STANDARD_NAME BRUINS_UVC_RESPONSE_MIDDLE SYSTEMATIC_NAME M2249 COLLECTION C2:CGP MSIGDB_URL https://www.gsea-msigdb.org/gsea/msigdb/human/geneset/BRUINS_UVC_RESPONSE_MIDDLE NAMESPACE MOUSE_SEQ_ACCESSION DESCRIPTION_BRIEF Middle response genes: differentially expressed in the period between 3 h and 12 h after UV-C irradiation of MEF cells (embryonic fibroblast). DESCRIPTION_FULL Phosphorylation is important in p53-mediated DNA damage responses. After UV irradiation, p53 is phosphorylated specifically at murine residue Ser389. Phosphorylation mutant p53.S389A cells and mice show reduced apoptosis and compromised tumor suppression after UV irradiation. We investigated the underlying cellular processes by time-series analysis of UV-induced gene expression responses in wild-type, p53.S389A, and p53(-/-) mouse embryonic fibroblasts. The absence of p53.S389 phosphorylation already causes small endogenous gene expression changes for 2,253, mostly p53-dependent, genes. These genes showed basal gene expression levels intermediate to the wild type and p53(-/-), possibly to readjust the p53 network. Overall, the p53.S389A mutation lifts p53-dependent gene repression to a level similar to that of p53(-/-) but has lesser effect on p53-dependently induced genes. In the wild type, the response of 6,058 genes to UV irradiation was strictly biphasic. The early stress response, from 0 to 3 h, results in the activation of processes to prevent the accumulation of DNA damage in cells, whereas the late response, from 12 to 24 h, relates more to reentering the cell cycle. Although the p53.S389A UV gene response was only subtly changed, many cellular processes were significantly affected. The early response was affected the most, and many cellular processes were phase-specifically lost, gained, or altered, e.g., induction of apoptosis, cell division, and DNA repair, respectively. Altogether, p53.S389 phosphorylation seems essential for many p53 target genes and p53-dependent processes. PMID 18195040 GEOID AUTHORS Bruins W,Bruning O,Jonker MJ,Zwart E,van der Hoeven TV,Pennings JL,Rauwerda H,de Vries A,Breit TM CONTRIBUTOR Arthur Liberzon CONTRIBUTOR_ORG MSigDB Team EXACT_SOURCE Table 2S: Found in=WT_II FILTERED_BY_SIMILARITY EXTERNAL_NAMES_FOR_SIMILAR_TERMS EXTERNAL_DETAILS_URL SOURCE_MEMBERS AB010318,AB043586,AE000663,AF034580,AF075136,AF141311,AF229643,AF274973,AJ005350,AJ131957,AJ243418,AK003661,AK003880,AK004173,AK004319,AK004405,AK004708,AK005239,AK005431,AK006115,AK008492,AK009264,AK009425,AK009540,AK010254,AK010356,AK012513,AK012625,AK012941,AK013668,AK015009,AK015275,AK015640,AK016224,AK019097,AK019105,AK019150,AK019768,AK019874,AK020882,AL078630,BC002280,BC003284,BC003333,BC003341,BC004753,BC004766,BC005625,BC005638,BC006704,BC006858,BC006964,BC009125,BC009145,BC011308,BC011512,BC013499,BC014757,D14336,D32137,L16846,M31585,NM_007477,NM_007570,NM_007596,NM_007837,NM_007855,NM_007859,NM_007982,NM_007997,NM_008005,NM_008254,NM_008838,NM_009372,NM_009420,NM_009423,NM_009469,NM_009564,NM_009569,NM_009811,NM_009833,NM_010718,NM_010830,NM_011599,NM_013632,NM_013709,NM_015763,NM_015796,NM_016675,NM_016910,NM_019967,NM_020483,NM_020560,NM_020583,NM_023233,NM_023815,NM_025294,NM_026034,NM_026411,NM_028712,NM_030260,NM_030720,NM_031873,U20239,X58472,X80431,Z49086 GENE_SYMBOLS ZNF263,RPRM,TRBV13,KNOP1,SAP30,HILPDA,USP27X,PIDD1,,SAC3D1,ARVCF,ZFYVE21,CHST11,,ELOVL5,ATP23,WDR73,CDAN1,TTC23,IFT43,DUSP11,FASTKD3,SEC24D,CLUAP1,SLC7A6OS,DEF6,,,CMTM6,,ADAL,OTUD4,NAA30,,C10orf88,TEPSIN,SLC25A12,,GMIP,SHISAL2B,OR2H2,MTERF4,DCAF4,RBM43,GPN3,L3HYPDH,PTCD1,MRM1,FAM220A,DYRK3,FCHSD1,ZNF622,NSMCE2,IMP3,DDX41,TMEM41A,DEPDC7,SPRYD4,POLR1E,OVGP1,BTG1,ICAM1,,BTG2,CAMLG,DDIT3,TWIST2,DFFB,PTK2,FDXR,FGF18,HMGCL,PIGF,TGIF1,CRISP2,TRAF4,ULK1,ZFP64,ZFPM1,CASP6,CCNT1,LIMK2,MSH6,TLE1,PNP,SH3YL1,LPIN1,FBXO17,CLDN2,PPM1D,BRINP1,SAP30BP,MRPS31,ISG20,TRIM13,TP53RK,NATD1,ARMC10,MTRES1,RAP2B,ZXDC,GPR84,TAS1R2,FBRS,KIN,PPP2R5D,EPHB3 FOUNDER_NAMES