E-mail: nikolacurik@centrum.cz
Odborné práce publikované na Linkos.cz
Přehled odborných textů publikovaných autorem na portálu Linkos.cz. Jsou zde uvedeny knihy a brožury, články v Klinické onkologii, tuzemská abstrakta z databáze abstrakt a další texty. Rejstřík není v žádném případě úplným autorským rejstříkem, protože jsou zde uvedeny pouze texty zveřejněné na portálu Linkos.cz.
Publikovaná abstrakta
- 5-Azacytidine and G-CSF Derepressed Chromatin Structure of PU.1 and Its Targets Cebpa and Cbfb In Myelodysplastic Syndrome (MDS)
- Activation of Chromatin Structure Upstream PU.1 Gene and in Vitro Differentiation in High Risk Myelodysplastic Syndrome Following 5-Azacytidine
- Active Chromatin Structure near MYB Occupancy at the Mir-155 Host Gene Promoter Coincides with Increased Mir-155 and MYB Levels In Chronic Lymphocytic Leukemia
- Divalent Metal Transporter 1 (DMT1) Regulates EPO Receptor Gene Expression Via GATA-1
- Epigenetic regulation of miR155 expression - insights into pathogenesis of CLL
- Erythroid Transcription Factor GATA-1 Binds and Represses PU.1 Gene – Candidate Mechanism Of Epigenetic Repression Of PU.1 and Inefficient Erythropoiesis In MDS
- Fog1 and Cebpa Are DNA Targets of GATA-1/PU.1 Antagonism during Leukemia Differentiation.
- Gata1 Regulates Erythroid Transcription by Cooperating with Chromatin Remodeling Protein Snf2h
- INTERFERON-ΑLPHA REVISITED: INDIVIDUALIZED IMMUNE-MODULATION EASED UP SELECTION PRESSURE OF TKI ON BCR-ABL MUTATED CLONES AND IMPROVES MOLECULAR RESPONSE IN HIGH-RISK CML PATIENTS
- ISWI Chromatin Remodeling ATPase Smarca5 (Snf2h) Is Required for Murine Erythroid Development and Globin Gene Regulation
- MicroRNA Mir-155 and Myb Proto-Oncogene Family Members Cooperate in Pathogenesis of Chronic Lymphocytic Leukemia
- Mutation Of The Divalent Metal Transporter (Dmt1) Gene Results In Inefficient Induction Of The Erythroid Transcriptional Program Due To Latter Onset Of GATA-1 and Epor Expression
- Mutual Regulatory Loop between miR-155 and PU.1 Is a Candidate Pathogenesis Factor in CLL.
- Patients with Chronic Myeloid Leukemia Show Different Modulation of MYB-Dependent Oncogenic Pathway in the Course of Hematopoietic Differentiation upon Sensitivity to the TKI Treatment
- PU.1 Dose-Dependently Induces Granulocyte or Macrophage Commitment by Targeting Lineage Restricted Genes and by Regulating Transcription Factors Egr2, Nab2, Cebpa and Gfi1.
- PU.1 Relieves Its GATA-1-Mediated Repression near Cebpa and Cbfb During Transdifferentiation of Murine Erythroleukemia - Tool of Inducing Leukemic Blasts to Differentiate
- Retroviral rescue with PU.1 induces derepression of both PU.1 and miR155 target genes - possible therapeutic implications for CLL
- Smarca5 Regulates Ctcf Recruitment to Chromatin, Including to Regulatory Loci Involved In Control of Globin Gene Expression In Erythroleukemia
- SNPs in the Promoter of the Gene Encoding Transmembrane Transporter SLC22A4 (hOCTN1) Are Significantly Associated with an Alteration of Gene Expression and with Resistance to the Imatinib Treatment in Chronic Myeloid Leukemia
- Transcription Factor CTCF Inhibits Effects of 5-Azacitidine in MDS/AML Cells
