Kosinsky, Robyn Laura

[["dc.bibliographiccitation.firstpage","37906"],["dc.bibliographiccitation.issue","35"],["dc.bibliographiccitation.journal","Oncotarget"],["dc.bibliographiccitation.lastpage","37918"],["dc.bibliographiccitation.volume","6"],["dc.contributor.author","Kosinsky, Robyn L."],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Hellbach, Nicole"],["dc.contributor.author","Dobbelstein, Matthias"],["dc.contributor.author","Mansouri, Ahmed"],["dc.contributor.author","Vogel, Tanja"],["dc.contributor.author","Begus-Nahrmann, Yvonne"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2019-07-09T11:42:03Z"],["dc.date.available","2019-07-09T11:42:03Z"],["dc.date.issued","2015-11-10"],["dc.description.abstract","Epigenetic regulatory mechanisms play a central role in controlling gene expression during development, cell differentiation and tumorigenesis. Monoubiquitination of histone H2B is one epigenetic modification which is dynamically regulated by the opposing activities of specific ubiquitin ligases and deubiquitinating enzymes (DUBs). The Ubiquitin-specific Protease 22 (USP22) is the ubiquitin hydrolase component of the human SAGA complex which deubiquitinates histone H2B during transcription. Recently, many studies have investigated an oncogenic potential of USP22 overexpression. However, its physiological function in organ maintenance, development and its cellular function remain largely unknown. A previous study reported embryonic lethality in Usp22 knockout mice. Here we describe a mouse model with a global reduction of USP22 levels which expresses the LacZ gene under the control of the endogenous Usp22 promoter. Using this reporter we found Usp22 to be ubiquitously expressed in murine embryos. Notably, adult Usp22lacZ/lacZ displayed low residual Usp22 expression levels coupled with a reduced body size and weight. Interestingly, the reduction of Usp22 significantly influenced the frequency of differentiated cells in the small intestine and the brain while H2B and H2Bub1 levels remained constant. Taken together, we provide evidence for a physiological role for USP22 in controlling cell differentiation and lineage specification."],["dc.identifier.doi","10.18632/oncotarget.5412"],["dc.identifier.pmid","26431380"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12736"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58576"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1949-2553"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Usp22 deficiency impairs intestinal epithelial lineage specification in vivo."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","705"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Calcified Tissue International"],["dc.bibliographiccitation.lastpage","719"],["dc.bibliographiccitation.volume","102"],["dc.contributor.author","Saul, D."],["dc.contributor.author","Harlas, B."],["dc.contributor.author","Ahrabi, A."],["dc.contributor.author","Kosinsky, R. L."],["dc.contributor.author","Hoffmann, D. B."],["dc.contributor.author","Wassmann, M."],["dc.contributor.author","Wigger, R."],["dc.contributor.author","Böker, K. O."],["dc.contributor.author","Sehmisch, S."],["dc.contributor.author","Komrakova, M."],["dc.date.accessioned","2020-06-10T14:22:48Z"],["dc.date.available","2020-06-10T14:22:48Z"],["dc.date.issued","2017"],["dc.description.abstract","Osteoporosis is often accompanied by sarcopenia. The effect of strontium ranelate (SR) on muscle tissue has not been investigated sufficiently. In this study, the effect of different SR treatments on muscle was studied. Additionally, the lumbar vertebrae were analyzed. Three-month-old female rats were divided into five groups (n = 12): Group 1: untreated (NON-OVX); Group 2: ovariectomized and left untreated (OVX); Group 3: SR after OVX until the study ended (13 weeks, SR prophylaxis and therapy = pr+th); Group 4: OVX and SR for 8 weeks (SR prophylaxis = pr); Group 5: SR for 5 weeks from the 8 week after OVX (SR therapy = SR th). SR was applied in food (630 mg/kg body weight). The size of muscle fibers, capillary density, metabolic enzymes, and mRNA expression were assessed in soleus, gastrocnemius, and longissimus muscles. The vertebral bodies underwent micro-CT, biomechanical, and ashing analyses. In general, SR did not alter the muscle histological parameters. The changes in fiber size and capillary ratio were related to the body weight. Myostatin mRNA was decreased in Sr pr+th; protein expression was not changed. SR th led to increase in mRNA expression of vascular endothelial growth factor (Vegf-B). In lumbar spine, SR pr+th enhanced biomechanical properties, bone mineral density, trabecular area, density, and thickness and cortical density. The reduced calcium/phosphate ratio in the SR pr+th group indicates the replacement of calcium by strontium ions. SR has no adverse effects on muscle tissue and it shows a favorable time-dependent effect on vertebrae. A functional analysis of muscles could verify these findings."],["dc.identifier.doi","10.1007/s00223-017-0374-0"],["dc.identifier.pmid","29242963"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66222"],["dc.language.iso","en"],["dc.relation.eissn","1432-0827"],["dc.relation.issn","0171-967X"],["dc.title","Effect of Strontium Ranelate on the Muscle and Vertebrae of Ovariectomized Rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","401"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","International Journal of Molecular Sciences"],["dc.bibliographiccitation.volume","22"],["dc.contributor.affiliation","Saul, Dominik; \t\t \r\n\t\t Kogod Center on Aging and Division of Endocrinology, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA, Saul.Dominik@mayo.edu\t\t \r\n\t\t Department of Trauma, Orthopedics and Reconstructive Surgery, Georg-August-University of Goettingen, 37075 Goettingen, Germany, Saul.Dominik@mayo.edu"],["dc.contributor.affiliation","Kosinsky, Robyn Laura; \t\t \r\n\t\t Division of Gastroenterology and Hepatology, Mayo Clinic, 200 First St SW, Rochester, MN 55905, USA, Kosinsky.RobynLaura@mayo.edu"],["dc.contributor.author","Saul, Dominik"],["dc.contributor.author","Kosinsky, Robyn Laura"],["dc.date.accessioned","2021-04-14T08:29:43Z"],["dc.date.available","2021-04-14T08:29:43Z"],["dc.date.issued","2021"],["dc.date.updated","2022-09-06T08:44:48Z"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.description.sponsorship","Deutsche Krebshilfe"],["dc.identifier.doi","10.3390/ijms22010401"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82970"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1422-0067"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Epigenetics of Aging and Aging-Associated Diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","6334"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Nucleic Acids Research"],["dc.bibliographiccitation.lastpage","6349"],["dc.bibliographiccitation.volume","45"],["dc.contributor.author","Mishra, Vivek Kumar"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Kosinsky, Robyn Laura"],["dc.contributor.author","Sen, Madhobi"],["dc.contributor.author","Baumgartner, Roland"],["dc.contributor.author","Wulff, Tanja"],["dc.contributor.author","Siveke, Jens T."],["dc.contributor.author","Schildhaus, Hans-Ulrich"],["dc.contributor.author","Najafova, Zeynab"],["dc.contributor.author","Kari, Vijayalakshmi"],["dc.contributor.author","Kohlhof, Hella"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2018-11-07T10:22:37Z"],["dc.date.available","2018-11-07T10:22:37Z"],["dc.date.issued","2017"],["dc.description.abstract","Pancreatic ductal adenocarcinoma (PDAC) is a highly aggressive cancer with a particularly dismal prognosis. Histone deacetylases (HDAC) are epigenetic modulators whose activity is frequently deregulated in various cancers including PDAC. In particular, class-I HDACs (HDAC 1, 2, 3 and 8) have been shown to play an important role in PDAC. In this study, we investigated the effects of the class Ispecific HDAC inhibitor (HDACi) 4SC-202 in multiple PDAC cell lines in promoting tumor cell differentiation. We show that 4SC-202 negatively affects TGF beta signaling and inhibits TGF beta-induced epithelial-tomesenchymal transition (EMT). Moreover, 4SC-202 markedly induced p21 (CDKN1A) expression and significantly attenuated cell proliferation. Mechanistically, genome-wide studies revealed that 4SC-202-induced genes were enriched for Bromodomain-containing Protein-4 (BRD4) and MYC occupancy. BRD4, a well-characterized acetyllysine reader, has been shown to play a major role in regulating transcription of selected subsets of genes. Importantly, BRD4 and MYC are essential for the expression of a subgroup of genes induced by class-I HDACi. Taken together, our study uncovers a previously unknown role of BRD4 and MYC in eliciting the HDACi-mediated induction of a subset of genes and provides molecular insight into the mechanisms of HDACi action in PDAC."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2017"],["dc.identifier.doi","10.1093/nar/gkx212"],["dc.identifier.isi","000403693000023"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14605"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42309"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1362-4962"],["dc.relation.issn","0305-1048"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Histone deacetylase class-I inhibition promotes epithelial gene expression in pancreatic cancer cells in a BRD4-and MYC-dependent manner"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3126"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Saul, Dominik"],["dc.contributor.author","Kosinsky, Robyn Laura"],["dc.date.accessioned","2021-12-01T09:23:03Z"],["dc.date.available","2021-12-01T09:23:03Z"],["dc.date.issued","2021"],["dc.description.abstract","The human aging process is associated with molecular changes and cellular degeneration, resulting in a significant increase in cancer incidence with age. Despite their potential correlation, the relationship between cancer- and ageing-related transcriptional changes is largely unknown. In this study, we aimed to analyze aging-associated transcriptional patterns in publicly available bulk mRNA-seq and single-cell RNA-seq (scRNA-seq) datasets for chronic myelogenous leukemia (CML), colorectal cancer (CRC), hepatocellular carcinoma (HCC), lung cancer (LC), and pancreatic ductal adenocarcinoma (PDAC). Indeed, we detected that various aging/senescence-induced genes (ASIGs) were upregulated in malignant diseases compared to healthy control samples. To elucidate the importance of ASIGs during cell development, pseudotime analyses were performed, which revealed a late enrichment of distinct cancer-specific ASIG signatures. Notably, we were able to demonstrate that all cancer entities analyzed in this study comprised cell populations expressing ASIGs. While only minor correlations were detected between ASIGs and transcriptome-wide changes in PDAC, a high proportion of ASIGs was induced in CML, CRC, HCC, and LC samples. These unique cellular subpopulations could serve as a basis for future studies on the role of aging and senescence in human malignancies."],["dc.description.abstract","The human aging process is associated with molecular changes and cellular degeneration, resulting in a significant increase in cancer incidence with age. Despite their potential correlation, the relationship between cancer- and ageing-related transcriptional changes is largely unknown. In this study, we aimed to analyze aging-associated transcriptional patterns in publicly available bulk mRNA-seq and single-cell RNA-seq (scRNA-seq) datasets for chronic myelogenous leukemia (CML), colorectal cancer (CRC), hepatocellular carcinoma (HCC), lung cancer (LC), and pancreatic ductal adenocarcinoma (PDAC). Indeed, we detected that various aging/senescence-induced genes (ASIGs) were upregulated in malignant diseases compared to healthy control samples. To elucidate the importance of ASIGs during cell development, pseudotime analyses were performed, which revealed a late enrichment of distinct cancer-specific ASIG signatures. Notably, we were able to demonstrate that all cancer entities analyzed in this study comprised cell populations expressing ASIGs. While only minor correlations were detected between ASIGs and transcriptome-wide changes in PDAC, a high proportion of ASIGs was induced in CML, CRC, HCC, and LC samples. These unique cellular subpopulations could serve as a basis for future studies on the role of aging and senescence in human malignancies."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.3390/cells10113126"],["dc.identifier.pii","cells10113126"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94549"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","2073-4409"],["dc.relation.orgunit","Klinik für Unfallchirurgie, Orthopädie und Plastische Chirurgie"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Single-Cell Transcriptomics Reveals the Expression of Aging- and Senescence-Associated Genes in Distinct Cancer Cell Populations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","unpublished"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1000191"],["dc.bibliographiccitation.issue","01"],["dc.bibliographiccitation.journal","Journal of Osteoporosis and Physical Activity"],["dc.bibliographiccitation.volume","05"],["dc.contributor.author","Saul, D."],["dc.contributor.author","Schilling, A. F."],["dc.contributor.author","Kosinsky, R. L."],["dc.date.accessioned","2019-07-09T11:43:26Z"],["dc.date.available","2019-07-09T11:43:26Z"],["dc.date.issued","2017"],["dc.description.abstract","In an aging population, the decline in muscle mass and strength in combination with a high prevalence of osteoporosis and cancer leads to a multitude of clinical manifestations. In the recent years, mouse models of wasting in cancer and inflammation, including xenograft, genetic and chemically induced models, allowed to uncover several key mechanisms underlying muscle loss. These include inflammation, hormone alterations and deregulated protein degradation. Inflammation is associated with increased expression of tumor necrosis factor α (TNF-α), nuclear factor κB (NF-κB), and interleukin (IL)-6 and is therefore linked to inflammatory bowel diseases or chronic obstructive pulmonary disease (COPD). Moreover, active NF-κB signaling and IL-6 secretion commonly occurs in malignancies and cancer-induced cachexia. The ubiquitin proteasome-mediated degradation of proteins represents a second pathway underlying sarcopenia and is partially initiated by inflammatory signaling. Consequently, increased levels of the E3 ligases Muscle RING-Finger Protein-1 (MuRF1), Atrogin-1/Muscle Atrophy F-box (MAFbx), and tumor necrosis factor α receptor adaptor protein 6 (TRAF6) are associated with high rates of protein degradation. Furthermore, hormonal alterations, such as the aging-related decline of growth hormone (GH) and insulin-like growth factor 1 (IGF-1), lead to a reduction of muscle mass. Interestingly, experimental targeting of several of those sarcopenia-associated factors in vivo resulted in a rescue of muscle mass and function. While therapeutic options nowadays still need to be evaluated regarding their clinical practicability, IL-6 antibodies, inhibition of cyclooxygenases and inhibitors of myostatin appear promising."],["dc.identifier.doi","10.4172/2329-9509.1000191"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/14528"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58888"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2329-9509"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Why Age Matters: Inflammation, Cancer and Hormones in the Development of Sarcopenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Saul, Dominik"],["dc.contributor.author","Kosinsky, Robyn Laura"],["dc.contributor.author","Atkinson, Elizabeth J."],["dc.contributor.author","Doolittle, Madison L."],["dc.contributor.author","Zhang, Xu"],["dc.contributor.author","LeBrasseur, Nathan K."],["dc.contributor.author","Pignolo, Robert J."],["dc.contributor.author","Robbins, Paul D."],["dc.contributor.author","Niedernhofer, Laura J."],["dc.contributor.author","Ikeno, Yuji"],["dc.contributor.author","Khosla, Sundeep"],["dc.date.accessioned","2022-09-01T09:50:03Z"],["dc.date.available","2022-09-01T09:50:03Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract\n Although cellular senescence drives multiple age-related co-morbidities through the senescence-associated secretory phenotype, in vivo senescent cell identification remains challenging. Here, we generate a gene set (SenMayo) and validate its enrichment in bone biopsies from two aged human cohorts. We further demonstrate reductions in SenMayo in bone following genetic clearance of senescent cells in mice and in adipose tissue from humans following pharmacological senescent cell clearance. We next use SenMayo to identify senescent hematopoietic or mesenchymal cells at the single cell level from human and murine bone marrow/bone scRNA-seq data. Thus, SenMayo identifies senescent cells across tissues and species with high fidelity. Using this senescence panel, we are able to characterize senescent cells at the single cell level and identify key intercellular signaling pathways. SenMayo also represents a potentially clinically applicable panel for monitoring senescent cell burden with aging and other conditions as well as in studies of senolytic drugs."],["dc.description.sponsorship"," Dr. Mildred Scheel Stiftung für Krebsforschung https://doi.org/10.13039/501100005973"],["dc.description.sponsorship"," Foundation for the National Institutes of Health https://doi.org/10.13039/100000009"],["dc.identifier.doi","10.1038/s41467-022-32552-1"],["dc.identifier.pii","32552"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113610"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-597"],["dc.relation.eissn","2041-1723"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","A new gene set identifies senescent cells and predicts senescence-associated pathways across tissues"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Cell Death & Disease"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Kosinsky, Robyn Laura"],["dc.contributor.author","Helms, Marlena"],["dc.contributor.author","Zerche, Maria"],["dc.contributor.author","Wohn, Luisa"],["dc.contributor.author","Dyas, Anna"],["dc.contributor.author","Prokakis, Evangelos"],["dc.contributor.author","Kazerouni, Zahra Basir"],["dc.contributor.author","Bedi, Upasana"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2020-12-10T18:09:43Z"],["dc.date.available","2020-12-10T18:09:43Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1038/s41419-019-2141-9"],["dc.identifier.eissn","2041-4889"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17081"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73737"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","USP22-dependent HSP90AB1 expression promotes resistance to HSP90 inhibition in mammary and colorectal cancer"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","4"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nutrition & Metabolism"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Saul, Dominik"],["dc.contributor.author","Weber, Marie"],["dc.contributor.author","Zimmermann, Marc Hendrik"],["dc.contributor.author","Kosinsky, Robyn Laura"],["dc.contributor.author","Hoffmann, Daniel Bernd"],["dc.contributor.author","Menger, Björn"],["dc.contributor.author","Taudien, Stefan"],["dc.contributor.author","Lehmann, Wolfgang"],["dc.contributor.author","Komrakova, Marina"],["dc.contributor.author","Sehmisch, Stephan"],["dc.date.accessioned","2019-07-09T11:49:50Z"],["dc.date.accessioned","2020-06-09T07:03:29Z"],["dc.date.available","2019-07-09T11:49:50Z"],["dc.date.available","2020-06-09T07:03:29Z"],["dc.date.issued","2019"],["dc.description.abstract","Background Osteoporosis is one of the world’s major medical burdens in the twenty-first century. Pharmaceutical intervention currently focusses on decelerating bone loss, but phytochemicals such as baicalein, which is a lipoxygenase inhibitor, may rescue bone loss. Studies evaluating the effect of baicalein in vivo are rare. Methods We administered baicalein to sixty-one three-month-old female Sprague-Dawley rats. They were divided into five groups, four of which were ovariectomized (OVX) and one non-ovariectomized (NON-OVX). Eight weeks after ovariectomy, bilateral tibial osteotomy with plate osteosynthesis was performed and bone formation quantified. Baicalein was administered subcutaneously using three doses (C1: 1 mg/kg BW; C2: 10 mg/kg BW; and C3: 100 mg/kg BW) eight weeks after ovariectomy for four weeks. Finally, femora and tibiae were collected. Biomechanical tests, micro-CT, ashing, histological and gene expression analyses were performed. Results Biomechanical properties were unchanged in tibiae and reduced in femora. In tibiae, C1 treatment enhanced callus density and cortical width and decreased callus area. In the C3 group, callus formation was reduced during the first 3 weeks after osteotomy, correlating to a higher mRNA expression of Osteocalcin, Tartrate-resistant acid phosphatase and Rankl. In femora, baicalein treatments did not alter bone parameters. Conclusions Baicalein enhanced callus density and cortical width but impaired early callus formation in tibiae. In femora, it diminished the biomechanical properties and calcium-to-phosphate ratio. Thus, it is not advisable to apply baicalein to treat early bone fractures. To determine the exact effects on bone healing, further studies in which baicalein treatments are started at different stages of healing are needed."],["dc.identifier.doi","10.1186/s12986-018-0327-2"],["dc.identifier.pmid","30651746"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15789"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59640"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/66212"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1743-7075"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Effect of the Lipoxygenase Inhibitor Baicalein on Bone Tissue and Bone Healing in Ovariectomized Rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Clinical Epigenetics"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Sen, Madhobi"],["dc.contributor.author","Wang, Xin"],["dc.contributor.author","Hamdan, Feda H."],["dc.contributor.author","Rapp, Jacobe"],["dc.contributor.author","Eggert, Jessica"],["dc.contributor.author","Kosinsky, Robyn Laura"],["dc.contributor.author","Wegwitz, Florian"],["dc.contributor.author","Kutschat, Ana Patricia"],["dc.contributor.author","Younesi, Fereshteh S."],["dc.contributor.author","Gaedcke, Jochen"],["dc.contributor.author","Grade, Marian"],["dc.contributor.author","Hessmann, Elisabeth"],["dc.contributor.author","Papantonis, Argyris"],["dc.contributor.author","Strӧbel, Philipp"],["dc.contributor.author","Johnsen, Steven A."],["dc.date.accessioned","2020-12-10T18:39:06Z"],["dc.date.available","2020-12-10T18:39:06Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1186/s13148-019-0690-5"],["dc.identifier.eissn","1868-7083"],["dc.identifier.issn","1868-7075"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16438"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77543"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","ARID1A facilitates KRAS signaling-regulated enhancer activity in an AP1-dependent manner in colorectal cancer cells"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]