DOCSLIB.ORG

5 0 5 10 Log2 Fold Change FDR Adjust P Value Volcano Plot 0 50 100 150

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
5 0 5 10 Log2 Fold Change FDR Adjust P Value Volcano Plot 0 50 100 150 A Volcano plot Not significant 150 Up regulated Down regulated 100 50 FDR adjust P value 0 −5 0 5 10 log2 Fold Change B PCDHB11 ZNF675 ZNF85 NAT16 ZNF519 LPPR4 N4BP2L1 PCDHA4 CUEDC1 CCER2 C4orf6 FAM189B GAL3ST4 GRAMD1B GOLPH3L UNC119B PRDM7GCSAML BPIFB4 ENSG00000181638 ZNF560 ADAMDEC1 GRAMD1A ARL17A DCAF4L1 TSGA10IP CXorf36 LDLRAD1 ZNF391 CYP2W1 CST2 CCDC169 LYG1SCGB3A1 ANKLE1 PCDHA7 BNIPL TMC4 ARL17B BTNL8 GRAMD1C C3orf55 CARD18 AGAP4 SBK3 TSPAN5 NUDCD1 ZNF114 LRRC63 MAP7D2 ERICH6B SLC22A15 ZNF273 GLOD5 RTKN2 SERHL2 HEPACAM2 ACBD7 ZNF530 EFHD1 STXBP4 C1orf95 PROKR1 C12orf73 ZFP69B NXPH4 C9orf57 PRR5L FDCSP BPIFA2 ZNF71 BEX2NT5DC4 ZNF532 LRRC19 SLC45A4 DRICH1 PADI3 SLC38A8CCDC71L WDR17 FNDC4LRRC37A BEND6 FAM110CSLC26A7 PCDHB16 DPEP2 AQP10 LRRC37A3 ONECUT3 CYP27C1ANKS6 GPR64 ZSCAN9GPR115 FAM198A BANF2 FAHD2A OTOGL ZSWIM5 TSPAN11 RUFY4 MROH6 LIPH TTC9 DEFB132 TIGD5 CST5 ZNF454 POPDC3TM4SF20 CWH43 ZNF251 SSC4D EPPK1 SLC5A10 MFSD6 HHIPL2 ASIC5 CDH19C11orf53 FAM151A SLC25A47PNRC1 C8orf59 RGS17 OTOP3 CEP128 CTAGE15 EDDM3A NAALAD2 SAMD12 SEC14L3FSTL4 SCUBE1 PBLDPPEF1 FRMD3 FAM171A2ANO9 DNASE1L3 OCLM C1orf116FAM57BSLCO5A1 C1orf198 CLRN3ZPLD1 WDYHV1 CLVS1CEMIP CLDN15 GSDMC CUZD1 JRKL ANKAR DAPK2 C6orf132 RNF125 PADI1 PRDM12 IMPG2 HMCN2TMC7 LRRC36TMEM106C LPPR1 MCCD1 CCDC112C5orf34 SLC5A11 MYO16 TMEM191B PTCHD4 HSD17B13 SLC4A3 KLHDC7B PLSCR5TSPAN10 JRKPSAPL1 SLC38A6 AQPEP AIFM3 SPATA21 UQCC2 C21orf62 UCN2 SLC26A9 NIPAL2 AP3B2GPR161C15orf59 ABCB9 PKDCC ILDR2 SLC4A5 GPR146B4GALNT4 PLEKHS1 RASL10B MYO7BPDZD7 PCDHGA1 SSC5D GALNT13 PNMA3 PLEKHH1 SLC38A5 FAM178BMATN4 C21orf91NUGGCMFAP3LMSANTD1 C11orf96 LGALS12 SMIM24 LRRC39SLC7A6 CNGB1 C1orf158 FAM180A PAGE2 STC1 FIBCD1RDH8 CD302PAPLN GPR88 NRIP2 PRRG3 BAI3 LGI2 PLXDC1CHST5 SCN7APLSCR4 MIP 43528 SSUH2 SCGB1D2 ABHD12B AQP8 CST1 NAALADL2 TMCO3YJEFN3 ATP13A4 ILDR1 OLAH STRA6 NDRG2 ANKRD29LRRC55 ZNF711DSCR8 SPRYD4 CYP4V2 JSRP1 AVIL MRO BFSP2 MPPED2 TMEM25 RBM46 DAGLA GLB1L3 SLMO1 BEND4IRF2BPL SLC7A4 SLC6A15 CDH24NKAIN2ZNF404ANO4OR51E1 GAL3ST2 FITM1 SLC13A4 CCDC154 CA5B CPNE7TBX19 SHISA6KIAA1324 PXMP2 JAKMIP3 ASIC3 CPED1 LRRC26 GULP1SLC4A11 FAM149ARGS13 CRYBB1 DSCR4 ZNF793 CELA3A CHST6 MFSD2ACDH26 KRT6BESYT3 CHST4GXYLT2 PRIMA1 ODAM SERPINB4 SLC22A10EHD3 TCTEX1D1 RTBDNNTN5 CLDN18 CLIC6 CRYBA2 LAMP5 MCF2L2 RHBDL1 TMPRSS15 BCAT1 GPR50 RDH5 PNMT LRRC66SLC6A9 AVPI1 ISX MUC12 ATHL1 KCNJ14ABCA4 KCNJ15 SCNN1BKCNK10SLC38A11 NWD2 CAMK2N2 KIAA1211L TMEM178B C15orf48 TBC1D16 CPA5 FSCN2RUSC1 KCNK12EPS8L3 EFCAB12 SPATC1LPCDHGA2 ACSM1 TPSG1 SLC41A2 HS3ST3A1BPIFB1 TSPEARSLC9B2 GPR123 BEND3 BEST4 SCNM1 AMOTL2 C1QTNF9BUROC1 SPATA18CTRB2 REG1B MGAT3SLC7A8LYG2 AQP5 ANO2 CLDN19CCDC85APMEPA1 PRRT4 KCNJ13 MCC ACADSB MUCL1SCGB2A1 GDPD3 RGS20 AQP3TM6SF2TRPM5 RS1FCGBPCNTN1RUNDC3A GATSSAMD5ZBTB21 WSCD1 SEZ6L FAM222A GALNT5 MALRD1 SLC38A2PCNXL2 PCDH9 ABLIM2 LHFPL3 NOL4 CDH12 SOWAHB FAM212B ANGPTL6 LOC93432 GPR1 CRLF1 LRAT WBSCR28 PRKAA2 C9orf152ALS2CLENSG00000279362PI15 PLAC8L1 C1QL1 PLEKHD1 NIPAL1RIPPLY2 ADIG FRMD4B RHBG PRELPBCO2CPA2 MAFANKIRAS1SLC46A2DOK7SLC35E4PCSK1N MEP1B CPNE5 CCDC141GPR160 FAM19A4NDUFA4L2 ATP8A2 SYNDIG1 ELFN2BAIAP2L2 PRSS56 HIC2 KBTBD11 PTPN14 PCDHB8 PLEK2 B3GNT4 B3GNT3 SLC9A9INS-IGF2 WNK2 PDE1C OSR1 RIPPLY3 DDN GPR114 AQP7SLC12A1 TMEM35 TTYH3 VSIG10L C6orf163 CST4MS4A7 ATP11C MGAT5BMUC15 SLC1A7GALNT16CNGA1PLP2 CEND1MKRN3 PRR15L APOBEC3A KAAG1 ZNF385C SLC7A14ST3GAL6GLYATCHST8 TUSC5MEP1A CADPS GABRQPKD1L1 DSG4PRRT3KCNH6 FER1L5ZFR2 RRAGDMRAP2PXDNL CLUL1 RASD2 SLITRK3SOCS7 HAP1RIMS3S100A3MPPED1SLC6A17VAMP1 VPS45FRMPD1BICC1 PCDHA6 QRICH2 AQP6ACSM3 TMEM108 CSN2ZG16VN1R1 BPIFA1LYPD8CRHBPSCGNGJB6 STRCSYT8PDE6G OLFM3 SOWAHA C8orf4TMEM200A KIAA1462 SLAIN1 GDPD1 ZNF365 ALDH8A1 ABHD6 SLC34A3MDGA2 PPP1R1B EDIL3 KRT81 CCDC108 TTC13 VSIG1 TGM3 MPC1 CTRB1CPA1NMNAT2 ADRBK2 ANKRD52 REEP2 CRYBA4 VSTM5 LCNL1 RASGEF1B SLC16A11SLC44A3 CPA6 REG1A CHST10CILPHAPLN3 P2RX3 PTCHD2RIMS2 MGAT4C CLEC2L FAM186AENSG00000248919 CXCL17MS4A6A GPR27SLC14A2ADM2 RIMKLA TIMD4PEG3CHRNDLSAMP CLCNKASLC6A14HS3ST4 TTYH1OR2B6GLDNANKRD23APOBEC2 CORO6 EGFL6NREP RDH16 PLVAP CD300EPOU6F2 EPHX4 CCDC102B UTS2 GPR97DNASE1SYNGR3CNIH2 ASIC1 OR51E2 KRT12 FOXS1CIB2AIM1LPOPDC2 SLC22A17 PNMA5 TTC36 PEX5L SLC38A1 SLC6A12GNAT1 SLC26A3 DOC2AGRIK2SGSM1 SEZ6L2CAPN14RNF157 ANXA13 TMIEFER1L6 PIANP LRP4 UPK3ASLC9A2 PLCXD3TMEM132BBSNDSLC26A6SLC6A2ANKRD22KCNH1 MCOLN3CNTN4 SYT5 GJA3 ZNF285ENSG00000157654TMEM151A ZNF605 SIGLEC11 REG3A PDZK1IP1DEFA5 RBP2 FAM132A B4GALNT1SLC16A3CCL28KLK4 ARR3DBNDD1CRB1 SLC17A8 SCN11AUNC13AKCNJ6 ENPP5TIGD1 SLITRK6 GALNT10HPSE2 PLIN1 SLC16A14 SLC5A4CNGB3KLF11 GABRA3JPH2 GABRG3 AATK VEPH1CCDC36 COX4I2 ODF3L1 REG3G TMEM8C KLHL35 NPY5RSLC7A2 QRFPRGUCA2APROK1 LPHN1SLC7A10MDGA1 GABRA2CLEC3B KCNU1AIF1L KRT23CKMT1B IL1RAPL2COX7B2 FHL5 VCX PLA2R1 CHST1 HMGCLL1 CXCL14 CTSE PKD2L1AVPR1A AGPAT4NMB NPFFR2CHRM3APELAARHGAP28OXCT1NETO2 PDE6CART3DFNB31 KIRREL2SLC45A2 SEZ6 ZNF169 SAMD11C11orf80 SDK1 GPR128 GCNT3SLC16A4ST8SIA1CEL GLP1R AP1M2 UNC5D PDE2ASLC46A3MAP3K15WNK4 STRIP2CAPN12 PRR15 SLC29A4ACADL C1R PTGER2SCTRCA4GPR83SLC1A1ADRB1CRHR1 SLC9A3 CLDN4PACSIN1RBPJLFXYD3 GJB3 KCNK2 ENTHD1 SEC14L5 SYTL5 EFCAB5 SCIMP ACADS CLEC4MB3GNTL1GCDH GIPRHCAR1PON3 STAB2MUC13 BAI1 TECTBCACNG4 KCNK9 LYPD1KCNE1 STX11 BCAS1PPFIA4ENSG00000204176ADAM11 BFSP1 MYEF2 SULT1C2POU2F3 CCL23 ZBTB12 SI GNA14 TECTAEDNRB TRPC3 NPTX1PHLDA1CATSPERB EIF4E3NAAA ACAA1 IYDPLIN2CCL4L1MMP10ETFDHTRPM8 ATP1A4 MGPDPYSL4PDZD2 RTDR1 SYT13 C1orf204 DLK2 ALG1L EXTL1 SLC13A3 SMPDL3BPAMR1PPAP2C SSTR3BDKRB1CCRN4L POF1BSLC2A14 GNAZDAND5ASPHABCA3 CLN3 SH3GL3OCA2LHFPL4 SP5 HTRA4C5orf46 IGSF11 NDRG3 CES3 PEX11GTMEM82ACOT2NDST3SPINK1NDST4ACAA2TBXA2RHGFACCCL13 GRPR TMEM132AKISS1R ADRA1DATP1B1TMEM130CEACAM7NTM FAM163B CSMD1GABREGDAP1L1 CLVS2BMP8BFOXD2CAPN8GJC1LYPD6 DRP2ERVFRD-1 PCDHA3FAXC KIAA1549L SERPINB9 HTRA3 TTC39B UPK1A CORIN B3GNT5PNLIPSULT4A1SLC16A2GLS2ADAM12PRKD1PDE6ADUSP26RHO CACNA2D3CLCN1CKMT2SLC6A3MYBPHLSNAP91 LRFN2ARHGEF26CAMK1G SERPINI2ATP1B3HHATLNXPH3 SVEP1 TMSNB KIAA1614 CES5A IL27 AADAT SLC2A5SLC35D1GPR150 CRHR2 NTNG2 UTS2BCNTN5 MYO18BCLDN6 SCN4ANDRG4 CCDC170 GPR158 SUSD4KRT85 COA6 ACAD11FERMT1B4GALNT2LPGAT1CA8 SULT1A2 SSTR5MLYCDIAPP GSTM5ADRA2BVIPR1 TACSTD2OXTNTS GHRHRTMEM27 PTGDSCALML6TRPC4SMTNL2 PITPNM3DACH2 KBTBD12 CXorf22 DHRS2 CNNM1SIGLEC14 KELAQP1GAL CPT1B TMEM220SHANK1LYPD2GABRR3 BOLA2BKIAA0319 SLC8A2 LGI3 GJA10 HAGHL LRRC69 ELOVL4SPTSSB NPBWR1TAS2R5PTGIRMUC5ACSLC5A1 GRM8GABBR2KMONPY1RCHRM2 TMEM59LCNTN3ALLCSGIP1STK39 GUCY2DCRYABSMPXKCNH5FAM134BCASKIN1CSDC2 SYT6 VGLL2 KLHDC8A C22orf23 CYP4F2 FCN1 BCHE RXFP1DRD4PDLIM7ADRA2CCALCBQRFP GOLM1SLC12A5PLEKHG4BEPHB1 EPB41L1TMPRSS4SCAMP5 FREM2 ENSG00000259305SIRPB1 SLCO2A1MARCO GDF6 UAP1L1 ACSL1 CCR3 P2RY12SLC9C2PTGFRFFAR2HTR2CARG2ADRA1A THBS4 CALN1GABRD SDK2 STXBP6SH3D21IL1RAPL1 C1orf64 PGLYRP2 C14orf180G0S2 SLC47A2ADH1AACSL6 LIPEPPP1R3BLPAR3XK BPIFB2TAS2R4GCGR GASTGNGT1GP2HCN2 CLTCL1 GGT5PRSS21GGN TTYH2ATP1A2 S100A1GJB2 SLC52A3 LY6G5B ACACBRIC3ADH6 GNPATFUT2MUC5B PTGDR2ST6GAL2 GPR37L1 LY6EFAM46AAVPR2VGF TRPM6NR3C2CHGBASPHD1SCN1ABEGAINPSD2DLGAP2KCNH2 KCNN2PCP4 ZIC4CDH8 MEGF11 LRP12PLA2G5 DMBT1 SCINGLP2R BCAMHKDC1CNR1ADRA1BPADI4GPR35 PDE4CGNALGRIK4F2RL3GRIN2BCASQ1OXTRPRND CKMT1A CALY PIEZO2PRDM15AGAP5TRPM3ATP10A CCDC13 LRRC16B PCDHA1 ST8SIA5PTH2R BDKRB2PTGDR SLC26A2P2RY13GLSTAS2R20DUSP5PLCD4CHRM1SEL1L3HAPLN1 MNX1PTPRR CACNA1B GCM1FAM227ASIPA1L2 DMRTB1 SHISA2 SLC22A11 CCL26AGXT2 C6 TREH CXCR1CTSCFPR2SLC22A2PSCAPTGISGRM2 CDS1DLK1NDRG1 TRPA1RASEFCPLX1CACNG8GRIN2CKCNMB3RIPK4RHBDL3SCNN1GDIRAS2PTPN5HCN4CATSPER1LRRC10B SLITRK5 COX6B2 SSX3 PLD5 GPR63 HS6ST2 SRD5A1DIO2CPA4 ARHGAP20CCR10 LHX4-AS1NMUR1ALDH3A1HTR1DAGTR2ADORA1PODXL CAMK2BSLC4A4 KRT20ATP1A1RNASE1NRXN1DLX2 MYBPC2PCDH17ITPKA CATSPER2MYO1A CDH18 CRYGSEGFL8 HUNK AMN SLC22A12 TSPO2CYP2C19 PLA2G6CCR1SPP2TMEM65C8A APOD HTR4 IGDCC3TACR1 DACH1 ITPR3TRPV4CACNA1SCACNA1FLY6KGABRG2 SCAMP3MICAL1CPLX2 DNER TMEM81 PNPLA7 ARHGEF38TMEM156 ST6GALNAC1RTL1CPD SLC7A11 MCHR1 TSPAN8SLC1A3 MC1R DLGAP1GUCY2C SLC26A8 RXRGLOXHD1 ECEL1 RGAG4 SPINK5SLCO1C1 SLC16A9 CXCR2ADMCLIC1 CEACAM3LRRC52GLULSLC6A4SRPX MPP2KCNJ5 ANKRD34ACACNA1ISTX1AGPRIN1RASGRF1USH1CPI16CDH9NOVA1COX6A2NLRP2 TRNP1IGDCC4 ABCA12APRG1 THRSPPANK1 TDO2 CYP1B1 F9 DGKKPCK1PTGER3MASP1A1BGGCG SULF1ANGPT2 VNN2NPHS1PVALBSLCO4C1 GRIA2CLIC5COCHCDH22 CACNB4 GPNMB TRIM54PKIB BMP8A CCL14 CPXM1CYP26A1ST6GALNAC5SAA4VSIG4 APLN CD109ATF3MFI2REG4CNTNAP1SSTDLG5NRXN3DNM3SNAP25 HOMER3 KCNN3 BCL2L15ANKRD2CCDC77 KIAA0907 RNF24 CRTAC1 MEGF10FTCDPTGESAPOA5 KLKB1GALR2TAC3 KCNC2MPZNOS2SAA1AGRN ADRB2ABCC8SLC19A3 DSCAMPRPF3GRIN2ACHGAPCSK1LY6HDCC RNF43TIAM1CELF4 UQCRBPEA15 COX6C FSTL5 COLCA2 DCST1 TREML4 SAA2-SAA4 ACOXLWFDC1ST8SIA6PROZTOMM40L CLEC1B C5AR1 GPC2CALCRMNS1 CCL25 GPM6AAGTR1RENCKBDGKI FAIM2 CDH11SPARCL1 NTN4TRPC1 LGI1 TRDNTNNC1C20orf96SOX21 C8orf76 FCRLA SLC27A5 PLA2G4CMOGAT2ADH4CTSACYP24A1FBP1MTNR1BC9ASPA PLAC8CAPN13 ABCC9MSLNENO3 GRIN1 SYT3ERC2LRRN3FRAS1 DRGX KIAA1751EML5 TMEM198 C2CD4B UGT1A8SLC16A8 SLC35F3 GPSM1QPCTFGD1CCL20ACSL4SCG3PIK3R2ERICH4GRM7CGACALCAHK2 GNG4 SH3PXD2BFAM155ASCG2 CFAP45SYT2RAPSN CACNA1EDCXATP6V1B1 TRIM72TCF15 PHYHIPL NR1I2 TAGLN2PLA2G4FGALR3 SLC5A2 BSGGRM4CXCL5OGDHLPLCB4 TH EPHA5CAMK2ARFX6CNTN2HSF4 RAB3B LRRC4 43711 CDHR2 LSMEM1 ALS2CR11 FMO1 ST6GALNAC2PRSS3P2SLC5A5 GPX2 CLPS MFGE8ADCY8AGR2LRP8ASS1 PAEP DNAJC6EPHA2 APLP1 CHN1 CDH13SLC6A11FOXH1ARHGAP10 GIPC2 CAPN11 CYP3A43 C6orf25 PAQR5ELOVL3 S100A12 CCL4 ALPI TP63ADCY6POSTN LHX9DBH CALB1KCNT1KCNJ4 IFITM5MAP2K3GPR56SCN5ASLC35F1RASGRF2RHCG BACE2C2orf40 ZNF385D LIX1 CCDC185MYOM3CDH7 CYP39A1FCN2UGT2B11 AKR1C3ABCC4CD1A IL1RAPPPBPGLYATL1 GNRH1DCNATP6V0D2PGCPNMAL2NGF GCH1NKX3-1 JPH1 GJA5PRR16MLANAFAT4 ANKS1BFLJ22184 KANK4 KRT86CNIH4 IGFN1 UGT2B7 FLRT1 ENSG00000160200KCNH4LPCAT1INHAPLA2G1BNELL1CXCL2TNR
Load more

Recommended publications
  • Genetic Associations Between Voltage-Gated Calcium Channels (Vgccs) and Autism Spectrum Disorder (ASD)
    Liao and Li Molecular Brain (2020) 13:96 https://doi.org/10.1186/s13041-020-00634-0 REVIEW Open Access Genetic associations between voltage- gated calcium channels and autism spectrum disorder: a systematic review Xiaoli Liao1,2 and Yamin Li2* Abstract Objectives: The present review systematically summarized existing publications regarding the genetic associations between voltage-gated calcium channels (VGCCs) and autism spectrum disorder (ASD). Methods: A comprehensive literature search was conducted to gather pertinent studies in three online databases. Two authors independently screened the included records based on the selection criteria. Discrepancies in each step were settled through discussions. Results: From 1163 resulting searched articles, 28 were identified for inclusion. The most prominent among the VGCCs variants found in ASD were those falling within loci encoding the α subunits, CACNA1A, CACNA1B, CACN A1C, CACNA1D, CACNA1E, CACNA1F, CACNA1G, CACNA1H, and CACNA1I as well as those of their accessory subunits CACNB2, CACNA2D3, and CACNA2D4. Two signaling pathways, the IP3-Ca2+ pathway and the MAPK pathway, were identified as scaffolds that united genetic lesions into a consensus etiology of ASD. Conclusions: Evidence generated from this review supports the role of VGCC genetic variants in the pathogenesis of ASD, making it a promising therapeutic target. Future research should focus on the specific mechanism that connects VGCC genetic variants to the complex ASD phenotype. Keywords: Autism spectrum disorder, Voltage-gated calcium
    [Show full text]
  • Supplemental Figure 1. Vimentin
    Double mutant specific genes Transcript gene_assignment Gene Symbol RefSeq FDR Fold- FDR Fold- FDR Fold- ID (single vs. Change (double Change (double Change wt) (single vs. wt) (double vs. single) (double vs. wt) vs. wt) vs. single) 10485013 BC085239 // 1110051M20Rik // RIKEN cDNA 1110051M20 gene // 2 E1 // 228356 /// NM 1110051M20Ri BC085239 0.164013 -1.38517 0.0345128 -2.24228 0.154535 -1.61877 k 10358717 NM_197990 // 1700025G04Rik // RIKEN cDNA 1700025G04 gene // 1 G2 // 69399 /// BC 1700025G04Rik NM_197990 0.142593 -1.37878 0.0212926 -3.13385 0.093068 -2.27291 10358713 NM_197990 // 1700025G04Rik // RIKEN cDNA 1700025G04 gene // 1 G2 // 69399 1700025G04Rik NM_197990 0.0655213 -1.71563 0.0222468 -2.32498 0.166843 -1.35517 10481312 NM_027283 // 1700026L06Rik // RIKEN cDNA 1700026L06 gene // 2 A3 // 69987 /// EN 1700026L06Rik NM_027283 0.0503754 -1.46385 0.0140999 -2.19537 0.0825609 -1.49972 10351465 BC150846 // 1700084C01Rik // RIKEN cDNA 1700084C01 gene // 1 H3 // 78465 /// NM_ 1700084C01Rik BC150846 0.107391 -1.5916 0.0385418 -2.05801 0.295457 -1.29305 10569654 AK007416 // 1810010D01Rik // RIKEN cDNA 1810010D01 gene // 7 F5 // 381935 /// XR 1810010D01Rik AK007416 0.145576 1.69432 0.0476957 2.51662 0.288571 1.48533 10508883 NM_001083916 // 1810019J16Rik // RIKEN cDNA 1810019J16 gene // 4 D2.3 // 69073 / 1810019J16Rik NM_001083916 0.0533206 1.57139 0.0145433 2.56417 0.0836674 1.63179 10585282 ENSMUST00000050829 // 2010007H06Rik // RIKEN cDNA 2010007H06 gene // --- // 6984 2010007H06Rik ENSMUST00000050829 0.129914 -1.71998 0.0434862 -2.51672
    [Show full text]
  • The Mineralocorticoid Receptor Leads to Increased Expression of EGFR
    www.nature.com/scientificreports OPEN The mineralocorticoid receptor leads to increased expression of EGFR and T‑type calcium channels that support HL‑1 cell hypertrophy Katharina Stroedecke1,2, Sandra Meinel1,2, Fritz Markwardt1, Udo Kloeckner1, Nicole Straetz1, Katja Quarch1, Barbara Schreier1, Michael Kopf1, Michael Gekle1 & Claudia Grossmann1* The EGF receptor (EGFR) has been extensively studied in tumor biology and recently a role in cardiovascular pathophysiology was suggested. The mineralocorticoid receptor (MR) is an important efector of the renin–angiotensin–aldosterone‑system and elicits pathophysiological efects in the cardiovascular system; however, the underlying molecular mechanisms are unclear. Our aim was to investigate the importance of EGFR for MR‑mediated cardiovascular pathophysiology because MR is known to induce EGFR expression. We identifed a SNP within the EGFR promoter that modulates MR‑induced EGFR expression. In RNA‑sequencing and qPCR experiments in heart tissue of EGFR KO and WT mice, changes in EGFR abundance led to diferential expression of cardiac ion channels, especially of the T‑type calcium channel CACNA1H. Accordingly, CACNA1H expression was increased in WT mice after in vivo MR activation by aldosterone but not in respective EGFR KO mice. Aldosterone‑ and EGF‑responsiveness of CACNA1H expression was confrmed in HL‑1 cells by Western blot and by measuring peak current density of T‑type calcium channels. Aldosterone‑induced CACNA1H protein expression could be abrogated by the EGFR inhibitor AG1478. Furthermore, inhibition of T‑type calcium channels with mibefradil or ML218 reduced diameter, volume and BNP levels in HL‑1 cells. In conclusion the MR regulates EGFR and CACNA1H expression, which has an efect on HL‑1 cell diameter, and the extent of this regulation seems to depend on the SNP‑216 (G/T) genotype.
    [Show full text]
  • Table S1 the Four Gene Sets Derived from Gene Expression Profiles of Escs and Differentiated Cells
    Table S1 The four gene sets derived from gene expression profiles of ESCs and differentiated cells Uniform High Uniform Low ES Up ES Down EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol EntrezID GeneSymbol 269261 Rpl12 11354 Abpa 68239 Krt42 15132 Hbb-bh1 67891 Rpl4 11537 Cfd 26380 Esrrb 15126 Hba-x 55949 Eef1b2 11698 Ambn 73703 Dppa2 15111 Hand2 18148 Npm1 11730 Ang3 67374 Jam2 65255 Asb4 67427 Rps20 11731 Ang2 22702 Zfp42 17292 Mesp1 15481 Hspa8 11807 Apoa2 58865 Tdh 19737 Rgs5 100041686 LOC100041686 11814 Apoc3 26388 Ifi202b 225518 Prdm6 11983 Atpif1 11945 Atp4b 11614 Nr0b1 20378 Frzb 19241 Tmsb4x 12007 Azgp1 76815 Calcoco2 12767 Cxcr4 20116 Rps8 12044 Bcl2a1a 219132 D14Ertd668e 103889 Hoxb2 20103 Rps5 12047 Bcl2a1d 381411 Gm1967 17701 Msx1 14694 Gnb2l1 12049 Bcl2l10 20899 Stra8 23796 Aplnr 19941 Rpl26 12096 Bglap1 78625 1700061G19Rik 12627 Cfc1 12070 Ngfrap1 12097 Bglap2 21816 Tgm1 12622 Cer1 19989 Rpl7 12267 C3ar1 67405 Nts 21385 Tbx2 19896 Rpl10a 12279 C9 435337 EG435337 56720 Tdo2 20044 Rps14 12391 Cav3 545913 Zscan4d 16869 Lhx1 19175 Psmb6 12409 Cbr2 244448 Triml1 22253 Unc5c 22627 Ywhae 12477 Ctla4 69134 2200001I15Rik 14174 Fgf3 19951 Rpl32 12523 Cd84 66065 Hsd17b14 16542 Kdr 66152 1110020P15Rik 12524 Cd86 81879 Tcfcp2l1 15122 Hba-a1 66489 Rpl35 12640 Cga 17907 Mylpf 15414 Hoxb6 15519 Hsp90aa1 12642 Ch25h 26424 Nr5a2 210530 Leprel1 66483 Rpl36al 12655 Chi3l3 83560 Tex14 12338 Capn6 27370 Rps26 12796 Camp 17450 Morc1 20671 Sox17 66576 Uqcrh 12869 Cox8b 79455 Pdcl2 20613 Snai1 22154 Tubb5 12959 Cryba4 231821 Centa1 17897
    [Show full text]
  • Supplementary Table S1. Upregulated Genes Differentially
    Supplementary Table S1. Upregulated genes differentially expressed in athletes (p < 0.05 and 1.3-fold change) Gene Symbol p Value Fold Change 221051_s_at NMRK2 0.01 2.38 236518_at CCDC183 0.00 2.05 218804_at ANO1 0.00 2.05 234675_x_at 0.01 2.02 207076_s_at ASS1 0.00 1.85 209135_at ASPH 0.02 1.81 228434_at BTNL9 0.03 1.81 229985_at BTNL9 0.01 1.79 215795_at MYH7B 0.01 1.78 217979_at TSPAN13 0.01 1.77 230992_at BTNL9 0.01 1.75 226884_at LRRN1 0.03 1.74 220039_s_at CDKAL1 0.01 1.73 236520_at 0.02 1.72 219895_at TMEM255A 0.04 1.72 201030_x_at LDHB 0.00 1.69 233824_at 0.00 1.69 232257_s_at 0.05 1.67 236359_at SCN4B 0.04 1.64 242868_at 0.00 1.63 1557286_at 0.01 1.63 202780_at OXCT1 0.01 1.63 1556542_a_at 0.04 1.63 209992_at PFKFB2 0.04 1.63 205247_at NOTCH4 0.01 1.62 1554182_at TRIM73///TRIM74 0.00 1.61 232892_at MIR1-1HG 0.02 1.61 204726_at CDH13 0.01 1.6 1561167_at 0.01 1.6 1565821_at 0.01 1.6 210169_at SEC14L5 0.01 1.6 236963_at 0.02 1.6 1552880_at SEC16B 0.02 1.6 235228_at CCDC85A 0.02 1.6 1568623_a_at SLC35E4 0.00 1.59 204844_at ENPEP 0.00 1.59 1552256_a_at SCARB1 0.02 1.59 1557283_a_at ZNF519 0.02 1.59 1557293_at LINC00969 0.03 1.59 231644_at 0.01 1.58 228115_at GAREM1 0.01 1.58 223687_s_at LY6K 0.02 1.58 231779_at IRAK2 0.03 1.58 243332_at LOC105379610 0.04 1.58 232118_at 0.01 1.57 203423_at RBP1 0.02 1.57 AMY1A///AMY1B///AMY1C///AMY2A///AMY2B// 208498_s_at 0.03 1.57 /AMYP1 237154_at LOC101930114 0.00 1.56 1559691_at 0.01 1.56 243481_at RHOJ 0.03 1.56 238834_at MYLK3 0.01 1.55 213438_at NFASC 0.02 1.55 242290_at TACC1 0.04 1.55 ANKRD20A1///ANKRD20A12P///ANKRD20A2///
    [Show full text]
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
    Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated.
    [Show full text]
  • Genomic Comparison of Indigenous African and Northern European
    Animal Science Publications Animal Science 5-2017 Genomic Comparison of Indigenous African and Northern European Chickens Reveals Putative Mechanisms of Stress Tolerance Related to Environmental Selection Pressure Damarius S. Fleming Iowa State University Steffen Weigend Friedrich-Loeffler-Institut Henner Simianer University of Göttingen Annett eiW gend Friedrich-Loeffler-Institut Follow this and additional works at: https://lib.dr.iastate.edu/ans_pubs MaxP aRrothschit of theldAgriculture Commons, Ecology and Evolutionary Biology Commons, Genetics and GeIowanomic State Usn Civommonersity, mfrsoth, asndc@i theastaPteoultr.edu y or Avian Science Commons TheSee nex tompc page forle addte bitioniblaiol agruthorapshic information for this item can be found at https://lib.dr.iastate.edu/ ans_pubs/368. For information on how to cite this item, please visit http://lib.dr.iastate.edu/ howtocite.html. This Article is brought to you for free and open access by the Animal Science at Iowa State University Digital Repository. It has been accepted for inclusion in Animal Science Publications by an authorized administrator of Iowa State University Digital Repository. For more information, please contact [email protected]. Genomic Comparison of Indigenous African and Northern European Chickens Reveals Putative Mechanisms of Stress Tolerance Related to Environmental Selection Pressure Abstract Global climate change is increasing the magnitude of environmental stressors, such as temperature, pathogens, and drought, that limit the survivability and sustainability of livestock production. Poultry production and its expansion is dependent upon robust animals that are able to cope with stressors in multiple environments. Understanding the genetic strategies that indigenous, noncommercial breeds have evolved to survive in their environment could help to elucidate molecular mechanisms underlying biological traits of environmental adaptation.
    [Show full text]
  • Supplementary Figure S4
    18DCIS 18IDC Supplementary FigureS4 22DCIS 22IDC C D B A E (0.77) (0.78) 16DCIS 14DCIS 28DCIS 16IDC 28IDC (0.43) (0.49) 0 ADAMTS12 (p.E1469K) 14IDC ERBB2, LASP1,CDK12( CCNE1 ( NUTM2B SDHC,FCGR2B,PBX1,TPR( CD1D, B4GALT3, BCL9, FLG,NUP21OL,TPM3,TDRD10,RIT1,LMNA,PRCC,NTRK1 0 ADAMTS16 (p.E67K) (0.67) (0.89) (0.54) 0 ARHGEF38 (p.P179Hfs*29) 0 ATG9B (p.P823S) (0.68) (1.0) ARID5B, CCDC6 CCNE1, TSHZ3,CEP89 CREB3L2,TRIM24 BRAF, EGFR (7p11); 0 ABRACL (p.R35H) 0 CATSPER1 (p.P152H) 0 ADAMTS18 (p.Y799C) 19q12 0 CCDC88C (p.X1371_splice) (0) 0 ADRA1A (p.P327L) (10q22.3) 0 CCNF (p.D637N) −4 −2 −4 −2 0 AKAP4 (p.G454A) 0 CDYL (p.Y353Lfs*5) −4 −2 Log2 Ratio Log2 Ratio −4 −2 Log2 Ratio Log2 Ratio 0 2 4 0 2 4 0 ARID2 (p.R1068H) 0 COL27A1 (p.G646E) 0 2 4 0 2 4 2 EDRF1 (p.E521K) 0 ARPP21 (p.P791L) ) 0 DDX11 (p.E78K) 2 GPR101, p.A174V 0 ARPP21 (p.P791T) 0 DMGDH (p.W606C) 5 ANP32B, p.G237S 16IDC (Ploidy:2.01) 16DCIS (Ploidy:2.02) 14IDC (Ploidy:2.01) 14DCIS (Ploidy:2.9) -3 -2 -1 -3 -2 -1 -3 -2 -1 -3 -2 -1 -3 -2 -1 -3 -2 -1 Log Ratio Log Ratio Log Ratio Log Ratio 12DCIS 0 ASPM (p.S222T) Log Ratio Log Ratio 0 FMN2 (p.G941A) 20 1 2 3 2 0 1 2 3 2 ERBB3 (p.D297Y) 2 0 1 2 3 20 1 2 3 0 ATRX (p.L1276I) 20 1 2 3 2 0 1 2 3 0 GALNT18 (p.F92L) 2 MAPK4, p.H147Y 0 GALNTL6 (p.E236K) 5 C11orf1, p.Y53C (10q21.2); 0 ATRX (p.R1401W) PIK3CA, p.H1047R 28IDC (Ploidy:2.0) 28DCIS (Ploidy:2.0) 22IDC (Ploidy:3.7) 22DCIS (Ploidy:4.1) 18IDC (Ploidy:3.9) 18DCIS (Ploidy:2.3) 17q12 0 HCFC1 (p.S2025C) 2 LCMT1 (p.S34A) 0 ATXN7L2 (p.X453_splice) SPEN, p.P677Lfs*13 CBFB 1 2 3 4 5 6 7 8 9 10 11
    [Show full text]
  • Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
    Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase
    [Show full text]
  • (SLC3A2) Sustains Amino Acid and Nucleotide Availability for Cell Cycle
    www.nature.com/scientificreports OPEN CD98hc (SLC3A2) sustains amino acid and nucleotide availability for cell cycle progression Received: 16 April 2019 Sara Cano-Crespo1, Josep Chillarón2, Alexandra Junza3,4, Gonzalo Fernández-Miranda1, Accepted: 13 September 2019 Judit García5,6, Christine Polte7, Laura R. de la Ballina 8,9, Zoya Ignatova7, Óscar Yanes 3,4, Published: xx xx xxxx Antonio Zorzano 1,4,10, Camille Stephan-Otto Attolini 1 & Manuel Palacín1,6,10 CD98 heavy chain (CD98hc) forms heteromeric amino acid (AA) transporters by interacting with diferent light chains. Cancer cells overexpress CD98hc-transporters in order to meet their increased nutritional and antioxidant demands, since they provide branched-chain AA (BCAA) and aromatic AA (AAA) availability while protecting cells from oxidative stress. Here we show that BCAA and AAA shortage phenocopies the inhibition of mTORC1 signalling, protein synthesis and cell proliferation caused by CD98hc ablation. Furthermore, our data indicate that CD98hc sustains glucose uptake and glycolysis, and, as a consequence, the pentose phosphate pathway (PPP). Thus, loss of CD98hc triggers a dramatic reduction in the nucleotide pool, which leads to replicative stress in these cells, as evidenced by the enhanced DNA Damage Response (DDR), S-phase delay and diminished rate of mitosis, all recovered by nucleoside supplementation. In addition, proper BCAA and AAA availability sustains the expression of the enzyme ribonucleotide reductase. In this regard, BCAA and AAA shortage results in decreased content of deoxynucleotides that triggers replicative stress, also recovered by nucleoside supplementation. On the basis of our fndings, we conclude that CD98hc plays a central role in AA and glucose cellular nutrition, redox homeostasis and nucleotide availability, all key for cell proliferation.
    [Show full text]
  • Abnormal Spermatogenesis and Reduced Fertility in Transition Nuclear Protein 1-Deficient Mice
    Abnormal spermatogenesis and reduced fertility in transition nuclear protein 1-deficient mice Y. Eugene Yu*†,Yun Zhang*, Emmanual Unni*‡, Cynthia R. Shirley*, Jian M. Deng§, Lonnie D. Russell¶, Michael M. Weil*, Richard R. Behringer§, and Marvin L. Meistrich*ʈ Departments of *Experimental Radiation Oncology, and §Molecular Genetics, University of Texas M. D. Anderson Cancer Center, Houston, TX 77030-4095; and ¶Department of Physiology, Southern Illinois University, School of Medicine, Carbondale, IL 62901 Edited by Richard D. Palmiter, University of Washington School of Medicine, Seattle, WA, and approved February 22, 2000 (received for review May 3, 1999) Transition nuclear proteins (TPs), the major proteins found in (15), suggesting some functional relationship between the three chromatin of condensing spermatids, are believed to be important proteins exists. Tnp1, however, is on a separate chromosome and for histone displacement and chromatin condensation during is not clearly related to the other three proteins. mammalian spermatogenesis. We generated mice lacking the ma- In vitro, TP1 decreases the melting temperature of DNA (16) jor TP, TP1, by targeted deletion of the Tnp1 gene in mouse and relaxes the DNA in nucleosomal core particles (17), which embryonic stem cells. Surprisingly, testis weights and sperm pro- led to the proposal that TP1 reduces the interaction of DNA duction were normal in the mutant mice, and only subtle abnor- with the nucleosome core. In contrast, TP2 increases the malities were observed in sperm morphology. Electron microscopy melting temperature of DNA and compacts the DNA in revealed large rod-like structures in the chromatin of mutant step nucleosomal cores, suggesting that it is a DNA-condensing 13 spermatids, in contrast to the fine chromatin fibrils observed in protein (18).
    [Show full text]
  • Ion Channels
    UC Davis UC Davis Previously Published Works Title THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: Ion channels. Permalink https://escholarship.org/uc/item/1442g5hg Journal British journal of pharmacology, 176 Suppl 1(S1) ISSN 0007-1188 Authors Alexander, Stephen PH Mathie, Alistair Peters, John A et al. Publication Date 2019-12-01 DOI 10.1111/bph.14749 License https://creativecommons.org/licenses/by/4.0/ 4.0 Peer reviewed eScholarship.org Powered by the California Digital Library University of California S.P.H. Alexander et al. The Concise Guide to PHARMACOLOGY 2019/20: Ion channels. British Journal of Pharmacology (2019) 176, S142–S228 THE CONCISE GUIDE TO PHARMACOLOGY 2019/20: Ion channels Stephen PH Alexander1 , Alistair Mathie2 ,JohnAPeters3 , Emma L Veale2 , Jörg Striessnig4 , Eamonn Kelly5, Jane F Armstrong6 , Elena Faccenda6 ,SimonDHarding6 ,AdamJPawson6 , Joanna L Sharman6 , Christopher Southan6 , Jamie A Davies6 and CGTP Collaborators 1School of Life Sciences, University of Nottingham Medical School, Nottingham, NG7 2UH, UK 2Medway School of Pharmacy, The Universities of Greenwich and Kent at Medway, Anson Building, Central Avenue, Chatham Maritime, Chatham, Kent, ME4 4TB, UK 3Neuroscience Division, Medical Education Institute, Ninewells Hospital and Medical School, University of Dundee, Dundee, DD1 9SY, UK 4Pharmacology and Toxicology, Institute of Pharmacy, University of Innsbruck, A-6020 Innsbruck, Austria 5School of Physiology, Pharmacology and Neuroscience, University of Bristol, Bristol, BS8 1TD, UK 6Centre for Discovery Brain Science, University of Edinburgh, Edinburgh, EH8 9XD, UK Abstract The Concise Guide to PHARMACOLOGY 2019/20 is the fourth in this series of biennial publications. The Concise Guide provides concise overviews of the key properties of nearly 1800 human drug targets with an emphasis on selective pharmacology (where available), plus links to the open access knowledgebase source of drug targets and their ligands (www.guidetopharmacology.org), which provides more detailed views of target and ligand properties.
    [Show full text]