Matches in SemOpenAlex for { <https://semopenalex.org/work/W2156801167> ?p ?o ?g. }
- W2156801167 abstract "NASP (Nuclear Autoantigenic Sperm Protein) is a linker histone chaperone required for normal cell division. Changes in NASP expression significantly affect cell growth and development; loss of gene function results in embryonic lethality. However, the mechanism by which NASP exerts its effects in the cell cycle is not understood. To understand the pathways and networks that may involve NASP function, we evaluated gene expression in HeLa cells in which NASP was either overexpressed or depleted by siRNA. Total RNA from HeLa cells overexpressing NASP or depleted of NASP by siRNA treatment was converted to cRNA with incorporation of Cy5-CTP (experimental samples), or Cy3-CTP (control samples). The labeled cRNA samples were hybridized to whole human genome microarrays (Agilent Technologies, Wilmington, Delaware, USA). Various gene expression analysis techniques were employed: Significance Analysis of Microarrays (SAM), Expression Analysis Systematic Explorer (EASE), and Ingenuity Pathways Analysis (IPA). From approximately 36 thousand genes present in a total human genome microarray, we identified a set of 47 up-regulated and 7 down-regulated genes as a result of NASP overexpression. Similarly we identified a set of 56 up-regulated and 71 down-regulated genes as a result of NASP siRNA treatment. Gene ontology, molecular network and canonical pathway analysis of NASP overexpression demonstrated that the most significant changes were in proteins participating in organismal injury, immune response, and cellular growth and cancer pathways (major hubs: TNF, FOS, EGR1, NFκB, IRF7, STAT1, IL6). Depletion of NASP elicited the changed expression of proteins involved in DNA replication, repair and development, followed by reproductive system disease, and cancer and cell cycle pathways (major hubs: E2F8, TP53, FGF, FSH, FST, hCG, NFκB, TRAF6). This study has demonstrated that NASP belongs to a network of genes and gene functions that are critical for cell survival. We have confirmed the previously reported interactions between NASP and HSP90, HSP70, histone H1, histone H3, and TRAF6. Overexpression and depletion of NASP identified overlapping networks that included TNF as a core protein, confirming that both high and low levels of NASP are detrimental to cell cycle progression. Networks with cancer-related functions had the highest significance, however reproductive networks containing follistatin and FSH were also significantly affected, which confirmed NASP's important role in reproductive tissues. This study revealed that, despite some overlap, each response was associated with a unique gene signature and placed NASP in important cell regulatory networks." @default.
- W2156801167 created "2016-06-24" @default.
- W2156801167 creator A5055347417 @default.
- W2156801167 creator A5068729549 @default.
- W2156801167 creator A5082137245 @default.
- W2156801167 date "2009-05-13" @default.
- W2156801167 modified "2023-10-17" @default.
- W2156801167 title "Analysis of gene expression profiles in HeLa cells in response to overexpression or siRNA-mediated depletion of NASP" @default.
- W2156801167 cites W1576773659 @default.
- W2156801167 cites W1975859486 @default.
- W2156801167 cites W1977636458 @default.
- W2156801167 cites W1977681402 @default.
- W2156801167 cites W1980590293 @default.
- W2156801167 cites W1981419171 @default.
- W2156801167 cites W1985326610 @default.
- W2156801167 cites W1989375033 @default.
- W2156801167 cites W2002399698 @default.
- W2156801167 cites W2007571492 @default.
- W2156801167 cites W2010398513 @default.
- W2156801167 cites W2013320221 @default.
- W2156801167 cites W2013845759 @default.
- W2156801167 cites W2020288787 @default.
- W2156801167 cites W2024853196 @default.
- W2156801167 cites W2031000162 @default.
- W2156801167 cites W2041071598 @default.
- W2156801167 cites W2041941722 @default.
- W2156801167 cites W2043522660 @default.
- W2156801167 cites W2049175197 @default.
- W2156801167 cites W2049371771 @default.
- W2156801167 cites W2061096783 @default.
- W2156801167 cites W2072380594 @default.
- W2156801167 cites W2076611205 @default.
- W2156801167 cites W2077169782 @default.
- W2156801167 cites W2079870321 @default.
- W2156801167 cites W2084809191 @default.
- W2156801167 cites W2095516078 @default.
- W2156801167 cites W2097255042 @default.
- W2156801167 cites W2098456169 @default.
- W2156801167 cites W2110307590 @default.
- W2156801167 cites W2110817748 @default.
- W2156801167 cites W2113495229 @default.
- W2156801167 cites W2123087827 @default.
- W2156801167 cites W2127938920 @default.
- W2156801167 cites W2128036243 @default.
- W2156801167 cites W2128985829 @default.
- W2156801167 cites W2134140342 @default.
- W2156801167 cites W2137082708 @default.
- W2156801167 cites W2138726369 @default.
- W2156801167 cites W2140576556 @default.
- W2156801167 cites W2145349694 @default.
- W2156801167 cites W2154579710 @default.
- W2156801167 cites W2157615753 @default.
- W2156801167 cites W2159942494 @default.
- W2156801167 cites W2171118762 @default.
- W2156801167 cites W4246619137 @default.
- W2156801167 cites W4294107304 @default.
- W2156801167 doi "https://doi.org/10.1186/1477-7827-7-45" @default.
- W2156801167 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2686705" @default.
- W2156801167 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19439102" @default.
- W2156801167 hasPublicationYear "2009" @default.
- W2156801167 type Work @default.
- W2156801167 sameAs 2156801167 @default.
- W2156801167 citedByCount "24" @default.
- W2156801167 countsByYear W21568011672012 @default.
- W2156801167 countsByYear W21568011672013 @default.
- W2156801167 countsByYear W21568011672015 @default.
- W2156801167 countsByYear W21568011672016 @default.
- W2156801167 countsByYear W21568011672018 @default.
- W2156801167 countsByYear W21568011672019 @default.
- W2156801167 countsByYear W21568011672021 @default.
- W2156801167 countsByYear W21568011672022 @default.
- W2156801167 crossrefType "journal-article" @default.
- W2156801167 hasAuthorship W2156801167A5055347417 @default.
- W2156801167 hasAuthorship W2156801167A5068729549 @default.
- W2156801167 hasAuthorship W2156801167A5082137245 @default.
- W2156801167 hasBestOaLocation W21568011671 @default.
- W2156801167 hasConcept C104317684 @default.
- W2156801167 hasConcept C119056186 @default.
- W2156801167 hasConcept C150194340 @default.
- W2156801167 hasConcept C153911025 @default.
- W2156801167 hasConcept C29537977 @default.
- W2156801167 hasConcept C502942594 @default.
- W2156801167 hasConcept C54355233 @default.
- W2156801167 hasConcept C8415881 @default.
- W2156801167 hasConcept C86803240 @default.
- W2156801167 hasConcept C95444343 @default.
- W2156801167 hasConceptScore W2156801167C104317684 @default.
- W2156801167 hasConceptScore W2156801167C119056186 @default.
- W2156801167 hasConceptScore W2156801167C150194340 @default.
- W2156801167 hasConceptScore W2156801167C153911025 @default.
- W2156801167 hasConceptScore W2156801167C29537977 @default.
- W2156801167 hasConceptScore W2156801167C502942594 @default.
- W2156801167 hasConceptScore W2156801167C54355233 @default.
- W2156801167 hasConceptScore W2156801167C8415881 @default.
- W2156801167 hasConceptScore W2156801167C86803240 @default.
- W2156801167 hasConceptScore W2156801167C95444343 @default.
- W2156801167 hasIssue "1" @default.
- W2156801167 hasLocation W21568011671 @default.
- W2156801167 hasLocation W21568011672 @default.
- W2156801167 hasLocation W21568011673 @default.