Sökning: "parp"
Visar resultat 1 - 5 av 46 avhandlingar innehållade ordet parp.
1. Post-translational modifications in DNA base excision repair : The roles of CK2 and PARP-1
Sammanfattning : Base lesions and DNA single-strand breaks (SSBs) are very common types of DNA damage. The base excision repair (BER) and single-strand break repair (SSBR) machineries both require a succession of enzymatic events in order to remove these types of endogenous lesions and to restore the DNA. LÄS MER
2. Allosteric control of ALC1-catalyzed nucleosome remodeling
Sammanfattning : The genetic information of eukaryotic cells is packaged inside the nucleus as chromatin. This packaging restricts access to the DNA and therefore represents a barrier for processes such as DNA replication, repair, and gene expression. LÄS MER
3. Transcriptional Silencing in the Imprinted Igf2-H19 Loci: The Mystique of Epigenetics
Sammanfattning : Genomic imprinting marks a subset of autosomal loci expressed in parent of origin-dependent monoallelic expression in a non-Mendelian fashion. To restore totipotency and to reset the imprint according to the sex of the individual, the mark must be erased during germline development. LÄS MER
4. Synthesis of Small Molecules Targeting ADP-Ribosyltransferases and Total Synthesis of Resveratrol Based Natural Products
Sammanfattning : Diphtheria Toxin-like ADP-RibosyltransferasesThe Human ADP-ribosyl transferases (ARTDs) are a group of poorly studied enzymes which are believed to be involved in e.g. DNA repair, protein degradation, transcription regulation and cell death. Medicinal chemistry programmes aimed at developing selective inhibitors of these ARTDs were initiated. LÄS MER
5. Mechanisms of leukemia-induced immunosuppression
Sammanfattning : This thesis aimed to define the role of reactive oxygen species (ROS), produced by the NADPH oxidase of myeloid cells, in the regulation of lymphocyte function with focus on ROS-induced dysfunction of natural killer (NK) cells and T lymphocytes in myeloid leukemia. In Paper I, a novel mechanism is presented by which specifically activated T lymphocytes evade inactivation by ROS after antigen presentation. LÄS MER