Schizophrenia risk candidate protein ZNF804A interacts with STAT2 and influences interferon-mediated gene transcription in mammalian cells.

[1]  Olanzapine , 2019, Reactions Weekly.

[2]  T. Decker,et al.  A molecular switch from STAT2-IRF9 to ISGF3 underlies interferon-induced gene transcription , 2019, Nature Communications.

[3]  E. Vannoni,et al.  The Anti-amyloid Compound DO1 Decreases Plaque Pathology and Neuroinflammation-Related Expression Changes in 5xFAD Transgenic Mice. , 2019, Cell chemical biology.

[4]  Annie W Shieh,et al.  Transcriptome-wide isoform-level dysregulation in ASD, schizophrenia, and bipolar disorder , 2018, Science.

[5]  Sigrid Schnoegl,et al.  LuTHy: a double‐readout bioluminescence‐based two‐hybrid technology for quantitative mapping of protein–protein interactions in mammalian cells , 2018, Molecular systems biology.

[6]  H. Xi,et al.  Interactome analysis reveals ZNF804A, a schizophrenia risk gene, as a novel component of protein translational machinery critical for embryonic neurodevelopment , 2017, Molecular Psychiatry.

[7]  M. Hill,et al.  Psychosis Risk Candidate ZNF804A Localizes to Synapses and Regulates Neurite Formation and Dendritic Spine Structure , 2017, Biological Psychiatry.

[8]  N. Stevenson,et al.  Advances in anti-viral immune defence: revealing the importance of the IFN JAK/STAT pathway , 2017, Cellular and Molecular Life Sciences.

[9]  X. Xiao,et al.  The schizophrenia risk gene ZNF804A: clinical associations, biological mechanisms and neuronal functions , 2017, Molecular Psychiatry.

[10]  Peilin Jia,et al.  SZGR 2.0: a one-stop shop of schizophrenia candidate genes , 2016, Nucleic Acids Res..

[11]  A. Vita,et al.  Schizophrenia , 2016, The Lancet.

[12]  K. Błaszczyk,et al.  The unique role of STAT2 in constitutive and IFN-induced transcription and antiviral responses. , 2016, Cytokine & growth factor reviews.

[13]  Konrad Klockmeier,et al.  DULIP: A Dual Luminescence-Based Co-Immunoprecipitation Assay for Interactome Mapping in Mammalian Cells. , 2015, Journal of molecular biology.

[14]  M. Schwarz,et al.  The role of inflammation in schizophrenia , 2015, Front. Neurosci..

[15]  D. Zheng,et al.  ZNF804A Transcriptional Networks in Differentiating Neurons Derived from Induced Pluripotent Stem Cells of Human Origin , 2015, PloS one.

[16]  Paul J. Harrison,et al.  Expression of ZNF804A in human brain and alterations in schizophrenia, bipolar disorder, and major depressive disorder: a novel transcript fetally regulated by the psychosis risk variant rs1344706. , 2014, JAMA psychiatry.

[17]  D. Atkinson,et al.  Schizophrenia: overview and treatment options. , 2014, P & T : a peer-reviewed journal for formulary management.

[18]  C. Spencer,et al.  Biological Insights From 108 Schizophrenia-Associated Genetic Loci , 2014, Nature.

[19]  Ilia N. Karatsoreos,et al.  Links between Circadian Rhythms and Psychiatric Disease , 2014, Front. Behav. Neurosci..

[20]  B. Rost,et al.  PredictProtein—an open resource for online prediction of protein structural and functional features , 2014, Nucleic Acids Res..

[21]  S. Glatt,et al.  How might ZNF804A variants influence risk for schizophrenia and bipolar disorder? A literature review, synthesis, and bioinformatic analysis , 2014, American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics.

[22]  H. Steen,et al.  STAT2 phosphorylation and signaling , 2013, JAK-STAT.

[23]  J. Mintern,et al.  Enhanced survival of lung tissue-resident memory CD8+ T cells during infection with influenza virus due to selective expression of IFITM3 , 2013, Nature Immunology.

[24]  M. Hill,et al.  Evidence that schizophrenia risk variation in the ZNF804A gene exerts its effects during fetal brain development. , 2012, The American journal of psychiatry.

[25]  Alan S. Brown Epidemiologic studies of exposure to prenatal infection and risk of schizophrenia and autism , 2012, Developmental neurobiology.

[26]  J. Darnell,et al.  The JAK-STAT pathway at twenty. , 2012, Immunity.

[27]  M. Hill,et al.  Knockdown of the psychosis susceptibility gene ZNF804A alters expression of genes involved in cell adhesion. , 2012, Human molecular genetics.

[28]  B. Maher,et al.  ZNF804a Regulates Expression of the Schizophrenia-Associated Genes PRSS16, COMT, PDE4B, and DRD2 , 2012, PloS one.

[29]  M. Schwarz,et al.  Inflammatory processes in schizophrenia: a promising neuroimmunological target for the treatment of negative/cognitive symptoms and beyond. , 2011, Pharmacology & therapeutics.

[30]  P. Sullivan,et al.  Schizophrenia genetics: where next? , 2011, Schizophrenia bulletin.

[31]  D. Rujescu,et al.  Fine mapping of ZNF804A and genome-wide significant evidence for its involvement in schizophrenia and bipolar disorder , 2011, Molecular Psychiatry.

[32]  Aaron Klug,et al.  The discovery of zinc fingers and their applications in gene regulation and genome manipulation. , 2010, Annual review of biochemistry.

[33]  Alan S. Brown,et al.  Prenatal infection and schizophrenia: a review of epidemiologic and translational studies. , 2010, The American journal of psychiatry.

[34]  C. Spencer,et al.  Identification of loci associated with schizophrenia by genome-wide association and follow-up , 2008, Nature Genetics.

[35]  D. Levy,et al.  JAK-STAT Signaling: From Interferons to Cytokines* , 2007, Journal of Biological Chemistry.

[36]  R. Singh,et al.  Olanzapine Increases RGS7 Protein Expression via Stimulation of the Janus Tyrosine Kinase-Signal Transducer and Activator of Transcription Signaling Cascade , 2007, Journal of Pharmacology and Experimental Therapeutics.

[37]  K. Honda,et al.  IRFs: master regulators of signalling by Toll-like receptors and cytosolic pattern-recognition receptors , 2006, Nature Reviews Immunology.

[38]  H. Lehrach,et al.  A Human Protein-Protein Interaction Network: A Resource for Annotating the Proteome , 2005, Cell.

[39]  E. Susser,et al.  Serologic evidence for prenatal influenza in the etiology of schizophrenia , 2003, Schizophrenia Research.

[40]  R. Hoffman,et al.  Schizophrenia as a disorder of developmentally reduced synaptic connectivity. , 2000, Archives of general psychiatry.

[41]  S. Anderson,et al.  Is schizophrenia due to excessive synaptic pruning in the prefrontal cortex? The Feinberg hypothesis revisited. , 1994, Journal of psychiatric research.

[42]  I. Mosweu,et al.  The Societal Cost of Schizophrenia: A Systematic Review , 2016, PharmacoEconomics.

[43]  I. Feinberg,et al.  Schizophrenia: caused by a fault in programmed synaptic elimination during adolescence? , 1982, Journal of psychiatric research.