Supplementary Figure 1

Total Page:16

File Type:pdf, Size:1020Kb

Supplementary Figure 1 CRHBP APOA2 MMP26 CTSA COL6A2 THBS3 GLB1 CELA1 LRG1 RBM12 C3AR1 UCN MST1 B AMBP CFP C1S CDH19 A C2 CFB MASP1 CTRB1 C1R CDH18 CPN1 HPN THBS2 DEFA1B HIST1H2BJ C1QC HIST1H1B DEFA1 ISOC2 CFI F13A1 DHDDS PDK1 HPS6 COL6A3 HIC2 IL10RB APOD HLA-DPB1 PROC AICDA F7 DLAT IL10 MINA CFH DPYSL3 TFPI CDH6 USP49 CROCC LRRFIP2 SPOCK1 HAPLN1 C5 HPS5 PLA2G5 LOX MMRN1 TBC1D4 SERPING1 F11 LUC7L ADAMTS4 TRIM7 THOC1 C7 HRG BCAN NEU1 PROS1 DMC1 GIGYF2 TMPRSS6 TNFAIP8 HGFAC BNC2 LEP F10 NPNT F5 RWDD2BBRD3 COL5A3 SERPINE2 LRRFIP1NFIB TRIP11 NCOA5 ADAMTS1 C1QB KLKB1 RSL24D1 FUT4 CFHR3 IGFBP1 PDHA1 TNXB SAA1 GTF3C2 C8B AGR3 SAA2 FST APOBEC3F DCK MED30 KAL1 MFAP2 MED17 ITGAM CFHR5 REG3A CLEC3B COL13A1 KIAA1524 HLA-DPA1 ACAN HABP2 ANKRD13A MMP9 DPT SUPT3H ITGA8 MMP25 CRP ELN RBBP5RECQL PARP10 ZNF622 COL7A1 CELF2 MED22 MSH4 IPO5 BDP1 ANGPTL3 SERPINA1 WISP1 RPA4 C3 GYG2 PDK2 VSIG4 LPA LAMA3 ESM1 PTX3 OSM KPNA4 ARID3B EMCN SPOCK3 FGG CD93 CDH9 MED19 MORF4L1 ITGAX GNAT1 RECK WISP2 RAB31 A1CF APOBEC1 XPO4 XPOT HIST2H2AC LCN2 COL4A4 LST1 AEBP1 TIMP2 CD151 F2 PRELP DDX19B KDM5B APCS COL4A6 TBC1D17 OLFM4 CP SERPINI1 SNAPC3 TGFBI AGXT VEGFB NFIC PDHX RANBP3SERPINB2 HELB FGA COMP C20orf27 TSKU C5AR2 NRP2 ELANE EIF5A CCNB1IP1 LRP1B PLAU ATG5 PCGF2 LIN9 PGF CXCL12 LAMA1 FN1 SERPINF2 ATG7 RPA3 TREX1 CFHR4 MRC1 CDH7 HIST1H2BF NFIX SRP19 SEMA3F LYZ BHLHE41 MED12 FRK CD97 LACRT HGF HIST1H2BG MED4 CCNF INHA MRPL44 GPI SEPT8 IPO7 EP400 MMP3 PF4 CTRL GPNMB BFSP1HIST1H2BD LMO4 CIDEA YAE1D1 PDGFA RANGAP1 EMR2 GAS6 LGALS3BP APOH SELP ICAM4 SERPINA3 USP13 TFAP2B HBP1 GPC1 IGFBP4 HIST1H2BI IL10RA MMP13 ITGB8 ATG3 APOBEC3G SCGB1A1 IGFALS THAP1 DNMT3L TNR SPARC PUF60 IL13RA2 ST14 TUSC3 KLC3 PSMB9 SUV420H2 GYG1 TOM1L2 CDH10 AK1 KIF15 MED8 NR1D1 IL4 TSPAN4 THBS1 MIA IGFBP2 SIN3B FSD1 DFFB MUC7 LCN1 CYR61 FANCB ARMCX2 RAD54B NXT1 CR1 MEP1A FBLN2 SEPT4 HIST1H4A PLIN3 TMEM123 SRP68 COL18A1 KLK4 ATG10 MPP3 RAD1 SSRP1 NEK1 CEL LOR C9 KNG1 EID1 PPIL1 ITGAD NID1 CTRC AEBP2 MBD3 COL5A1 GALNT6 DCTD AIMP1 MXI1 ITLN1 COL4A1 MUTYH DYRK2 POLL HIST2H3A RING1 HP C1QA CTSK MARCKSL1 SFI1 MKI67 NR1D2 FBN1 BAZ1A CD74 IGFBP7 IPO11 HIST2H3C GGT1 TIMP3 MMP2 PLG CHMP1B BUB1B CIDEB SNAPC5MYCN ICAM2 UPP2 EPN3 OGDH NFYC HIST1H4KPPHLN1 MAF MMP1 BGN PSMB10 HUS1 PDPN EIF5AL1 EFTUD2 MAFB HK3 RRM2B AKTIP MLH1 RANBP2HIST4H4 CCNT2 HIST1H2BCCHAF1B SELL FIGF DRP2 SERPINC1 SYT9 PABPN1 RBBP7 PARGTNPO1 F2RL2 COL14A1 GULP1 CBX3 IL7 DPYSL5 NGF COL4A3 OSBP2 HIST1H1B MBD2 BCL11A FCGR1A TNFRSF11BDCN RBBP9 RPA1 HIST1H4B MOK HHLA3 VWF GNG7 PLK2 DPYSL2 TRIM28 CSF2 MMP7 UPP1 TRIM22 BCAR3 CTSD PTGFR PCED1A DNM1LC10orf54 GTF2F1 B4GALT1 MORF4L2 HIST1H4F PHPT1 HIST2H3DHIST1H2AMSNAPC1 SIGLEC1 RALYL ZNF652 TWIST2 KLK3 COL1A2 SERPINA5 SLIT2 SIRT6 HERC1 ID3 RBP1 TP53BP1 BRMS1L KLF9 DYSF MMP14 ITGA2B RNF168 KLF1 CBX4PURA NEK9 CRLF2 COL4A5 GABRB2SPAG8 BUB3 ICAM1 TF SELENBP1 TRAIP GCNT1 OPTNL3MBTL1 CDK11A MELK VEGFC PLAUR SFTPD COL4A2 SLC35A2 TRAP1 TOMM34HOPX F3 RBBP8 NFE2L2ERG BRF1 GGA2 MNDA HIST1H4L CCDC109B IGF1 GNG5 TLX2 CEBPE CTBP2 GGA1 MTA2 RABIF INHBA PTGER2 CCDC33 FUBP1 TAF1B LEPR WRN XBP1 JAM2 CD53 TNC RAI2 HMG20B RIF1 TRIM29 HIST1H4I DNMT3B EIF1AX OSGEP RCN1 TXNRD1 NRCAM GALNT10 ITGA5 LAMA2 IGF2 TRIOBP HIST1H2BE PARK7 PAX5GSTP1 NUP153 TYRO3 CTGF LUM MNS1 FEM1B IFI16 SMARCA5 SIX3 FGF9 PTGER1 KRT6B LAPTM5 SERBP1MAFG SKP2 SFPQ SAP30 RNF40 GALNT12 FCER2 P2RY2 ITGAVFERMT2HBEGF UBAC1 HEY1 ORC2 HIST1H4J ATAD2 BCL11B RANGRF JAM3 CLIP1 PEX5 RFX1 FANCA PRDM2 VGLL4 THY1 CD82 NSMF RIBC2 RLIM RAD51E2F4 HIST2H4A CHD9 RGN VNN2 PSD MPHOSPH8 TRAM2 MPRIP AATF NIPSNAP1 FLOT1 HLA-DQB1 CTSL FANCG GTF2F2 MAX SP100 USP4 NRP1 MT2A ITGB6 SMCP WFDC2 ACIN1 RAG1 VPS35 COL1A1 RRM2RRM1 PAFAH1B1 SUMO3 TRIM27 SATB1 VEGFA SPINT1 NEU4 RAB11B RPLP1DCAF6 RBL2 HIST1H4H CCNA1 GZMA GP6 SGTB PNN ONECUT1 LSM4 CD55 SPOCK2 FCGR3A TNS2 ENKD1 NUTF2 SUMO2 SMARCB1 GCSH HIST1H2AI C17orf70 GNGT1 RAB3IL1 ZEB2 PCBP1 RAD9A HUWE1PSMD10 RBBP4RELBDNMT3A TRAPPC4 ITGA3 HSPG2 PLAC8 SPI1 HOXB2 RCC1 VGLL2 IL2 F2RL1 CLU TNF COL2A1 ATG12 RAB11FIP5 SEPT5 GOLM1 ZBTB17 COPS3 E2F3 PTPRB CD46LGALS1 DAG1 IGSF1 YIPF3 GYS1 MCRS1 PPP1R15A XPA CBX5 GADD45GIP1 ELAVL1 REV1 SCEL DSCAML1 DNAJC1 CTSB GGA3MCM7 MDM4 HIST1H4E IFI35 SOCS2 PLCE1 CD36 SDC2 RGS11 RBM41 PTMA GORASP1 M6PRNR2C1 GALNT1 FBLN1 LTBP1 HGH1 HAP1 LSM2 XPO1 FLII TEAD1 PDE5A SERPINE1 BRD1 RPN1 MRGBP SIN3A NR2E3 NECAP2 PON1 CD9 FBLIM1 DGCR6L CXADR CPE NR1H2 KPNA1 ITGB2 LAMA5 TTK BRMS1 BRD7 SET MAPK15 HDAC9 FLT4 CTSG IGFBP6 EPN1 SMARCD1WT1 RIMS1 SUV39H1 GALNT15 SNX1 SLIT1 DLK2 APIPNOC4L PCM1 HIST2H2BE TRRAP HDDC3 TAC1 F2R IGFBP3 KRT7 NUP50 FMR1 RARGRPS6KA5 APEX1 PLAT TGFBR3 NEK7 RGS6 RAB11FIP1 ARL8B SPG7 UTP14AING5 ETV1 PPARGC1A PPP1R16A EMILIN1 CD4 USHBP1RAD52 CCNT1 RAN MYL3 GALNT2 AHSG CPSF3L EIF6SGOL1 CARM1MCM2 PRKDCE2F1 FANCCCEBPA NR0B2 HIST1H4D PTCH1 CLEC5A TGFB1 FSTL3 ID1IRF8 HNRNPUL1 SMARCD3 MATN2 IP6K2 CCER1 C10orf10 DCUN1D1MEN1 KDM5A SREBF2 ATF2 MEF2D CREG1 NAA11 CD24 FCGR2A IGFBP5 QKI RPS3 SMARCC1ASCC2 CRCT1 CEBPD DPPA4 SOX9 IL13 GIPC1 USP2 PLEKHM1 SMARCE1 MAP6 KLRC3 TGFA ITGB3 ACVR2B GNG3 KAT7 TAF1 ID2 KPNA2NFATC2 NR1I2CBFA2T3MALT1 HMGB2 STMN4 TGFB3 RPA2 BLMUSP7 UBE2IPCNA CDC5L POU1F1 BPHL CD38 FLOT2 TCTEX1D4 PCBP2MYCBP PKMYT1 NR2F6 COL3A1 TGFB2 MTA1 HDAC2 PRAM1MXD1 POU2F2 ICAM3 RAPSN TSLP HDAC6 RBM23 HIST2H4B SNW1 PLA2G4A SIGLEC14 C5AR1 EPHA4 PRTN3 ANTXR2 WDR44 MID1 CEP76 NAP1L1 PPARA DFFA GATA4 PRPF6 S100A7 CIR1 NCR2 GPLD1 PODXL AXL NT5E MED9 ACVR2A LMO2 RPL18A HIST1H4C RBL1 PARP2 ETS2 MCAM ITGA2 CHRDL2 NTN4 BARD1ACTL6ACBFA2T2 DCTN1SGK1 GTF2BRB1GATA1 TSNAXING1 ELF1 MEF2CESRRA PTMS TNS1 SDC1 C10orf62 EIF3J FXR1 PPP1R12APITX2 HOXB6 MCM5 MYC RUNX1 SKI PAPSS1 CALR DHRS1 MID2 NFYBSF3B1 PRDX1 NR4A3USF1 ARSF VPREB1 RDX CSF3R CD58 ITGB1 LTBP3 RGS9 KXD1 DTX2 SF1 CRY1 NCOR1 HDAC1 HDAC3 ARID3A NMI IL7R LRP8 CDCP1 VTN MYO5AALS2CR11 CCDC85B BRCA2 TBP DHX30 RARBREM1 KIR2DS2 TREM1 CLDN4 TEK ITGA4 CD81 DEFB1 KRT15 KIAA1377 FBXW7 CCND2 CDK6CDC6 SPEN PPAP2B SACS HBA1 RAB11FIP4 SOX10 SRF JDP2 E4F1 SRP72RBAK EIF5B GNB5 PPP2R5E KRT19 STK35 GADD45GRBM48 MAGEA11FLI1 HDAC5 HDAC4NCOA1 NR0B1 FHL1 SOCS3 ERBB4 FLT1 CANX PTPRD ENG GDI2 SYNCRIP NUDT18 SLC25A4 SNIP1DNMT1 CUL1 KAT2B SNRNP70 VLDLR NDC80 RAB8B ARL3 GADD45B ZFP36 TXNIP NAA15 CD300E ADAM12 GH2 DDX17 POU2F1 CDC27 KLRK1 PDGFRA ZNF764 NR1H3 MCM3 MEF2A MAPK7 ANP32ATHAP11 HIST1H2AG FGFR2 PHIP LIMS2 KRT20 EXOC8 DVL1 PIAS4 HSF1 TNFAIP3 BCL6 CD22 CD14 EFEMP1 RABGGTB LMO3 EPB41L3 SMAD5 APAF1 MYOD1 RFC1 FCER1G BST1 SPN BEND5 PTGDS ROBO2 GLRX3 PSME1NPDC1 CHEK2ILF3 NR5A1 SFTPA1 COL4A3BP PGLS VIM LNX1SNCAIPCTBP1 PRMT2 CDK2PRMT1 TREM2 SH2D2A TOM1L1 LOC101929889 S100A6 SDCCAG3 HOOK2 TNFRSF11ARUNX2 FOSTOP2ACOPS5 KPNA6 ENC1 JAK3AP3D1 MYOC MED15 ELF3 PSMD11 CCNB1 MED1 METTL1 LTA4H KIR2DL3 IL2RG CD59 KLK6 KLK2 HOXA1 ARHGEF28 RHPN2 TFG GAP43 BHLHE40LEF1 THRB FZR1 RARA UBE2J1 RPL26 FLT3 CD47 LRP2 NRAS BEND5 PPP2R5C KAT5PLCB1 VDR JUNHIST3H3 CDC25B IRF1 LAX1 CTLA4 DOK1 CEACAM1 SHBG CTNNA2 ITGB5 ACVR1B BMPER NEDD4LHEYL UBE4B STAT6 SPAG9 HIST1H2AK KIDINS220 ACTN3 PAPPA2 TMOD2 DCTN2 RPL9 FXR2 MAP3K3CDK11B NRIP1 DDX54 KLRC4-KLRK1 SHB SPRY2 CNTN1 PIWIL2 PGS1 FBXL18SH3YL1 RAB11A AGR2 MDFIEPN2 BTBD2 TCF3 PML HMGA1 PKP1 GHR DIAPH2 IVNS1ABPS100A2 NIF3L1 KIAA0408 MED31 FAF1 PPP3CA MAP2K7 SMARCA4 MNAT1 SLAMF1 CD44 INS NR6A1 RAB7A NCALD RPS6KA1 BRCA1ETS1NCOR2PPARG TOP1 E2F2 KIR3DS1 PDGFRB POM121 PLK1COPS2RUNX1T1 EP300 SP1 XRCC5YY1 MMS19 EPOR IL2RB LTF PALLD TNFSF13 GREM2 ZNF638 HEY2 SMAD9HABP4 PAX2PHBCFLARDEDD SH2B3 MAGI3 MGP RNF11CHD3 EEDCDC25CXPO5 PSIP1 THNSL2 TYROBP LRP1VTCN1 KCNA2 RERE HAND1 CEBPB CDK4 KIR3DL3 YES1 CLDN1 APP NEK9 NOG GNG4 PHLDA1 ZNF408 NCAN ADD1 GOLGB1HSPE1SNX6 SP3 STAT4CETP VPREB3 LAT CSF1R TXK SNX2ADAM17 LIMS1 PTBP1HNRNPC FHL3SAT1 HSPA1BTGM2COPS6 TCEA2 CREBBP NCOA3 TPR CSE1L SIT1 TYK2 KDR PAPPA BMP2 AGO1 PLSCR4 NFKB1 SUMO1 DMTF1 GRAP FGF2 NELL1 MID1IP1 STX4 NME2 ZMYND8 DGKZ CDC25APIAS1 CD72 ADORA2A MYOT FGFBP1 IDE OLFM2 PSMD7 PPP2CB TNNT1 BEGAIN SETDB1 PPL XRCC6 ZBTB16 NCOA2 TTBK1 OTUD5 KLRC4 GAB3 TSHR TLN1CAV3 FGFR4 MEP1B ROBO1 TP53 HIPK2 ANXA2 RAPGEF2 PIWIL1 DICER1 MAPKAPK5 CIC BIRC3 LIME1 SPHK1 SPP1 TOB1 CRMP1 TFAP2A LMNB1 NR4A1 SMARCA2 HIST1H2AL NAA10 LAT2 BTLA SYNJ2BP TARBP2 EWSR1 ARHGEF6CDK1 CREB1 POLA1 BIRC6 UBXN11 PBX1 TACR1 SKAP1 CRKL DOK4 SH3BP2 AREG USH2A NELL2 CHRD MYOZ2YLPM1RAB11FIP3 LAMA4TLE1PFDN4THRASMAD2 PPARD PELP1 NPAS2 ECD CD19 PLA1A CLUAP1 PITPNM1 PTPRK DAZAP2 SMAD3 RELA BIRC5 SCN1B UTRN RHOD FAM103A1 MX1 CAST CRIP1 PPP1R8 AHR MCL1IKBKG LGALS4 PTPN11 RIMS2 HBA2 PPP2R5D KRTAP4-12ABLIM1 GDF9 PTN MAP3K4 TUBBWEE1 NFKBIA MAPKAPK2 TDP2 HPR SNX6 HIVEP2 RPH3A VCLKRT8 MAPK9 MAPK14 STK3 MYOZ1 MED28 ARPC3 CR2 ADAM9 SYT6 GREM1 RHOH PARK2 CDK9 KRT18 BNIP3L RXRB CASP8AP2 PIK3R2 SYT1 LRIF1TRAF4 CDKN1AGBP2CDKN1BNFKB2 CDKN2BBNIP3ESR1 PARP1 UBR5 AIFM1 NLRP3 ITGB7 TNFRSF13B TRIP13 PLSCR1 IRF2TUBGCP4EEF1D PKN1PRKRA DLSTDAXX SMAD4 NR3C1CYBAETV6 ELK3 PGR CD3D TUB PLCG2 PIK3CA JAK1 CAPNS2 ZNF581 RAPGEF2 AKAP1 S100A8 SMAD1 BUB1 GSK3B KPNB1BCL2L1LMNA AKAP8 BIRC2 SHC2 EZR CAV2 CDH5 FGFR1 MALLTM2D1 TGM2 PSMA1 SLC27A6FBF1WWP1 ZHX1 YWHAH AR SARS2 GJA8 FCER1A IGJ KIT JAK2 CSF2RB PTPRF FGFR3 TNFRSF11ASYNPO NELL1 IGBP1 PPP2R2A PDLIM1 NEDD4 MDM2 CCNE1 MARK4 XIAP DIABLO PDE10A SH2D1A PTPRE SSX2IP ERBB2 LYPLA1 TNFSF11 CTNNBIP1 PIWIL4 NEFL HNRNPK MAP4EIF4E GSPT1SOX18 IL27RA GAB2 SDC3 PECAM1 MED28 TNFAIP8 GGN DVL2 PTGES3 RABEP1NUMB MAP3K14SFN FADD PPP1CC SOX4 HIVEP3 CD27 OS9 CPSF6 YWHAG EIF2AK2 TRAF2 BAG1 NCOA6 KCNK9 HTRA2 DOK2 MUC1 APBB2 CD99 BMP4 BMP7 DKK3 FGFR1OP STRN3 UBTFCOIL STAU1HTT CASP3TSC2 MAPK8 EPHB4 FAM46A ARL4C GDF7 ADAMTSL4 CDC42EP1 GFAP PPP1CATUBA3D CCND1 RANBP9 NCL WDR4 CLDN8 ANXA5 MTSS1 FANCL GDF5 SYT11 TNFRSF10C PFKM HSPA1A MAPT CDK16 NR2C2 MKNK1 MAGEA1 POP1 NPHS2 ITIH2 SKAP2 SGTA BRD4 HK2 UBQLN1 PFDN5
Recommended publications
  • 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]
  • The Metabotropic Glutamate Receptor Mglur1 Regulates the Voltage-Gated Potassium Channel Kv1.2 Through Agonist-Dependent and Agonist-Independent Mechanisms
    University of Vermont ScholarWorks @ UVM Graduate College Dissertations and Theses Dissertations and Theses 2019 The etM abotropic glutamate receptor mGluR1 regulates the voltage-gated potassium channel Kv1.2 through agonist-dependent and agonist- independent mechanisms Sharath Chandra Madasu University of Vermont Follow this and additional works at: https://scholarworks.uvm.edu/graddis Part of the Cell Biology Commons, Neuroscience and Neurobiology Commons, and the Pharmacology Commons Recommended Citation Madasu, Sharath Chandra, "The eM tabotropic glutamate receptor mGluR1 regulates the voltage-gated potassium channel Kv1.2 through agonist-dependent and agonist-independent mechanisms" (2019). Graduate College Dissertations and Theses. 982. https://scholarworks.uvm.edu/graddis/982 This Dissertation is brought to you for free and open access by the Dissertations and Theses at ScholarWorks @ UVM. It has been accepted for inclusion in Graduate College Dissertations and Theses by an authorized administrator of ScholarWorks @ UVM. For more information, please contact [email protected]. THE METABOTROPIC GLUTAMATE RECEPTOR MGLUR1 REGULATES THE VOLTAGE-GATED POTASSIUM CHANNEL KV1.2 THROUGH AGONIST-DEPENDENT AND AGONIST-INDEPENDENT MECHANISMS. A Dissertation Presented by Sharath Chandra Madasu to The Faculty of the Graduate College of The University of Vermont In Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy Specializing in Cellular Molecular and Biomedical Science January, 2019 Defense Date: September 27, 2018 Dissertation Examination Committee: Anthony D. Morielli, PhD., Advisor John Green, PhD., Chairperson Karen Lounsbury, Ph.D. Benedek Erdos, PhD. Cynthia J. Forehand, Ph.D., Dean of the Graduate College ABSTRACT The voltage gated potassium channel Kv1.2 plays a key role in the central nervous system and mutations in Kv1.2 cause neurological disorders such as epilepsies and ataxias.
    [Show full text]
  • Characterizing the Mechanisms of Kappa Opioid Receptor Signaling Within Mesolimbic Dopamine Circuitry Katie Reichard a Dissertat
    Characterizing the mechanisms of kappa opioid receptor signaling within mesolimbic dopamine circuitry Katie Reichard A dissertation submitted in partial fulfillment of the degree requirements for the degree of: Doctor of Philosophy University of Washington 2020 Reading Committee: Charles Chavkin, Chair Paul Phillips Larry Zweifel Program Authorized to Confer Degree: Neuroscience Graduate Program TABLE OF CONTENTS Summary/Abstract………………………………………………………………………….……..6 Dedication……………………………………………………………………………….………...9 Chapter 1 The therapeutic potential of the targeting the kappa opioid receptor system in stress- associated mental health disorders……………………………….………………………………10 Section 1.1 Activation of the dynorphin/kappa opioid receptor system is associated with dysphoria, cognitive disruption, and increased preference for drugs of abuse…………………..13 Section 1.2 Contribution of the dyn/KOR system to substance use disorder, anxiety, and depression………………………………………………………………………………………..15 Section 1.3 KORs are expressed on dorsal raphe serotonin neurons and contribute to stress- induced plasticity with serotonin circuitry……………………………………………………….17 Section 1.4 Kappa opioid receptor expression in the VTA contributes to the behavioral response to stress……………………………………………………………………………………....…..19 Section 1.5 Other brain regions contributing to the KOR-mediated response to stress…………23 Section 1.6 G Protein signaling at the KOR …………………………………………………….25 Chapter 2: JNK-Receptor Inactivation Affects D2 Receptor through both agonist action and norBNI-mediated cross-inactivation
    [Show full text]
  • An Advance About the Genetic Causes of Epilepsy
    E3S Web of Conferences 271, 03068 (2021) https://doi.org/10.1051/e3sconf/202127103068 ICEPE 2021 An advance about the genetic causes of epilepsy Yu Sun1, a, *, †, Licheng Lu2, b, *, †, Lanxin Li3, c, *, †, Jingbo Wang4, d, *, † 1The School of Molecular and Cellular Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801-3633, US 2High School Affiliated to Shanghai Jiao Tong University, Shanghai, 200441, China 3Applied Biology program, University of British Columbia, Vancouver, V6r3b1, Canada 4School of Chemical Machinery and Safety, Dalian University of Technology, Dalian, 116023, China †These authors contributed equally. Abstract: Human hereditary epilepsy has been found related to ion channel mutations in voltage-gated channels (Na+, K+, Ca2+, Cl-), ligand gated channels (GABA receptors), and G-protein coupled receptors, such as Mass1. In addition, some transmembrane proteins or receptor genes, including PRRT2 and nAChR, and glucose transporter genes, such as GLUT1 and SLC2A1, are also about the onset of epilepsy. The discovery of these genetic defects has contributed greatly to our understanding of the pathology of epilepsy. This review focuses on introducing and summarizing epilepsy-associated genes and related findings in recent decades, pointing out related mutant genes that need to be further studied in the future. 1 Introduction Epilepsy is a neurological disorder characterized by 2 Malfunction of Ion channel epileptic seizures caused by abnormal brain activity. 1 in Functional variation in voltage or ligand-gated ion 100 (50 million people) people are affected by symptoms channel mutations is a major cause of idiopathic epilepsy, of this disorder worldwide, with men, young children, and especially in rare genetic forms.
    [Show full text]
  • Ion Channels 3 1
    r r r Cell Signalling Biology Michael J. Berridge Module 3 Ion Channels 3 1 Module 3 Ion Channels Synopsis Ion channels have two main signalling functions: either they can generate second messengers or they can function as effectors by responding to such messengers. Their role in signal generation is mainly centred on the Ca2 + signalling pathway, which has a large number of Ca2+ entry channels and internal Ca2+ release channels, both of which contribute to the generation of Ca2 + signals. Ion channels are also important effectors in that they mediate the action of different intracellular signalling pathways. There are a large number of K+ channels and many of these function in different + aspects of cell signalling. The voltage-dependent K (KV) channels regulate membrane potential and + excitability. The inward rectifier K (Kir) channel family has a number of important groups of channels + + such as the G protein-gated inward rectifier K (GIRK) channels and the ATP-sensitive K (KATP) + + channels. The two-pore domain K (K2P) channels are responsible for the large background K current. Some of the actions of Ca2 + are carried out by Ca2+-sensitive K+ channels and Ca2+-sensitive Cl − channels. The latter are members of a large group of chloride channels and transporters with multiple functions. There is a large family of ATP-binding cassette (ABC) transporters some of which have a signalling role in that they extrude signalling components from the cell. One of the ABC transporters is the cystic − − fibrosis transmembrane conductance regulator (CFTR) that conducts anions (Cl and HCO3 )and contributes to the osmotic gradient for the parallel flow of water in various transporting epithelia.
    [Show full text]
  • Spatial Distribution of Leading Pacemaker Sites in the Normal, Intact Rat Sinoa
    Supplementary Material Supplementary Figure 1: Spatial distribution of leading pacemaker sites in the normal, intact rat sinoatrial 5 nodes (SAN) plotted along a normalized y-axis between the superior vena cava (SVC) and inferior vena 6 cava (IVC) and a scaled x-axis in millimeters (n = 8). Colors correspond to treatment condition (black: 7 baseline, blue: 100 µM Acetylcholine (ACh), red: 500 nM Isoproterenol (ISO)). 1 Supplementary Figure 2: Spatial distribution of leading pacemaker sites before and after surgical 3 separation of the rat SAN (n = 5). Top: Intact SAN preparations with leading pacemaker sites plotted during 4 baseline conditions. Bottom: Surgically cut SAN preparations with leading pacemaker sites plotted during 5 baseline conditions (black) and exposure to pharmacological stimulation (blue: 100 µM ACh, red: 500 nM 6 ISO). 2 a &DUGLDFIoQChDQQHOV .FQM FOXVWHU &DFQDG &DFQDK *MD &DFQJ .FQLS .FQG .FQK .FQM &DFQDF &DFQE .FQM í $WSD .FQD .FQM í .FQN &DVT 5\U .FQM &DFQJ &DFQDG ,WSU 6FQD &DFQDG .FQQ &DFQDJ &DFQDG .FQD .FQT 6FQD 3OQ 6FQD +FQ *MD ,WSU 6FQE +FQ *MG .FQN .FQQ .FQN .FQD .FQE .FQQ +FQ &DFQDD &DFQE &DOP .FQM .FQD .FQN .FQG .FQN &DOP 6FQD .FQD 6FQE 6FQD 6FQD ,WSU +FQ 6FQD 5\U 6FQD 6FQE 6FQD .FQQ .FQH 6FQD &DFQE 6FQE .FQM FOXVWHU V6$1 L6$1 5$ /$ 3 b &DUGLDFReFHSWRUV $GUDF FOXVWHU $GUDD &DY &KUQE &KUP &KJD 0\O 3GHG &KUQD $GUE $GUDG &KUQE 5JV í 9LS $GUDE 7SP í 5JV 7QQF 3GHE 0\K $GUE *QDL $QN $GUDD $QN $QN &KUP $GUDE $NDS $WSE 5DPS &KUP 0\O &KUQD 6UF &KUQH $GUE &KUQD FOXVWHU V6$1 L6$1 5$ /$ 4 c 1HXURQDOPURWHLQV
    [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]
  • A B C Supplementary Figure 1. Experimental Workflow And
    a c Ion channel activity Midbrain microdissection Cacna1c Cav1.2 Collected material Cacna1d Cav1.3 Cacna1g Cav3.1 SNc Hcn2 HCN2 SNr VTA Hcn4 HCN4 Scn2a1 Nav1.2 + Scn5a Nav1.5 TaqMan assays Scn8a Nav1.6 Kcna2 Kv1.2 Dissociated midbrain neurons Kcnb1 Kv2.1 Kcnd2 Kv4.2 Kcnd3 Kv4.3 Targeted reverse transcription Kcnip3 KCHIP3 and preamplification Kcnj11 Kir6.2 Abcc8 SUR1 Abcc9 SUR2B Fluorescence imaging Kcnj5 GIRK4 Kcnj6 GIRK2 GFP Kcnn3 SK3 DA metabolism & signaling Non-GFP Microfluidic quantitative PCR Th TH Slc6a3 DAT Assays Samples Slc18a2 VMAT2 Pipette harvesting Drd2 D2R Glia-specific markers Gfap GFAP Aldh1l1 FDH Calcium-ion-binding Calb1 CB Pvalb PV Other neuronal markers b 40 Slc17a6 VGLUT2 30 Gad1 GAD67 20 Gad2 GAD65 10 Chat CHAT Cell count 0 Penk ENK 16 GFP Neuronal structure Non-GFP 14 Ncam2 NCAM2 WT 12 Map2 MAP2 10 Nefm NEF3 Th (TH) 8 Neuronal activation x E Creb1 CREB 2 6 g DA neurons Fos C-FOS o 4 L (n=111) Bdnf BDNF 2 nDA neurons Housekeeping/ 0 (n=37) transcriptional factors 0 2 4 6 8 10 12 14 16 0 10 20 30 40 Hprt HGPRT Tbp TBP Log2Ex Slc6a3 (DAT) Cell count Tbx3 TBX3 Supplementary Figure 1. Experimental workflow and classification of DA and nDA neurons. a, schematic showing the workflow for the single-cell gene profiling. Left, neurons were manually collected after acute dissociation from microdissected midbrain slices containing the substantia nigra pars compacta and reticulata (SNc, SNr) and part of the ventral tegmental area (VTA) obtained from TH-GFP mice.
    [Show full text]
  • Information Topology of Gene Expression Profile in Dopaminergic Neurons
    bioRxiv preprint doi: https://doi.org/10.1101/168740; this version posted July 26, 2017. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. 1 Information topology of gene expression profile in dopaminergic neurons 2 Mónica TAPIA PACHECO1,§, Pierre BAUDOT1,§, Martial A. DUFOUR1,2, Christine 3 FORMISANO-TRÉZINY1, Simone TEMPORAL1, Manon LASSERRE1, Jean 4 GABERT1,3, Kazuto KOBAYASHI4 and Jean-Marc GOAILLARD1,5 5 6 1 Unité de Neurobiologie des Canaux Ioniques et de la Synapse, INSERM UMR 7 1072, Aix Marseille Université, 13015 Marseille, FRANCE 8 2 Current address: NYU Neuroscience Institute, New York University, New York, 9 NY 10016, USA 10 3 Department of Biochemistry & Molecular Biology, University Hospital Nord, 11 Marseille, FRANCE 12 4 Department of Molecular Genetics, Institute of Biomedical Sciences, Fukushima 13 Medical University, Fukushima, 960-1295, JAPAN 14 5 Corresponding author 15 § These authors contributed equally to this work 16 17 Author contributions: M.T.P, P.B., C.F.T. and J.M.G. designed research. M.T.P., 18 P.B., C.F.T., M.A.D., S.T., M.L., J.G., K.K. and J.M.G. performed research. M.T.P., 19 P.B., C.F.T. and J.M.G. analyzed data. M.T.P., P.B., C.F.T. and J.M.G. wrote the 20 manuscript. 21 Corresponding author: Jean-Marc GOAILLARD 22 UMR_S 1072, INSERM, Aix Marseille Université, Faculté de Médecine Secteur 23 Nord, Marseille, FRANCE. 24 Email: [email protected] 1 bioRxiv preprint doi: https://doi.org/10.1101/168740; this version posted July 26, 2017.
    [Show full text]
  • Gene List of the Targeted NGS MCD and CCA Gene Panel AKT3,ALX1
    Gene List of the targeted NGS MCD and CCA gene panel AKT3,ALX1,ALX3,ALX4,AMPD2,ARFGEF2,ARID1B,ARX,ASPM,ATR,ATRX,B3GALTL,BRPF1,c12orf57,C6orf70,CASK,CCND2,CDK5RAP2,CDON,C ENPJ,CEP170,CHMP1A,COL4A1,CREBBP,CYP11A1,DCHS1,DCLK1,DCX,DHCR24,DHCR7,DIS3L2,DISC1,DISP1,DLL1,DMRTA2,DYNC1H1,DYRK1 A,EARS2,EFNB1,EMX1,EOMES,EP300,ERBB4,ERMARD,EXOSC3,FAM36A,FGF8,FGFR1,FGFR2,FLNA,FOXC1,FOXG1,FOXH1,FZD10,GLI2,GLI3,GP R56,GPSM2,HCCS,HESX1,HNRNPU,IGBP1,IGFBP1,ISPD,ITPA,KAL1,KAT6B,KATNB1,KIAA1279,KIF14,KIF1A,KIF1B,KIF21A,KIF2A,KIF5C,KIF7,L1 CAM,LAMB1,LAMC3,LRP2,MCPH1,MED12,MID1,NDE1,NFIB,NPC1,NR2F1,NSD1,NTRK1,NTRK3,OCEL1,OPA1,OTX2,PAFAH1B1,PAX6,PEX1,PHF1 0,PIK3R2,POLR3A,POLR3B,POMT1,POMT2,PTCH1,PTPRS,PYCR1,RAB3GAP1,RARS2,RELN,RFX3,ROBO1,ROBO3,RPS6KA3,RTTN,SATB2,SEPSEC S,SHH,SIX3,SLC12A6,SOX2,SPOCK1,SRPX2,TBCD,TBCE,TCF4,TDGF1,TEAD1,THBS2,TMEM5,TSC1,TSC2,TSEN15,TSEN2,TSEN34,TSEN54,TUBA1 A,TUBA8,TUBB,TUBB2A,TUBB2B,TUBB3,TUBB4A,TUBG1,VAX1,VRK1,WDR47,WDR62,ZBTB18,ZEB2,ZIC2. Gene List of the targeted NGS epilepsy gene panel AARS, ADGRV1, ADRA2B, ADSL, ALDH4A1, ALDH7A1, ALG13, ALPL, ARHGEF15, ARHGEF9, ARX, ASAH1, ATP1A2, ATP1A3, BRD2, CACNA1A, CACNA1H, CACNA2D2, CACNB4, CBL, CDKL5, CERS1, CHD2, CHRNA2, CHRNA4, CHRNB2, CLCN2, CLCN4, CLN8, CLTC, CNKSR2, CNTNAP2, CPA6, CPLX1, CSNK1G1, CSNK2B, CTNND2, DEPDC5, DHDDS, DNM1, DOCK7, DYNC1H1, EEF1A2, EFHC1, EIF2S3, EMC1, EPM2A, FASN, FLNA, FOXG1, GABBR2, GABRA1, GABRA2, GABRA3, GABRB2, GABRB3, GABRD, GABRG2, GAL, GNAO1, GOSR2, GRIA1, GRIN1, GRIN2A, GRIN2B, HCN1, HCN4, HDAC4, HNRNPU, IDH3A, IQSEC2, JRK, KCNA1, KCNA2, KCNB1,
    [Show full text]
  • Anti-KCNA5 / Kv1.5 Antibody (ARG40377)
    Product datasheet [email protected] ARG40377 Package: 50 μg anti-KCNA5 / Kv1.5 antibody Store at: -20°C Summary Product Description Rabbit Polyclonal antibody recognizes KCNA5 / Kv1.5 Tested Reactivity Hu Predict Reactivity Bov Tested Application WB Host Rabbit Clonality Polyclonal Isotype IgG Target Name KCNA5 / Kv1.5 Antigen Species Human Immunogen Synthetic peptide corresponding to aa. 583-613 of Human KCNA5. (LEKCNVKAKSNVDLRRSLYALCLDTSRETDL) Conjugation Un-conjugated Alternate Names KV1.5; HK2; HPCN1; Potassium voltage-gated channel subfamily A member 5; PCN1; ATFB7; Voltage- gated potassium channel HK2; HCK1; Voltage-gated potassium channel subunit Kv1.5 Application Instructions Application table Application Dilution WB 0.1 - 0.5 µg/ml Application Note * The dilutions indicate recommended starting dilutions and the optimal dilutions or concentrations should be determined by the scientist. Calculated Mw 67 kDa Observed Size 67 kDa Properties Form Liquid Purification Affinity purification with immunogen. Buffer 0.2% Na2HPO4, 0.9% NaCl, 0.05% Sodium azide and 5% BSA. Preservative 0.05% Sodium azide Stabilizer 5% BSA Concentration 0.5 mg/ml Storage instruction For continuous use, store undiluted antibody at 2-8°C for up to a week. For long-term storage, aliquot and store at -20°C or below. Storage in frost free freezers is not recommended. Avoid repeated freeze/thaw cycles. Suggest spin the vial prior to opening. The antibody solution should be gently mixed www.arigobio.com 1/2 before use. Note For laboratory research only, not for drug, diagnostic or other use. Bioinformation Gene Symbol KCNA5 Gene Full Name potassium channel, voltage gated shaker related subfamily A, member 5 Background Potassium channels represent the most complex class of voltage-gated ino channels from both functional and structural standpoints.
    [Show full text]
  • Subcellular Localization of K+ Channels in Mammalian Brain Neurons: Remarkable Precision in the Midst of Extraordinary Complexity
    Neuron Review Subcellular Localization of K+ Channels in Mammalian Brain Neurons: Remarkable Precision in the Midst of Extraordinary Complexity James S. Trimmer1,2,* 1Department of Neurobiology, Physiology, and Behavior 2Department of Physiology and Membrane Biology University of California, Davis, Davis, CA 95616, USA *Correspondence: [email protected] http://dx.doi.org/10.1016/j.neuron.2014.12.042 Potassium channels (KChs) are the most diverse ion channels, in part due to extensive combinatorial assem- bly of a large number of principal and auxiliary subunits into an assortment of KCh complexes. Their structural and functional diversity allows KChs to play diverse roles in neuronal function. Localization of KChs within specialized neuronal compartments defines their physiological role and also fundamentally impacts their activity, due to localized exposure to diverse cellular determinants of channel function. Recent studies in mammalian brain reveal an exquisite refinement of KCh subcellular localization. This includes axonal KChs at the initial segment, and near/within nodes of Ranvier and presynaptic terminals, dendritic KChs found at sites reflecting specific synaptic input, and KChs defining novel neuronal compartments. Painting the remarkable diversity of KChs onto the complex architecture of mammalian neurons creates an elegant pic- ture of electrical signal processing underlying the sophisticated function of individual neuronal compart- ments, and ultimately neurotransmission and behavior. Introduction genes are expressed in distinct cellular expression patterns Mammalian brain neurons are distinguished from other cells by throughout the brain, such that particular neurons express spe- extreme molecular and structural complexity that is intimately cific combinations of KCh a and auxiliary subunits. However, the linked to the array of intra- and intercellular signaling events proteomic complexity of KChs is much greater, as KChs exist as that underlie brain function.
    [Show full text]