STANDARD_NAME CHANG_IMMORTALIZED_BY_HPV31_DN SYSTEMATIC_NAME M12051 COLLECTION C2:CGP MSIGDB_URL https://www.gsea-msigdb.org/gsea/msigdb/human/geneset/CHANG_IMMORTALIZED_BY_HPV31_DN NAMESPACE HUMAN_SEQ_ACCESSION DESCRIPTION_BRIEF Genes down-regulated in normal keratinocytes immortalized by infection with the high risk HPV31 (human papilloma virus) strain. DESCRIPTION_FULL Human papillomaviruses (HPVs) infect keratinocytes and induce proliferative lesions. In infected cells, viral gene products alter the activities of cellular proteins, such as Rb and p53, resulting in altered cell cycle response. It is likely that HPV gene products also alter expression of cellular genes. In this study we used microarray analysis to examine the global changes in gene expression induced by high-risk HPV type 31 (HPV31). Among 7,075 known genes and ESTs (expressed sequence tags) tested, we found that 178 were upregulated and 150 were downregulated twofold or more in HPV31 cells compared to normal human keratinocytes. While no specific pattern could be deduced from the list of genes that were upregulated, downregulated genes could be classified to three groups: genes that are involved in the regulation of cell growth, genes that are specifically expressed in keratinocytes, and genes whose expression is increased in response to interferon stimulation. The basal level of expression of several interferon-responsive genes was found to be downregulated in HPV31 cells by both microarray analysis and Northern blot analysis in different HPV31 cell lines. When cells were treated with alpha or gamma interferon, expression of interferon-inducible genes was impaired. At high doses of interferon, the effects were less pronounced. Among the genes repressed by HPV31 was the signal transducer and activator of transcription (Stat-1), which plays a major role in mediating the interferon response. Suppression of Stat-1 expression may contribute to a suppressed response to interferon as well as immune evasion. PMID 10756030 GEOID AUTHORS Chang YE,Laimins LA CONTRIBUTOR John Newman CONTRIBUTOR_ORG University of Washington EXACT_SOURCE Table 1: fold < 0 FILTERED_BY_SIMILARITY EXTERNAL_NAMES_FOR_SIMILAR_TERMS EXTERNAL_DETAILS_URL SOURCE_MEMBERS AA100757,AA255824,AA521454,AA741307,AA780043,AA905409,AB001928,AF002668,AF013970,AF034840,AF043325,AI004422,AJ000480,D28915,J04164,L06895,L33404,L33930,L34155,M14660,M20030,M21054,M22612,M23263,M30818,M33882,M34715,M55542,M77830,M87284,M95787,M97935,N24715,S73288,U04636,U09364,U49260,U50931,U62801,U65590,U67615,U72882,U79725,U92314,V00497,V01512,W73855,W76205,X03557,X04327,X04470,X04707,X13916,X56807,X57348,X59770,X67325,X74330,X77533,X82200,X86809,X89960,X90840,X97198,X99133,Y00630,Z85996 GENE_SYMBOLS HMGCS1,,PHF7,SAMD9,UBE3B,SNRPA1,CTSV,DEGS1,CBFA2T2,ENTPD3,NMT2,TEX29,TRIB1,IFI44,IFITM1,MXD1,KLK7,CD24,LAMA3,,SPRR2E,PLA2G1B,PRSS1,AR,MX2,MX1,PSG1,GBP1,DSP,OAS2,TAGLN,STAT1,,SPRR1A,PTGS2,,MVD,,KLK6,IL1RN,LYST,IFI35,GPA33,SULT2B1,HBB,FOS,DMKN,DSG1,IFIT1,BPGM,SLPI,THRB,LRP1,DSC2,,IL1R2,IFI27,PRIM1,ACVR2B,TRIM22,PEA15,SMCP,,PTPRU,LCN2,SERPINB2,CDKN1A FOUNDER_NAMES