Identification of differentially regulated genes upon overexpression of HLX in wild-type hematopoietic stem cells
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE27938 | GEO | 2012/09/14
SECONDARY ACCESSION(S): PRJNA141719
REPOSITORIES: GEO
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Project description:The goal was to study the role of Hlx in hematopoiesis. Sorted Lin-Kit+Sca-1+ cells from wild-type FVB/nJ bone marrow were infected with control (pCAD-IRES-GFP) or Hlx lentivirus (pCAD-IRES-GFP-Hlx) and cultured for 2 days in Iscove’s modified Dulbecco’s medium (IMDM) containing FBS, mIL-3, mIL-6 and mSCF with lentiviral supernatants in the presence of 8ug/ml polybrene. Subsequently, GFP+ cells were sorted by FACS and RNA was prepared. Three replicates of each, control vector transduced and HLX-transduced cells were used.
2012-09-14 | E-GEOD-27938 | biostudies-arrayexpress
Project description:To study the role of Hlx in hematopoietic differentiation and tumorigenesis, URE cells were infected with short-hairpin-containing pSIH1-H1-copGFP lentiviral vector (System Biosciences, Mountain View, CA) containing either nucleotide sequences targeting luciferase (shControl) or HLX (shHLX). After 24hrs incubation in Iscove’s modified Dulbecco’s medium (IMDM) containing FBS, mIL-3, mIL-6 and mSCF with lentiviral supernatants in the presence of 8ug/ml polybrene, cells were cultured in fresh medium for several days. Subsequently, GFP+ cells were sorted by FACS and RNA was prepared. URE cells were infected with short-hairpin-containing pSIH1-H1-copGFP lentiviral vector (System Biosciences, Mountain View, CA) containing either nucleotide sequences targeting luciferase (shControl) or HLX (shHLX). After 24hrs incubation in Iscove’s modified Dulbecco’s medium (IMDM) containing FBS, mIL-3, mIL-6 and mSCF with lentiviral supernatants in the presence of 8ug/ml polybrene, cells were cultured in fresh medium for several days. Subsequently, GFP+ cells were sorted by FACS and RNA was prepared. Three replicates of each, shControl and shHLX-transduced cells were used. The goal was to study the role of Hlx in hematopoietic differentiation and tumorigenesis.
2012-09-14 | E-GEOD-27939 | biostudies-arrayexpress
Project description:To study the role of Hlx in hematopoietic differentiation and tumorigenesis, URE cells were infected with short-hairpin-containing pSIH1-H1-copGFP lentiviral vector (System Biosciences, Mountain View, CA) containing either nucleotide sequences targeting luciferase (shControl) or HLX (shHLX). After 24hrs incubation in Iscove’s modified Dulbecco’s medium (IMDM) containing FBS, mIL-3, mIL-6 and mSCF with lentiviral supernatants in the presence of 8ug/ml polybrene, cells were cultured in fresh medium for several days. Subsequently, GFP+ cells were sorted by FACS and RNA was prepared.
2012-09-14 | GSE27939 | GEO
Project description:HLX was found as a VEGF-A induced gene in HUVEC (B.Schweighofer, submitted). In order to detect genes regulated by HLX HUVEC were infected by recombinant adenovirus expressing HLX for 4, 8, 16 and 32h. RNA was isolated and subjected to microarray analysis using Affymetrix microarray. HUVEC were infected with a MOI of 40 with either HLX expressing or empty adenovirus for 4, 8, 16 or 32 hours. HUVEC without an adenovirus infection were used as control.Total RNA was isolated with Trizol according to the instructions of the manufacturer. Gene expression was analysed with Affymetrix GeneChip Human Genome U133 Plus 2.0 Arrays according to the Affymetrix protocol.
2011-02-15 | E-GEOD-13054 | biostudies-arrayexpress
Project description:HLX was found as a VEGF-A induced gene in HUVEC (B.Schweighofer, submitted). In order to detect genes regulated by HLX HUVEC were infected by recombinant adenovirus expressing HLX for 4, 8, 16 and 32h. RNA was isolated and subjected to microarray analysis using Affymetrix microarray.
2011-02-15 | GSE13054 | GEO
Project description:NKL homeobox genes encode developmental transcription factors regulating basic processes in cell differentiation. According to their physiological expression pattern in early hematopoiesis and B-cell development, particular members of this homeobox gene subclass constitute an NKL-code. These B-cell specific genes generate a regulatory network and their deregulation is implicated in B-cell lymphomagenesis. Epstein-Barr virus (EBV) infects B-cells and influences the activity of signalling pathways including JAK/STAT and several genes encoding developmental regulators. Therefore, EBV-infection impacts the pathogenesis and the outcome of B-cell malignancies including Hodgkin lymphoma and diffuse large B-cell lymphoma (DLBCL). Here, we isolated EBV-positive and EBV-negative subclones from the DLBCL derived cell line DOHH-2. These subclones served as model to investigate the role of EBV in deregulation of the B-cell specific NKL-code members HHEX, HLX, MSX1 and NKX6-3. We showed that the EBV-encoded factors LMP1 and LMP2A activated the expression of HLX via STAT3. HLX in turn repressed NKX6-3, SPIB and IL4R which normally mediate plasma cell differentiation. In addition, HLX repressed pro-apoptotic factor BCL2L11/BIM supporting cell survival. Thus, EBV aberrantly activated HLX thereby disturbing both B-cell differentiation and apoptosis in DLBCL. The results of our study contribute to better understand the pathogenic role of EBV in B-cell malignancies.
2019-05-06 | GSE125420 | GEO
Project description:NKL homeobox genes encode developmental transcription factors regulating basic processes in cell differentiation. According to their physiological expression pattern in early hematopoiesis and B-cell development, particular members of this homeobox gene subclass constitute an NKL-code. These B-cell specific genes generate a regulatory network and their deregulation is implicated in B-cell lymphomagenesis. Epstein-Barr virus (EBV) infects B-cells and influences the activity of signalling pathways including JAK/STAT and several genes encoding developmental regulators. Therefore, EBV-infection impacts the pathogenesis and the outcome of B-cell malignancies including Hodgkin lymphoma and diffuse large B-cell lymphoma (DLBCL). Here, we isolated EBV-positive and EBV-negative subclones from the DLBCL derived cell line DOHH-2. These subclones served as model to investigate the role of EBV in deregulation of the B-cell specific NKL-code members HHEX, HLX, MSX1 and NKX6-3. We showed that the EBV-encoded factors LMP1 and LMP2A activated the expression of HLX via STAT3. HLX in turn repressed NKX6-3, SPIB and IL4R which normally mediate plasma cell differentiation. In addition, HLX repressed pro-apoptotic factor BCL2L11/BIM supporting cell survival. Thus, EBV aberrantly activated HLX thereby disturbing both B-cell differentiation and apoptosis in DLBCL. The results of our study contribute to better understand the pathogenic role of EBV in B-cell malignancies.
2020-09-10 | GSE146390 | GEO
Project description:NKL homeobox genes encode developmental transcription factors regulating basic processes in cell differentiation. According to their physiological expression pattern in early hematopoiesis and B-cell development, particular members of this homeobox gene subclass constitute an NKL-code. These B-cell specific genes generate a regulatory network and their deregulation is implicated in B-cell lymphomagenesis. Epstein-Barr virus (EBV) infects B-cells and influences the activity of signalling pathways including JAK/STAT and several genes encoding developmental regulators. Therefore, EBV-infection impacts the pathogenesis and the outcome of B-cell malignancies including Hodgkin lymphoma and diffuse large B-cell lymphoma (DLBCL). Here, we isolated EBV-positive and EBV-negative subclones from the DLBCL derived cell line DOHH-2. These subclones served as model to investigate the role of EBV in deregulation of the B-cell specific NKL-code members HHEX, HLX, MSX1 and NKX6-3. We showed that the EBV-encoded factors LMP1 and LMP2A activated the expression of HLX via STAT3. HLX in turn repressed NKX6-3, SPIB and IL4R which normally mediate plasma cell differentiation. In addition, HLX repressed pro-apoptotic factor BCL2L11/BIM supporting cell survival. Thus, EBV aberrantly activated HLX thereby disturbing both B-cell differentiation and apoptosis in DLBCL. The results of our study contribute to better understand the pathogenic role of EBV in B-cell malignancies.
2020-09-10 | GSE146389 | GEO
Project description:To gain more insights into the functional significance of lnc-HLX-2-7 in human medulloblastoma, genomic mapping of lnc-HLX-2-7 occupancy were analyzied by ChIRP DNA sequencing.
2023-11-01 | GSE232749 | GEO