Hoyer-Fender, Sigrid

[["dc.bibliographiccitation.firstpage","2677"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Rahimi, Amir Mohammad"],["dc.contributor.author","Cai, Mingfang"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.date.accessioned","2022-10-04T10:21:37Z"],["dc.date.available","2022-10-04T10:21:37Z"],["dc.date.issued","2022"],["dc.description.abstract","The embryonic mouse fibroblast cell line NIH3T3 is widely used in life science research, including the study of cell cycle control and primary cilia. Fibroblasts are the most important cell type in connective tissue, as they produce components of the extracellular matrix and determine tissue architecture. However, they are very heterogeneous and consist of subtypes specific to their organ of residence, among others. The NIH3T3 cell line was derived from whole mouse embryos that developed to pre-birth and is therefore most likely composed of different fibroblast subtypes. Furthermore, prolonged proliferation may have influenced their cellular composition. A heterogeneous cell population is unsuitable for any sophisticated research project. We found that the proportion of ciliated cells in the total NIH3T3 cell population was highly variable and asked whether this was a consequence of cellular heterogeneity and what molecular signatures were associated with it. We have established sub-cell lines by clonal expansion of single cells and characterized them morphologically and molecularly. Eventually, a myofibroblast-like and a fibroblast-like cell line were generated that differ in ciliation and proliferation. These homogeneous cell lines are valuable for a more detailed study of their molecular signatures, not least to uncover further the molecular pathways that contribute to the formation of the primary cilium."],["dc.identifier.doi","10.3390/cells11172677"],["dc.identifier.pii","cells11172677"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114456"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","2073-4409"],["dc.title","Heterogeneity of the NIH3T3 Fibroblast Cell Line"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2858"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","Human Molecular Genetics"],["dc.bibliographiccitation.lastpage","2866"],["dc.bibliographiccitation.volume","19"],["dc.contributor.author","Batsukh, Tserendulam"],["dc.contributor.author","Pieper, Lasse"],["dc.contributor.author","Koszucka, Anna M."],["dc.contributor.author","von Velsen, Nina"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.contributor.author","Elbracht, Miriam"],["dc.contributor.author","Bergman, Jorieke E. H."],["dc.contributor.author","Hoefsloot, Lies H."],["dc.contributor.author","Pauli, Silke"],["dc.date.accessioned","2018-11-07T08:41:21Z"],["dc.date.available","2018-11-07T08:41:21Z"],["dc.date.issued","2010"],["dc.description.abstract","CHARGE syndrome is an autosomal dominant disorder caused in about two-third of cases by mutations in the CHD7 gene. For other genetic diseases e.g. hereditary spastic paraplegia, it was shown that interacting partners are involved in the underlying cause of the disease. These data encouraged us to search for CHD7 binding partners by a yeast two-hybrid library screen and CHD8 was identified as an interacting partner. The result was confirmed by a direct yeast two-hybrid analysis, co-immunoprecipitation studies and by a bimolecular fluorescence complementation assay. To investigate the function of CHD7 missense mutations in the CHD7-CHD8 interacting area on the binding capacity of both proteins, we included three known missense mutations (p.His2096Arg, p.Val2102Ile and p.Gly2108Arg) and one newly identified missense mutation (p.Trp2091Arg) in the CHD7 gene and performed both direct yeast two-hybrid and co-immunoprecipitation studies. In the direct yeast two-hybrid system, the CHD7-CHD8 interaction was disrupted by the missense mutations p.Trp2091Arg, p.His2096Arg and p.Gly2108Arg, whereas in the co-immunoprecipitation studies disruption of the CHD7-CHD8 interaction by the mutations could not be observed. The results lead to the hypothesis that CHD7 and CHD8 proteins are interacting directly and indirectly via additional linker proteins. Disruption of the direct CHD7-CHD8 interaction might change the conformation of a putative large CHD7-CHD8 complex and could be a disease mechanism in CHARGE syndrome."],["dc.description.sponsorship","Medical School of the University of Gottingen"],["dc.identifier.doi","10.1093/hmg/ddq189"],["dc.identifier.isi","000279469100010"],["dc.identifier.pmid","20453063"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6228"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19448"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0964-6906"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","CHD8 interacts with CHD7, a protein which is mutated in CHARGE syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0274352"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLoS One"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Tomas-Roig, Jordi"],["dc.contributor.author","Ramasamy, Shyam"],["dc.contributor.author","Zbarsky, Diana"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.contributor.editor","Li, Xuan"],["dc.date.accessioned","2022-10-04T10:21:47Z"],["dc.date.available","2022-10-04T10:21:47Z"],["dc.date.issued","2022"],["dc.description.abstract","The dynamics of neuronal microtubules are essential for brain plasticity. Vesicular transport and synaptic transmission, additionally, requires acetylation of α-tubulin, and aberrant tubulin acetylation and neurobiological deficits are associated. Prolonged exposure to a stressor or consumption of drugs of abuse, like marihuana, lead to neurological changes and psychotic disorders. Here, we studied the effect of psychosocial stress and the administration of cannabinoid receptor type 1 drugs on α-tubulin acetylation in different brain regions of mice. We found significantly decreased tubulin acetylation in the prefrontal cortex in stressed mice. The impact of cannabinoid drugs on stress-induced microtubule disturbance was investigated by administration of the cannabinoid receptor agonist WIN55,212–2 and/or antagonist rimonabant. In both, control and stressed mice, the administration of WIN55,212–2 slightly increased the tubulin acetylation in the prefrontal cortex whereas administration of rimonabant acted antagonistically indicating a cannabinoid receptor type 1 mediated effect. The analysis of gene expression in the prefrontal cortex showed a consistent expression of\r\n ApoE\r\n attributable to either psychosocial stress or administration of the cannabinoid agonist. Additionally,\r\n ApoE\r\n expression inversely correlated with acetylated tubulin levels when comparing controls and stressed mice treated with WIN55,212–2 whereas rimonabant treatment showed the opposite."],["dc.description.sponsorship"," Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.description.sponsorship"," Deutsche Forschungsgemeinschaft http://dx.doi.org/10.13039/501100001659"],["dc.identifier.doi","10.1371/journal.pone.0274352"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114499"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.relation.eissn","1932-6203"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Psychosocial stress and cannabinoid drugs affect acetylation of α-tubulin (K40) and gene expression in the prefrontal cortex of adult mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Tapia Contreras, Constanza"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.date.accessioned","2021-04-14T08:23:12Z"],["dc.date.available","2021-04-14T08:23:12Z"],["dc.date.issued","2020"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2021"],["dc.identifier.doi","10.1038/s41598-020-71120-9"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17812"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/80827"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2045-2322"],["dc.relation.orgunit","Johann-Friedrich-Blumenbach-Institut für Zoologie und Anthropologie"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","The WD40-protein CFAP52/WDR16 is a centrosome/basal body protein and localizes to the manchette and the flagellum in male germ cells"],["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","216"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular and Cellular Biology"],["dc.bibliographiccitation.lastpage","225"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Yang, Kefei"],["dc.contributor.author","Meinhardt, Andreas"],["dc.contributor.author","Zhang, B."],["dc.contributor.author","Grzmil, Pawel"],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.date.accessioned","2018-11-07T09:16:11Z"],["dc.date.available","2018-11-07T09:16:11Z"],["dc.date.issued","2012"],["dc.description.abstract","Sperm motility and hence male fertility strictly depends on proper development of the sperm tail and its tight anchorage to the head. The main protein of sperm tail outer dense fibers, ODF1/HSPB10, belongs to the family of small heat shock proteins that function as molecular chaperones. However, the impact of ODF1 on sperm tail formation and motility and on male fecundity is unknown. We therefore generated mutant mice in which the Odf1 gene was disrupted. Heterozygous mutant male mice are fertile while sperm motility is reduced, but Odf1-deficient male mice are infertile due to the detachment of the sperm head. Although headless tails are somehow motile, transmission electron microscopy revealed disturbed organization of the mitochondrial sheath, as well as of the outer dense fibers. Our results thus suggest that ODF1, besides being involved in the correct arrangement of mitochondrial sheath and outer dense fibers, is essential for rigid junction of sperm head and tail. Loss of function of ODF1, therefore, might account for some of the cases of human infertility with decapitated sperm heads. In addition, since sperm motility is already affected in heterozygous mice, impairment of ODF1 might even account for some cases of reduced fertility in male patients."],["dc.identifier.doi","10.1128/MCB.06158-11"],["dc.identifier.isi","000298366000019"],["dc.identifier.pmid","22037768"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27875"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","1098-5549"],["dc.relation.issn","0270-7306"],["dc.title","The Small Heat Shock Protein ODF1/HSPB10 Is Essential for Tight Linkage of Sperm Head to Tail and Male Fertility in Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","49"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Histochemistry and Cell Biology"],["dc.bibliographiccitation.lastpage","59"],["dc.bibliographiccitation.volume","150"],["dc.contributor.author","Yang, Kefei"],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Meinhardt, Andreas"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.date.accessioned","2020-12-10T14:10:35Z"],["dc.date.available","2020-12-10T14:10:35Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s00418-018-1668-7"],["dc.identifier.eissn","1432-119X"],["dc.identifier.issn","0948-6143"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70808"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Ultra-structure of the sperm head-to-tail linkage complex in the absence of the spermatid-specific LINC component SPAG4"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","7657"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Molecular and Cellular Biology"],["dc.bibliographiccitation.lastpage","7664"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Adham, Ibrahim M."],["dc.contributor.author","Eck, T. J."],["dc.contributor.author","Mierau, K."],["dc.contributor.author","Mueller, N."],["dc.contributor.author","Sallam, M. A."],["dc.contributor.author","Paprotta, I."],["dc.contributor.author","Schubert, S."],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.contributor.author","Engel, Wolfgang"],["dc.date.accessioned","2018-11-07T10:56:24Z"],["dc.date.available","2018-11-07T10:56:24Z"],["dc.date.issued","2005"],["dc.description.abstract","Creb3l4 belongs to the CREB/ATF family of transcription factors that are involved in mediating transcription in response to intracellular signaling. This study shows that Creb3l4 is expressed at low levels in all organs and in different stages of embryogenesis but is present at very high levels in the testis, particularly in postmeiotic male germ cells. In contrast to CREB3L4 in the human prostate, of which specific expression was detected, Creb3l4 transcripts in the mouse prostate could be detected only by RT-PCR. To identify the physiological function of Creb3l4, the murine gene was inactivated by replacement with the gene encoding green fluorescent protein. Surprisingly, Creb3l4-deficient mice were born at expected ratios, were healthy, and displayed normal long-term survival rates. Despite a significant reduction in the number of spermatozoa in the epididymis of Creb3l4(-/-) mice, the breeding of mutant males with wild-type females was productive and the average litter size was not significantly altered in comparison to wild-type littermates. Further analyses revealed that the seminiferous tubules of Creb3l4(-/-) mice contained all of the developmental stages, though there was evidence for increased apoptosis of meiotic/postmeiotic germ cells. These results suggest that Creb3l4 plays a role in male germ cell development, but its loss is insufficient to completely compromise the production of spermatozoa."],["dc.identifier.doi","10.1128/MCB.25.17.7657-7664.2005"],["dc.identifier.isi","000231329300024"],["dc.identifier.pmid","16107712"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50005"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Amer Soc Microbiology"],["dc.relation.issn","0270-7306"],["dc.title","Reduction of spermatogenesis but not fertility in Creb314-deficient mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1795"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Cellular and Molecular Life Sciences"],["dc.bibliographiccitation.lastpage","1809"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Tylkowski, Marco Andreas"],["dc.contributor.author","Yang, Kefei"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.contributor.author","Stoykova, Anastassia"],["dc.date.accessioned","2018-11-07T09:58:04Z"],["dc.date.available","2018-11-07T09:58:04Z"],["dc.date.issued","2015"],["dc.description.abstract","Cortical glutamatergic neurons are generated by radial glial cells (RGCs), specified by the expression of transcription factor (TF) Pax6, in the germinative zones of the dorsal telencephalon. Here, we demonstrate that Pax6 regulates the structural assembly of the interphase centrosomes. In the cortex of the Pax6-deficient Small eye (Sey/Sey) mutant, we find a defect of the appendages of the mother centrioles, indicating incomplete centrosome maturation. Consequently, RGCs fail to generate primary cilia, and instead of staying in the germinative zone for renewal, RGCs detach from the ventricular surface thus affecting the interkinetic nuclear migration and they exit prematurely from mitosis. Mechanistically, we show that TF Pax6 directly regulates the activity of the Odf2 gene encoding for the appendage-specific protein Odf2 with a role for the assembly of mother centriole. Our findings demonstrate a molecular mechanism that explains important characteristics of the centrosome disassembly and malfunctioning in developing cortex lacking Pax6."],["dc.identifier.doi","10.1007/s00018-014-1766-1"],["dc.identifier.isi","000352791200011"],["dc.identifier.pmid","25352170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37296"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Basel"],["dc.relation.issn","1420-9071"],["dc.relation.issn","1420-682X"],["dc.title","Pax6 controls centriole maturation in cortical progenitors through Odf2"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","137"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Journal of Cell Biology"],["dc.bibliographiccitation.lastpage","146"],["dc.bibliographiccitation.volume","87"],["dc.contributor.author","Hueber, Daniela"],["dc.contributor.author","Geisler, Stephanie"],["dc.contributor.author","Monecke, Sebastian"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.date.accessioned","2018-11-07T11:17:30Z"],["dc.date.available","2018-11-07T11:17:30Z"],["dc.date.issued","2008"],["dc.description.abstract","The outer dense fiber protein ODF2 is the major component of the sperm tall cytoskeleton and a critical component of the mature centriole of the centrosome. Centriole maturation involves the formation of appendages and the recruitment of ODF2/Cenexin. ODF2 and Cenexin are alternative splice variants that differ in a short stretch of amino acids at their N-terminal regions encoded by exon 3b. Whereas Cenexin is ubiquitously expressed, Odf2 is the predominant transcript of testes [Huber, D., Hoyer-Fender, S., 2007. Alternative splicing of exon 3b gives rise to ODF2 and Cenexin. Cytogenet. Genome Res. 119, doi: 10. 1159/000109621]. Here, we show that testicular expression of Odf2 correlates with spermiogenesis and ongoing sperm tail formation thus implicating functional differences between ODF2 and Cenexin. By generation of a series of ODF2/Cenexin deletion constructs fused to GFP and inspection of their subcellular localization in transfected NIH3T3 cells we found that a peptide of 42 amino acids specific for Cenexin is necessary for targeting ODF2/Cenexin to the centrosome and the primary cilium. Additionally, this region is also necessary for the formation of ODF2/Cenexin fibers that are associated with acetylated microtubules. Centrosomal targeting of ODF2/Cenexin does not depend on dynein-mediated transport further supporting an alternative targeting mechanism. However, part of the C-terminal coiled-coil region of ODF2 is also important in centrosomal/ciliary targeting and fiber formation presumably by supporting self-association and the formation of higher-order structures. (C) 2007 Elsevier GmbH. All rights reserved."],["dc.identifier.doi","10.1016/j.ejcb.2007.10.004"],["dc.identifier.isi","000254299300002"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54825"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Gmbh, Urban & Fischer Verlag"],["dc.relation.issn","0171-9335"],["dc.title","Molecular dissection of ODF2/Cenexin revealed a short stretch of amino acids necessary for targeting to the centrosome and the primary cilium"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","28"],["dc.bibliographiccitation.journal","BMC Cell Biology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Burnicka-Turek, Ozanna"],["dc.contributor.author","Kata, Aleksandra"],["dc.contributor.author","Buyandelger, Byambajav"],["dc.contributor.author","Ebermann, Linda"],["dc.contributor.author","Kramann, Nadine"],["dc.contributor.author","Burfeind, Peter"],["dc.contributor.author","Hoyer-Fender, Sigrid"],["dc.contributor.author","Engel, Wolfgang"],["dc.contributor.author","Adham, Ibrahim M."],["dc.date.accessioned","2018-11-07T08:44:00Z"],["dc.date.available","2018-11-07T08:44:00Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Pelota (PELO) is an evolutionary conserved protein, which has been reported to be involved in the regulation of cell proliferation and stem cell self-renewal. Recent studies revealed the essential role of PELO in the No-Go mRNA decay, by which mRNA with translational stall are endonucleotically cleaved and degraded. Further, PELO-deficient mice die early during gastrulation due to defects in cell proliferation and/or differentiation. Results: We show here that PELO is associated with actin microfilaments of mammalian cells. Overexpression of human PELO in Hep2G cells had prominent effect on cell growth, cytoskeleton organization and cell spreading. To find proteins interacting with PELO, full-length human PELO cDNA was used as a bait in a yeast two-hybrid screening assay. Partial sequences of HAX1, EIF3G and SRPX protein were identified as PELO-interacting partners from the screening. The interactions between PELO and HAX1, EIF3G and SRPX were confirmed in vitro by GST pull-down assays and in vivo by co-immunoprecipitation. Furthermore, the PELO interaction domain was mapped to residues 268-385 containing the c-terminal and acidic tail domain. By bimolecular fluorescence complementation assay (BiFC), we found that protein complexes resulting from the interactions between PELO and either HAX1, EIF3G or SRPX were mainly localized to cytoskeletal filaments. Conclusion: We could show that PELO is subcellularly localized at the actin cytoskeleton, interacts with HAX1, EIF3G and SRPX proteins and that this interaction occurs at the cytoskeleton. Binding of PELO to cytoskeleton-associated proteins may facilitate PELO to detect and degrade aberrant mRNAs, at which the ribosome is stalled during translation."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft [Ad 129/2-1, 2]"],["dc.identifier.doi","10.1186/1471-2121-11-28"],["dc.identifier.isi","000277848800001"],["dc.identifier.pmid","20406461"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5678"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20108"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2121"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Pelota interacts with HAX1, EIF3G and SRPX and the resulting protein complexes are associated with the actin cytoskeleton"],["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"]]