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Article ; Online: Genome-wide CRISPR/Cas9 screen identifies regulators of BCMA expression on multiple myeloma cells.

Ajore, Ram / Mattsson, Jenny / Pertesi, Maroulio / Ekdahl, Ludvig / Ali, Zain / Hansson, Markus / Nilsson, Björn

2024 Volume 14, Issue 1, Page(s) 21

MeSH term(s)	Humans ; Multiple Myeloma/genetics ; Multiple Myeloma/metabolism ; B-Cell Maturation Antigen ; CRISPR-Cas Systems ; Cell Line, Tumor
Chemical Substances	B-Cell Maturation Antigen
Language	English
Publishing date	2024-01-25
Publishing country	United States
Document type	Letter ; Research Support, Non-U.S. Gov't
ZDB-ID	2600560-8
ISSN	2044-5385 ; 2044-5385
ISSN (online)	2044-5385
ISSN	2044-5385
DOI	10.1038/s41408-024-00986-z
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Article ; Online: MPRAscore: robust and non-parametric analysis of massively parallel reporter assays.

Niroula, Abhishek / Ajore, Ram / Nilsson, Björn

Bioinformatics (Oxford, England)

2019 Volume 35, Issue 24, Page(s) 5351–5353

Abstract: Motivation: Massively parallel reporter assays (MPRA) enable systematic screening of DNA sequence variants for effects on transcriptional activity. However, convenient analysis tools are still needed.: Results: We introduce MPRAscore, a novel tool to ...

Abstract	Motivation: Massively parallel reporter assays (MPRA) enable systematic screening of DNA sequence variants for effects on transcriptional activity. However, convenient analysis tools are still needed. Results: We introduce MPRAscore, a novel tool to infer allele-specific effects on transcription from MPRA data. MPRAscore uses a weighted, variance-regularized method to calculate variant effect sizes robustly, and a permutation approach to test for significance without assuming normality or independence. Availability and implementation: Source code (C++), precompiled binaries and data used in the paper at https://github.com/abhisheknrl/MPRAscore and https://www.ncbi.nlm.nih.gov/bioproject/PRJNA554195. Supplementary information: Supplementary data are available at Bioinformatics online.
MeSH term(s)	Alleles ; Biological Assay ; Software
Language	English
Publishing date	2019-07-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1422668-6
ISSN	1367-4811 ; 1367-4803
ISSN (online)	1367-4811
ISSN	1367-4803
DOI	10.1093/bioinformatics/btz591
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Article ; Online: Accelerating target deconvolution for therapeutic antibody candidates using highly parallelized genome editing.

Mattsson, Jenny / Ekdahl, Ludvig / Junghus, Fredrik / Ajore, Ram / Erlandsson, Eva / Niroula, Abhishek / Pertesi, Maroulio / Frendéus, Björn / Teige, Ingrid / Nilsson, Björn

Nature communications

2021 Volume 12, Issue 1, Page(s) 1277

Abstract: Therapeutic antibodies are transforming the treatment of cancer and autoimmune diseases. Today, a key challenge is finding antibodies against new targets. Phenotypic discovery promises to achieve this by enabling discovery of antibodies with therapeutic ... ...

Abstract	Therapeutic antibodies are transforming the treatment of cancer and autoimmune diseases. Today, a key challenge is finding antibodies against new targets. Phenotypic discovery promises to achieve this by enabling discovery of antibodies with therapeutic potential without specifying the molecular target a priori. Yet, deconvoluting the targets of phenotypically discovered antibodies remains a bottleneck; efficient deconvolution methods are needed for phenotypic discovery to reach its full potential. Here, we report a comprehensive investigation of a target deconvolution approach based on pooled CRISPR/Cas9. Applying this approach within three real-world phenotypic discovery programs, we rapidly deconvolute the targets of 38 of 39 test antibodies (97%), a success rate far higher than with existing approaches. Moreover, the approach scales well, requires much less work, and robustly identifies antibodies against the major histocompatibility complex. Our data establish CRISPR/Cas9 as a highly efficient target deconvolution approach, with immediate implications for the development of antibody-based drugs.
MeSH term(s)	Antibodies/metabolism ; CRISPR-Cas Systems/genetics ; Cell Line, Tumor ; Cell Survival/genetics ; Cell Survival/physiology ; Clustered Regularly Interspaced Short Palindromic Repeats/genetics ; Gene Editing ; Humans
Chemical Substances	Antibodies
Language	English
Publishing date	2021-02-24
Publishing country	England
Document type	Journal Article ; 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/s41467-021-21518-4
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Article ; Online: Accelerating target deconvolution for therapeutic antibody candidates using highly parallelized genome editing

Jenny Mattsson / Ludvig Ekdahl / Fredrik Junghus / Ram Ajore / Eva Erlandsson / Abhishek Niroula / Maroulio Pertesi / Björn Frendéus / Ingrid Teige / Björn Nilsson

Nature Communications, Vol 12, Iss 1, Pp 1-

2021 Volume 8

Abstract: Efficient deconvolution of antibody targets is needed for phenotype-based discovery. Here, the authors investigate a deconvolution approach based on pooled CRISPR Cas9 to achieve 97% deconvolution success rate. ...

Abstract	Efficient deconvolution of antibody targets is needed for phenotype-based discovery. Here, the authors investigate a deconvolution approach based on pooled CRISPR Cas9 to achieve 97% deconvolution success rate.
Keywords	Science ; Q
Language	English
Publishing date	2021-02-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Myeloid translocation gene-16 co-repressor promotes degradation of hypoxia-inducible factor 1.

Kumar, Parveen / Gullberg, Urban / Olsson, Inge / Ajore, Ram

PloS one

2015 Volume 10, Issue 5, Page(s) e0123725

Abstract: The myeloid translocation gene 16 (MTG16) co-repressor down regulates expression of multiple glycolytic genes, which are targets of the hypoxia-inducible factor 1 (HIF1) heterodimer transcription factor that is composed of oxygen-regulated labile HIF1α ... ...

Abstract	The myeloid translocation gene 16 (MTG16) co-repressor down regulates expression of multiple glycolytic genes, which are targets of the hypoxia-inducible factor 1 (HIF1) heterodimer transcription factor that is composed of oxygen-regulated labile HIF1α and stable HIF1β subunits. For this reason, we investigated whether MTG16 might regulate HIF1 negatively contributing to inhibition of glycolysis and stimulation of mitochondrial respiration. A doxycycline Tet-On system was used to control levels of MTG16 in B-lymphoblastic Raji cells. Results from co-association studies revealed MTG16 to interact with HIF1α. The co-association required intact N-terminal MTG16 residues including Nervy Homology Region 1 (NHR1). Furthermore, electrophoretic mobility shift assays demonstrated an association of MTG16 with hypoxia response elements (HREs) in PFKFB3, PFKFB4 and PDK1 promoters in-vitro. Results from chromatin immunoprecipitation assays revealed co-occupancy of these and other glycolytic gene promoters by HIF1α, HIF1β and MTG16 in agreement with possible involvement of these proteins in regulation of glycolytic target genes. In addition, MTG16 interacted with prolyl hydroxylase D2 and promoted ubiquitination and proteasomal degradation of HIF1α. Our findings broaden the area of MTG co-repressor functions and reveal MTG16 to be part of a protein complex that controls the levels of HIF1α.
MeSH term(s)	Aryl Hydrocarbon Receptor Nuclear Translocator/genetics ; Aryl Hydrocarbon Receptor Nuclear Translocator/metabolism ; B-Lymphocytes/cytology ; B-Lymphocytes/metabolism ; Cell Line, Tumor ; Chromatin Immunoprecipitation ; Gene Expression Regulation ; Glycolysis/genetics ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Hypoxia-Inducible Factor-Proline Dioxygenases/genetics ; Hypoxia-Inducible Factor-Proline Dioxygenases/metabolism ; Oxidative Phosphorylation ; Phosphofructokinase-2/genetics ; Phosphofructokinase-2/metabolism ; Promoter Regions, Genetic ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding ; Protein Stability ; Protein-Serine-Threonine Kinases/genetics ; Protein-Serine-Threonine Kinases/metabolism ; Proteolysis ; Pyruvate Dehydrogenase (Acetyl-Transferring) Kinase ; Repressor Proteins/genetics ; Repressor Proteins/metabolism ; Response Elements ; Signal Transduction ; Tumor Suppressor Proteins/genetics ; Tumor Suppressor Proteins/metabolism ; Ubiquitination
Chemical Substances	ARNT protein, human ; CBFA2T3 protein, human ; HIF1A protein, human ; Hypoxia-Inducible Factor 1, alpha Subunit ; PDK1 protein, human ; PFKFB4 protein, human ; Pyruvate Dehydrogenase (Acetyl-Transferring) Kinase ; Repressor Proteins ; Tumor Suppressor Proteins ; Aryl Hydrocarbon Receptor Nuclear Translocator (138391-32-9) ; EGLN1 protein, human (EC 1.14.11.2) ; Hypoxia-Inducible Factor-Proline Dioxygenases (EC 1.14.11.29) ; PFKFB3 protein, human (EC 2.7.1.105) ; Phosphofructokinase-2 (EC 2.7.1.105) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2015-05-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0123725
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Myeloid translocation gene-16 co-repressor promotes degradation of hypoxia-inducible factor 1.

Parveen Kumar / Urban Gullberg / Inge Olsson / Ram Ajore

PLoS ONE, Vol 10, Iss 5, p e

2015 Volume 0123725

Abstract	The myeloid translocation gene 16 (MTG16) co-repressor down regulates expression of multiple glycolytic genes, which are targets of the hypoxia-inducible factor 1 (HIF1) heterodimer transcription factor that is composed of oxygen-regulated labile HIF1α and stable HIF1β subunits. For this reason, we investigated whether MTG16 might regulate HIF1 negatively contributing to inhibition of glycolysis and stimulation of mitochondrial respiration. A doxycycline Tet-On system was used to control levels of MTG16 in B-lymphoblastic Raji cells. Results from co-association studies revealed MTG16 to interact with HIF1α. The co-association required intact N-terminal MTG16 residues including Nervy Homology Region 1 (NHR1). Furthermore, electrophoretic mobility shift assays demonstrated an association of MTG16 with hypoxia response elements (HREs) in PFKFB3, PFKFB4 and PDK1 promoters in-vitro. Results from chromatin immunoprecipitation assays revealed co-occupancy of these and other glycolytic gene promoters by HIF1α, HIF1β and MTG16 in agreement with possible involvement of these proteins in regulation of glycolytic target genes. In addition, MTG16 interacted with prolyl hydroxylase D2 and promoted ubiquitination and proteasomal degradation of HIF1α. Our findings broaden the area of MTG co-repressor functions and reveal MTG16 to be part of a protein complex that controls the levels of HIF1α.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2015-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Author Correction: Functional dissection of inherited non-coding variation influencing multiple myeloma risk.

Ajore, Ram / Niroula, Abhishek / Pertesi, Maroulio / Cafaro, Caterina / Thodberg, Malte / Went, Molly / Bao, Erik L / Duran-Lozano, Laura / Lopez de Lapuente Portilla, Aitzkoa / Olafsdottir, Thorunn / Ugidos-Damboriena, Nerea / Magnusson, Olafur / Samur, Mehmet / Lareau, Caleb A / Halldorsson, Gisli H / Thorleifsson, Gudmar / Norddahl, Gudmundur L / Gunnarsdottir, Kristbjorg / Försti, Asta /

Goldschmidt, Hartmut / Hemminki, Kari / van Rhee, Frits / Kimber, Scott / Sperling, Adam S / Kaiser, Martin / Anderson, Kenneth / Jonsdottir, Ingileif / Munshi, Nikhil / Rafnar, Thorunn / Waage, Anders / Weinhold, Niels / Thorsteinsdottir, Unnur / Sankaran, Vijay G / Stefansson, Kari / Houlston, Richard / Nilsson, Björn

Nature communications

2022 Volume 13, Issue 1, Page(s) 7725

Language	English
Publishing date	2022-12-13
Publishing country	England
Document type	Published Erratum
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-022-35411-1
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Article ; Online: Functional dissection of inherited non-coding variation influencing multiple myeloma risk.

Nature communications

2022 Volume 13, Issue 1, Page(s) 151

Abstract: Thousands of non-coding variants have been associated with increased risk of human diseases, yet the causal variants and their mechanisms-of-action remain obscure. In an integrative study combining massively parallel reporter assays (MPRA), expression ... ...

Abstract	Thousands of non-coding variants have been associated with increased risk of human diseases, yet the causal variants and their mechanisms-of-action remain obscure. In an integrative study combining massively parallel reporter assays (MPRA), expression analyses (eQTL, meQTL, PCHiC) and chromatin accessibility analyses in primary cells (caQTL), we investigate 1,039 variants associated with multiple myeloma (MM). We demonstrate that MM susceptibility is mediated by gene-regulatory changes in plasma cells and B-cells, and identify putative causal variants at six risk loci (SMARCD3, WAC, ELL2, CDCA7L, CEP120, and PREX1). Notably, three of these variants co-localize with significant plasma cell caQTLs, signaling the presence of causal activity at these precise genomic positions in an endogenous chromosomal context in vivo. Our results provide a systematic functional dissection of risk loci for a hematologic malignancy.
MeSH term(s)	Adaptor Proteins, Signal Transducing/genetics ; Adaptor Proteins, Signal Transducing/immunology ; Antineoplastic Combined Chemotherapy Protocols ; B-Lymphocytes/immunology ; B-Lymphocytes/pathology ; Base Sequence ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/immunology ; Chromatin/chemistry ; Chromatin/immunology ; Chromosomal Proteins, Non-Histone/genetics ; Chromosomal Proteins, Non-Histone/immunology ; DNA, Intergenic/genetics ; DNA, Intergenic/immunology ; Gene Expression Regulation, Neoplastic ; Genetic Predisposition to Disease ; Guanine Nucleotide Exchange Factors/genetics ; Guanine Nucleotide Exchange Factors/immunology ; Humans ; Inheritance Patterns ; Multiple Myeloma/drug therapy ; Multiple Myeloma/genetics ; Multiple Myeloma/immunology ; Multiple Myeloma/pathology ; Neoplasm Proteins/genetics ; Neoplasm Proteins/immunology ; Plasma Cells/immunology ; Plasma Cells/pathology ; Polymorphism, Genetic ; Primary Cell Culture ; Quantitative Trait Loci ; Repressor Proteins/genetics ; Repressor Proteins/immunology ; Risk Assessment ; Transcriptional Elongation Factors/genetics ; Transcriptional Elongation Factors/immunology
Chemical Substances	Adaptor Proteins, Signal Transducing ; CDCA7L protein, human ; CEP120 protein, human ; Cell Cycle Proteins ; Chromatin ; Chromosomal Proteins, Non-Histone ; DNA, Intergenic ; ELL2 protein, human ; Guanine Nucleotide Exchange Factors ; Neoplasm Proteins ; PREX1 protein, human ; Repressor Proteins ; SMARCD3 protein, human ; Transcriptional Elongation Factors ; WAC protein, human
Language	English
Publishing date	2022-01-10
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/s41467-021-27666-x
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Article ; Online: Author Correction: Germline variants at SOHLH2 influence multiple myeloma risk.

Duran-Lozano, Laura / Thorleifsson, Gudmar / Lopez de Lapuente Portilla, Aitzkoa / Niroula, Abhishek / Went, Molly / Thodberg, Malte / Pertesi, Maroulio / Ajore, Ram / Cafaro, Caterina / Olason, Pall I / Stefansdottir, Lilja / Bragi Walters, G / Halldorsson, Gisli H / Turesson, Ingemar / Kaiser, Martin F / Weinhold, Niels / Abildgaard, Niels / Andersen, Niels Frost / Mellqvist, Ulf-Henrik /

Waage, Anders / Juul-Vangsted, Annette / Thorsteinsdottir, Unnur / Hansson, Markus / Houlston, Richard / Rafnar, Thorunn / Stefansson, Kari / Nilsson, Björn

Blood cancer journal

2021 Volume 11, Issue 11, Page(s) 181

Language	English
Publishing date	2021-11-16
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2600560-8
ISSN	2044-5385 ; 2044-5385
ISSN (online)	2044-5385
ISSN	2044-5385
DOI	10.1038/s41408-021-00575-4
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Article ; Online: The leukemia associated ETO nuclear repressor gene is regulated by the GATA-1 transcription factor in erythroid/megakaryocytic cells

Gullberg Urban / Dhanda Rakesh / Ajore Ram / Olsson Inge

BMC Molecular Biology, Vol 11, Iss 1, p

2010 Volume 38

Abstract: Abstract Background The Eight-Twenty-One ( ETO ) nuclear co-repressor gene belongs to the ETO homologue family also containing Myeloid Translocation Gene on chromosome 16 (MTG16) and myeloid translocation Gene-Related protein 1 (MTGR1). By chromosomal ... ...

Abstract	Abstract Background The Eight-Twenty-One ( ETO ) nuclear co-repressor gene belongs to the ETO homologue family also containing Myeloid Translocation Gene on chromosome 16 (MTG16) and myeloid translocation Gene-Related protein 1 (MTGR1). By chromosomal translocations ETO and MTG16 become parts of fusion proteins characteristic of morphological variants of acute myeloid leukemia. Normal functions of ETO homologues have as yet not been examined. The goal of this work was to identify structural and functional promoter elements upstream of the coding sequence of the ETO gene in order to explore lineage-specific hematopoietic expression and get hints to function. Results A putative proximal ETO promoter was identified within 411 bp upstream of the transcription start site. Strong ETO promoter activity was specifically observed upon transfection of a promoter reporter construct into erythroid/megakaryocytic cells, which have endogeneous ETO gene activity. An evolutionary conserved region of 228 bp revealed potential cis -elements involved in transcription of ETO . Disruption of the evolutionary conserved GATA -636 consensus binding site repressed transactivation and disruption of the ETS1 -705 consensus binding site enhanced activity of the ETO promoter. The promoter was stimulated by overexpression of GATA-1 into erythroid/megakaryocytic cells. Electrophoretic mobility shift assay with erythroid/megakaryocytic cells showed specific binding of GATA-1 to the GATA -636 site. Furthermore, results from chromatin immunoprecipitation showed GATA-1 binding in vivo to the conserved region of the ETO promoter containing the -636 site. The results suggest that the GATA -636 site may have a role in activation of the ETO gene activity in cells with erythroid/megakaryocytic potential. Leukemia associated AML1 - ETO strongly suppressed an ETO promoter reporter in erythroid/megakaryocytic cells. Conclusions We demonstrate that the GATA-1 transcription factor binds and transactivates the ETO proximal promoter in an erythroid/megakaryocytic-specific manner. Thus, trans -acting factors that are essential in erythroid/megakaryocytic differentiation govern ETO expression.
Keywords	Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Subject code	570 ; 572
Language	English
Publishing date	2010-05-01T00:00:00Z
Publisher	BioMed Central
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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