Matches in SemOpenAlex for { <https://semopenalex.org/work/W2589061763> ?p ?o ?g. }
Showing items 1 to 86 of
86
with 100 items per page.
- W2589061763 abstract "Abstract Abstract 3369 Intact DNA damage response pathways are important for genomic fidelity of cells in order to avoid tumor formation. On the other hand, inhibition of DNA repair provides an important mechanism to enhance the therapeutic efficacy of DNA damaging agents such as gamma-irradiation. Thus, it is important to identify novel players in DNA damage response that might represent novel targets for combination therapies. Death-associated protein kinases (DAPK) are serine/threonine kinases believed to be involved in cell death and autophagy mechanisms, whereby particularly the role of DAPK1 has previously been investigated. The DAPK family is composed of five members: DAPK1, DAPK2 (or DRP-1), DAPK3 (or ZIP kinase), DRAK1 and DRAK2. DAPK1 and DAPK2 share 80% homology in the catalytic domain. Generally, the role of DAPK in DNA damage responses is not well studied. To analyze the role of DAPK1 and DAPK2 in response to gamma-irradiation, we used p53 wild-type REH B-cell acute lymphoblastic leukemia (B-ALL) cells as a model. In response to irradiation, DAPK1 protein expression increased paralleled by an increased of total p53, phospho-Ser20-p53 and p21WAF1/CIP1. DAPK2 expression, however, did not increase. Since upregulation of p21WAF1/CIP1, a classical p53 target in response to DNA damage leads to cell cycle arrest, we asked whether knocking down DAPK1 or DAPK2 might affect the cell cycle. Interestingly, knocking down DAPK2 but not DAPK1 led to a significant increase of S-phase cells upon irradiation. Moreover, knocking down DAPK2 attenuated the induction of DAPK1 upon irradiation indicating a DAPK2-DAPK1 cascade in DNA damage responses. Next, given the significant role of p21WAF1/CIP1 and p53 in DNA damage responses, we tested if DAPK2 might directly participate in a novel signaling pathway by interacting with these proteins. Indeed, pull down assays revealed that p21WAF1/CIP1 and p53 are novel DAPK2 interacting proteins. Clearly, further experiments are needed to define the DAPK2-DAPK1-p53- p21WAF1/CIP1 network in DNA repair pathways. In conclusion, we identified a novel role for DAPK1 and DAPK2 in DNA damage responses of B-ALL cells and propose a novel DAPK2/DAPK1/p53/ p21WAF1/CIP1 DNA damage regulatory pathway. Disclosures: No relevant conflicts of interest to declare." @default.
- W2589061763 created "2017-02-24" @default.
- W2589061763 creator A5000513493 @default.
- W2589061763 creator A5002388764 @default.
- W2589061763 creator A5005114043 @default.
- W2589061763 creator A5010633283 @default.
- W2589061763 creator A5018282746 @default.
- W2589061763 creator A5020867690 @default.
- W2589061763 creator A5032263445 @default.
- W2589061763 creator A5085075067 @default.
- W2589061763 date "2010-11-19" @default.
- W2589061763 modified "2023-10-17" @default.
- W2589061763 title "Involvement of Death-Associated Protein Kinases In DNA Damage Responses of B-ALL Cells." @default.
- W2589061763 doi "https://doi.org/10.1182/blood.v116.21.3369.3369" @default.
- W2589061763 hasPublicationYear "2010" @default.
- W2589061763 type Work @default.
- W2589061763 sameAs 2589061763 @default.
- W2589061763 citedByCount "0" @default.
- W2589061763 crossrefType "journal-article" @default.
- W2589061763 hasAuthorship W2589061763A5000513493 @default.
- W2589061763 hasAuthorship W2589061763A5002388764 @default.
- W2589061763 hasAuthorship W2589061763A5005114043 @default.
- W2589061763 hasAuthorship W2589061763A5010633283 @default.
- W2589061763 hasAuthorship W2589061763A5018282746 @default.
- W2589061763 hasAuthorship W2589061763A5020867690 @default.
- W2589061763 hasAuthorship W2589061763A5032263445 @default.
- W2589061763 hasAuthorship W2589061763A5085075067 @default.
- W2589061763 hasConcept C105696609 @default.
- W2589061763 hasConcept C134935766 @default.
- W2589061763 hasConcept C143425029 @default.
- W2589061763 hasConcept C178169997 @default.
- W2589061763 hasConcept C184235292 @default.
- W2589061763 hasConcept C190283241 @default.
- W2589061763 hasConcept C29537977 @default.
- W2589061763 hasConcept C31573885 @default.
- W2589061763 hasConcept C50001416 @default.
- W2589061763 hasConcept C502942594 @default.
- W2589061763 hasConcept C54086632 @default.
- W2589061763 hasConcept C54355233 @default.
- W2589061763 hasConcept C552990157 @default.
- W2589061763 hasConcept C86803240 @default.
- W2589061763 hasConcept C95444343 @default.
- W2589061763 hasConcept C97029542 @default.
- W2589061763 hasConceptScore W2589061763C105696609 @default.
- W2589061763 hasConceptScore W2589061763C134935766 @default.
- W2589061763 hasConceptScore W2589061763C143425029 @default.
- W2589061763 hasConceptScore W2589061763C178169997 @default.
- W2589061763 hasConceptScore W2589061763C184235292 @default.
- W2589061763 hasConceptScore W2589061763C190283241 @default.
- W2589061763 hasConceptScore W2589061763C29537977 @default.
- W2589061763 hasConceptScore W2589061763C31573885 @default.
- W2589061763 hasConceptScore W2589061763C50001416 @default.
- W2589061763 hasConceptScore W2589061763C502942594 @default.
- W2589061763 hasConceptScore W2589061763C54086632 @default.
- W2589061763 hasConceptScore W2589061763C54355233 @default.
- W2589061763 hasConceptScore W2589061763C552990157 @default.
- W2589061763 hasConceptScore W2589061763C86803240 @default.
- W2589061763 hasConceptScore W2589061763C95444343 @default.
- W2589061763 hasConceptScore W2589061763C97029542 @default.
- W2589061763 hasLocation W25890617631 @default.
- W2589061763 hasOpenAccess W2589061763 @default.
- W2589061763 hasPrimaryLocation W25890617631 @default.
- W2589061763 hasRelatedWork W1717397784 @default.
- W2589061763 hasRelatedWork W197000347 @default.
- W2589061763 hasRelatedWork W1971075697 @default.
- W2589061763 hasRelatedWork W1984888383 @default.
- W2589061763 hasRelatedWork W1985578078 @default.
- W2589061763 hasRelatedWork W2026677505 @default.
- W2589061763 hasRelatedWork W2030897839 @default.
- W2589061763 hasRelatedWork W2032603938 @default.
- W2589061763 hasRelatedWork W2037538933 @default.
- W2589061763 hasRelatedWork W2041279709 @default.
- W2589061763 hasRelatedWork W2088009068 @default.
- W2589061763 hasRelatedWork W2089277080 @default.
- W2589061763 hasRelatedWork W2093673674 @default.
- W2589061763 hasRelatedWork W2093823051 @default.
- W2589061763 hasRelatedWork W2095102493 @default.
- W2589061763 hasRelatedWork W2124679827 @default.
- W2589061763 hasRelatedWork W2132465015 @default.
- W2589061763 hasRelatedWork W2158199642 @default.
- W2589061763 hasRelatedWork W2341100407 @default.
- W2589061763 hasRelatedWork W3087125645 @default.
- W2589061763 isParatext "false" @default.
- W2589061763 isRetracted "false" @default.
- W2589061763 magId "2589061763" @default.
- W2589061763 workType "article" @default.