection ; Vasculitis ; Virus Replication
Chemical Substances	MAVS protein, human ; IPS-1 protein, mouse
Language	English
Publishing date	2023-08-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-40047-w
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Article ; Online: Single-cell multi-omics of human clonal hematopoiesis reveals that DNMT3A R882 mutations perturb early progenitor states through selective hypomethylation.

Nam, Anna S / Dusaj, Neville / Izzo, Franco / Murali, Rekha / Myers, Robert M / Mouhieddine, Tarek H / Sotelo, Jesus / Benbarche, Salima / Waarts, Michael / Gaiti, Federico / Tahri, Sabrin / Levine, Ross / Abdel-Wahab, Omar / Godley, Lucy A / Chaligne, Ronan / Ghobrial, Irene / Landau, Dan A

Nature genetics

2022 Volume 54, Issue 10, Page(s) 1514–1526

Abstract: Somatic mutations in cancer genes have been detected in clonal expansions across healthy human tissue, including in clonal hematopoiesis. However, because mutated and wild-type cells are admixed, we have limited ability to link genotypes with phenotypes. ...

Abstract	Somatic mutations in cancer genes have been detected in clonal expansions across healthy human tissue, including in clonal hematopoiesis. However, because mutated and wild-type cells are admixed, we have limited ability to link genotypes with phenotypes. To overcome this limitation, we leveraged multi-modality single-cell sequencing, capturing genotype, transcriptomes and methylomes in progenitors from individuals with DNMT3A R882 mutated clonal hematopoiesis. DNMT3A mutations result in myeloid over lymphoid bias, and an expansion of immature myeloid progenitors primed toward megakaryocytic-erythroid fate, with dysregulated expression of lineage and leukemia stem cell markers. Mutated DNMT3A leads to preferential hypomethylation of polycomb repressive complex 2 targets and a specific CpG flanking motif. Notably, the hypomethylation motif is enriched in binding motifs of key hematopoietic transcription factors, serving as a potential mechanistic link between DNMT3A mutations and aberrant transcriptional phenotypes. Thus, single-cell multi-omics paves the road to defining the downstream consequences of mutations that drive clonal mosaicism.
MeSH term(s)	Clonal Hematopoiesis ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA Methyltransferase 3A/genetics ; DNA Modification Methylases/genetics ; Hematopoiesis/genetics ; Humans ; Mutation ; Polycomb Repressive Complex 2/genetics
Chemical Substances	DNMT3A protein, human ; DNA Modification Methylases (EC 2.1.1.-) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; DNA Methyltransferase 3A (EC 2.1.1.37) ; Polycomb Repressive Complex 2 (EC 2.1.1.43)
Language	English
Publishing date	2022-09-22
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	1108734-1
ISSN	1546-1718 ; 1061-4036
ISSN (online)	1546-1718
ISSN	1061-4036
DOI	10.1038/s41588-022-01179-9
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Zs.A 3613: 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)
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Article ; Online: Jak2V617F Reversible Activation Shows Its Essential Requirement in Myeloproliferative Neoplasms.

Dunbar, Andrew J / Bowman, Robert L / Park, Young C / O'Connor, Kavi / Izzo, Franco / Myers, Robert M / Karzai, Abdul / Zaroogian, Zachary / Kim, Won Jun / Fernández-Maestre, Inés / Waarts, Michael R / Nazir, Abbas / Xiao, Wenbin / Codilupi, Tamara / Brodsky, Max / Farina, Mirko / Cai, Louise / Cai, Sheng F / Wang, Benjamin /

An, Wenbin / Yang, Julie L / Mowla, Shoron / Eisman, Shira E / Hanasoge Somasundara, Amritha Varshini / Glass, Jacob L / Mishra, Tanmay / Houston, Remie / Guzzardi, Emily / Martinez Benitez, Anthony R / Viny, Aaron D / Koche, Richard P / Meyer, Sara C / Landau, Dan A / Levine, Ross L

Cancer discovery

2024 Volume 14, Issue 5, Page(s) 737–751

Abstract: Gain-of-function mutations activating JAK/STAT signaling are seen in the majority of patients with myeloproliferative neoplasms (MPN), most commonly JAK2V617F. Although clinically approved JAK inhibitors improve symptoms and outcomes in MPNs, remissions ... ...

Abstract	Gain-of-function mutations activating JAK/STAT signaling are seen in the majority of patients with myeloproliferative neoplasms (MPN), most commonly JAK2V617F. Although clinically approved JAK inhibitors improve symptoms and outcomes in MPNs, remissions are rare, and mutant allele burden does not substantively change with chronic therapy. We hypothesized this is due to limitations of current JAK inhibitors to potently and specifically abrogate mutant JAK2 signaling. We therefore developed a conditionally inducible mouse model allowing for sequential activation, and then inactivation, of Jak2V617F from its endogenous locus using a combined Dre-rox/Cre-lox dual-recombinase system. Jak2V617F deletion abrogates MPN features, induces depletion of mutant-specific hematopoietic stem/progenitor cells, and extends overall survival to an extent not observed with pharmacologic JAK inhibition, including when cooccurring with somatic Tet2 loss. Our data suggest JAK2V617F represents the best therapeutic target in MPNs and demonstrate the therapeutic relevance of a dual-recombinase system to assess mutant-specific oncogenic dependencies in vivo. Significance: Current JAK inhibitors to treat myeloproliferative neoplasms are ineffective at eradicating mutant cells. We developed an endogenously expressed Jak2V617F dual-recombinase knock-in/knock-out model to investigate Jak2V617F oncogenic reversion in vivo. Jak2V617F deletion abrogates MPN features and depletes disease-sustaining MPN stem cells, suggesting improved Jak2V617F targeting offers the potential for greater therapeutic efficacy. See related commentary by Celik and Challen, p. 701. This article is featured in Selected Articles from This Issue, p. 695.
MeSH term(s)	Animals ; Humans ; Mice ; Disease Models, Animal ; Hematopoietic Stem Cells/metabolism ; Janus Kinase 2/genetics ; Janus Kinase 2/metabolism ; Mutation ; Myeloproliferative Disorders/genetics ; Myeloproliferative Disorders/drug therapy ; Signal Transduction
Chemical Substances	Janus Kinase 2 (EC 2.7.10.2) ; Jak2 protein, mouse (EC 2.7.10.2)
Language	English
Publishing date	2024-01-16
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2625242-9
ISSN	2159-8290 ; 2159-8274
ISSN (online)	2159-8290
ISSN	2159-8274
DOI	10.1158/2159-8290.CD-22-0952
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Article ; Online: Mapping genotypes to chromatin accessibility profiles in single cells.

Izzo, Franco / Myers, Robert M / Ganesan, Saravanan / Mekerishvili, Levan / Kottapalli, Sanjay / Prieto, Tamara / Eton, Elliot O / Botella, Theo / Dunbar, Andrew J / Bowman, Robert L / Sotelo, Jesus / Potenski, Catherine / Mimitou, Eleni P / Stahl, Maximilian / El Ghaity-Beckley, Sebastian / Arandela, JoAnn / Raviram, Ramya / Choi, Daniel C / Hoffman, Ronald /

Chaligné, Ronan / Abdel-Wahab, Omar / Smibert, Peter / Ghobrial, Irene M / Scandura, Joseph M / Marcellino, Bridget / Levine, Ross L / Landau, Dan A

Nature

2024

Abstract: In somatic tissue differentiation, chromatin accessibility changes govern priming and precursor commitment towards cellular ... ...

Abstract	In somatic tissue differentiation, chromatin accessibility changes govern priming and precursor commitment towards cellular fates
Language	English
Publishing date	2024-05-08
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/s41586-024-07388-y
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Zs.A 26: 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)
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Article ; Online: Specification of fetal liver endothelial progenitors to functional zonated adult sinusoids requires c-Maf induction.

Gómez-Salinero, Jesus Maria / Izzo, Franco / Lin, Yang / Houghton, Sean / Itkin, Tomer / Geng, Fuqiang / Bram, Yaron / Adelson, Robert P / Lu, Tyler M / Inghirami, Giorgio / Xiang, Jenny Zhaoying / Lis, Raphael / Redmond, David / Schreiner, Ryan / Rabbany, Sina Y / Landau, Dan A / Schwartz, Robert E / Rafii, Shahin

Cell stem cell

2022 Volume 29, Issue 4, Page(s) 593–609.e7

Abstract: The liver vascular network is patterned by sinusoidal and hepatocyte co-zonation. How intra-liver vessels acquire their hierarchical specialized functions is unknown. We study heterogeneity of hepatic vascular cells during mouse development through ... ...

Abstract	The liver vascular network is patterned by sinusoidal and hepatocyte co-zonation. How intra-liver vessels acquire their hierarchical specialized functions is unknown. We study heterogeneity of hepatic vascular cells during mouse development through functional and single-cell RNA-sequencing. The acquisition of sinusoidal endothelial cell identity is initiated during early development and completed postnatally, originating from a pool of undifferentiated vascular progenitors at E12. The peri-natal induction of the transcription factor c-Maf is a critical switch for the sinusoidal identity determination. Endothelium-restricted deletion of c-Maf disrupts liver sinusoidal development, aberrantly expands postnatal liver hematopoiesis, promotes excessive postnatal sinusoidal proliferation, and aggravates liver pro-fibrotic sensitivity to chemical insult. Enforced c-Maf overexpression in generic human endothelial cells switches on a liver sinusoidal transcriptional program that maintains hepatocyte function. c-Maf represents an inducible intra-organotypic and niche-responsive molecular determinant of hepatic sinusoidal cell identity and lays the foundation for the strategies for vasculature-driven liver repair.
MeSH term(s)	Animals ; Capillaries ; Endothelial Cells ; Endothelium ; Liver/pathology ; Liver Cirrhosis/pathology ; Liver Regeneration ; Mice ; Proto-Oncogene Proteins c-maf
Chemical Substances	Maf protein, mouse ; Proto-Oncogene Proteins c-maf
Language	English
Publishing date	2022-03-31
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2375354-7
ISSN	1875-9777 ; 1934-5909
ISSN (online)	1875-9777
ISSN	1934-5909
DOI	10.1016/j.stem.2022.03.002
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Article ; Online: Correction: Halting ErbB-2 isoforms retrograde transport to the nucleus as a new theragnostic approach for triple-negative breast cancer.

Madera, Santiago / Izzo, Franco / Chervo, María F / Dupont, Agustina / Chiauzzi, Violeta A / Bruni, Sofia / Petrillo, Ezequiel / Merin, Sharon S / De Martino, Mara / Montero, Diego / Levit, Claudio / Lebersztein, Gabriel / Anfuso, Fabiana / Roldán Deamicis, Agustina / Mercogliano, María F / Proietti, Cecilia J / Schillaci, Roxana / Elizalde, Patricia V / Cordo Russo, Rosalía I

Cell death & disease

2023 Volume 14, Issue 12, Page(s) 833

Language	English
Publishing date	2023-12-15
Publishing country	England
Document type	Published Erratum
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-023-06339-1
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Article ; Online: Halting ErbB-2 isoforms retrograde transport to the nucleus as a new theragnostic approach for triple-negative breast cancer.

Cell death & disease

2022 Volume 13, Issue 5, Page(s) 447

Abstract: Triple-negative breast cancer (TNBC) is clinically defined by the absence of estrogen and progesterone receptors and the lack of membrane overexpression or gene amplification of receptor tyrosine kinase ErbB-2/HER2. Due to TNBC heterogeneity, clinical ... ...

Abstract	Triple-negative breast cancer (TNBC) is clinically defined by the absence of estrogen and progesterone receptors and the lack of membrane overexpression or gene amplification of receptor tyrosine kinase ErbB-2/HER2. Due to TNBC heterogeneity, clinical biomarkers and targeted therapies for this disease remain elusive. We demonstrated that ErbB-2 is localized in the nucleus (NErbB-2) of TNBC cells and primary tumors, from where it drives growth. We also discovered that TNBC expresses both wild-type ErbB-2 (WTErbB-2) and alternative ErbB-2 isoform c (ErbB-2c). Here, we revealed that the inhibitors of the retrograde transport Retro-2 and its cyclic derivative Retro-2.1 evict both WTErbB-2 and ErbB-2c from the nucleus of BC cells and tumors. Using BC cells from several molecular subtypes, as well as normal breast cells, we demonstrated that Retro-2 specifically blocks proliferation of BC cells expressing NErbB-2. Importantly, Retro-2 eviction of both ErbB-2 isoforms from the nucleus resulted in a striking growth abrogation in multiple TNBC preclinical models, including tumor explants and xenografts. Our mechanistic studies in TNBC cells revealed that Retro-2 induces a differential accumulation of WTErbB-2 at the early endosomes and the plasma membrane, and of ErbB-2c at the Golgi, shedding new light both on Retro-2 action on endogenous protein cargoes undergoing retrograde transport, and on the biology of ErbB-2 splicing variants. In addition, we revealed that the presence of a functional signal peptide and a nuclear export signal (NES), both located at the N-terminus of WTErbB-2, and absent in ErbB-2c, accounts for the differential subcellular distribution of ErbB-2 isoforms upon Retro-2 treatment. Our present discoveries provide evidence for the rational repurposing of Retro-2 as a novel therapeutic agent for TNBC.
MeSH term(s)	Cell Nucleus/metabolism ; Humans ; Protein Isoforms/genetics ; Protein Isoforms/metabolism ; Receptor, ErbB-2/metabolism ; Receptors, Progesterone/metabolism ; Triple Negative Breast Neoplasms/pathology
Chemical Substances	Protein Isoforms ; Receptors, Progesterone ; Receptor, ErbB-2 (EC 2.7.10.1)
Language	English
Publishing date	2022-05-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2541626-1
ISSN	2041-4889 ; 2041-4889
ISSN (online)	2041-4889
ISSN	2041-4889
DOI	10.1038/s41419-022-04855-0
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Article: EpiMethylTag: simultaneous detection of ATAC-seq or ChIP-seq signals with DNA methylation

Lhoumaud, Priscillia / Sethia, Gunjan / Izzo, Franco / Sakellaropoulos, Theodore / Snetkova, Valentina / Vidal, Simon / Badri, Sana / Cornwell, Macintosh / Di Giammartino, Dafne Campigli / Kim, Kyu-Tae / Apostolou, Effie / Stadtfeld, Matthias / Landau, Dan Avi / Skok, Jane

Genome biology. 2019 Dec., v. 20, no. 1

2019

Abstract: Activation of regulatory elements is thought to be inversely correlated with DNA methylation levels. However, it is difficult to determine whether DNA methylation is compatible with chromatin accessibility or transcription factor (TF) binding if assays ... ...

Abstract	Activation of regulatory elements is thought to be inversely correlated with DNA methylation levels. However, it is difficult to determine whether DNA methylation is compatible with chromatin accessibility or transcription factor (TF) binding if assays are performed separately. We developed a fast, low-input, low sequencing depth method, EpiMethylTag, that combines ATAC-seq or ChIP-seq (M-ATAC or M-ChIP) with bisulfite conversion, to simultaneously examine accessibility/TF binding and methylation on the same DNA. Here we demonstrate that EpiMethylTag can be used to study the functional interplay between chromatin accessibility and TF binding (CTCF and KLF4) at methylated sites.
Keywords	DNA ; DNA methylation ; bisulfites ; chromatin ; chromatin immunoprecipitation ; regulatory sequences ; transcription factors
Language	English
Dates of publication	2019-12
Size	p. 248.
Publishing place	BioMed Central
Document type	Article
ZDB-ID	2040529-7
ISSN	1474-760X ; 1465-6906
ISSN (online)	1474-760X
ISSN	1465-6906
DOI	10.1186/s13059-019-1853-6
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