Supplementary Table 6. Human PPI Network Details for Significantly Changed Proteins, As Identified in 3.2, Underlying Each of the Five Functional Domains

Total Page:16

File Type:pdf, Size:1020Kb

Supplementary Table 6. Human PPI Network Details for Significantly Changed Proteins, As Identified in 3.2, Underlying Each of the Five Functional Domains Supplementary Table 6. Human PPI network details for significantly changed proteins, as identified in 3.2, underlying each of the five functional domains. The network nodes represent each significant protein, followed by the list of interactors. Note that identifiers were converted to gene names to facilitate PPI database queries. Functional Domain Node Interactors Development and CTSD HBA1 differentiation APP ATP6V0A1 MAPK1 GABARAPL1 ILK IFI16 RASSF9 RASSF7 RASSF10 H2AFX VCAM1 MARCH9 ATP6V1A Development and HSP90AB1 AARS differentiation ABL1 ACTB ACTG1 ACTN1 ACVR1B ACVR1C ACVR2B ADRBK1 AGO1 AGO2 AGO3 AGO4 AHSA1 AICDA AIP AKT2 ALDOA ALK ALPK1 AMHR2 ANAPC2 ANKMY2 ARAF AREL1 ARMC5 ARRB2 ASB17 ASB2 ASB3 ASB4 ASB6 ATF2 ATF3 AURKB AURKC AXL BBX BCR/ABL BLK BMPR1A BMX BRAF BTK BTRC C12orf10 C20orf194 CACYBP CAMK1G CAMK2A CAMK2B CAMK2D CAMK2G CAMK4 CAMKK1 CAMKK2 CAMKV CCDC117 CD247 CDC37 CDC37L1 CDC5L CDK10 CDK11A CDK14 CDK15 CDK18 CDK2 CDK3 CDK4 CDK5 CDK6 CDK7 CDK9 CDKN2A CEBPE CFTR CHEK1 CHORDC1 CHUK CLIC4 CLK2 CLK3 COPS5 CSF1R CSNK1A1 CSNK1E CSNK2A1 CUL1 CUL2 CUL3 CUL4A CUL4B CXXC1 CYP17A1 DAPK3 DBN1 DCLK2 DDR1 DDR2 DDX24 DET1 DLX6 DMPK DMRTA1 DNAJC7 DTX4 DYRK1B DYRK2 DYRK4 EEF2 EGFR EIF2AK1 EIF2AK2 EIF3H EIF3M EIF4EBP1 EL52 ENC1 ENO1 EPHA1 EPHA2 EPHA4 EPHB1 EPHB6 ERBB2 ERBB3 ERBB4 ESR1 FAM162A FASN FASTK FBXL12 FBXL13 FBXL14 FBXL15 FBXL18 FBXL2 FBXL3 FBXL8 FBXO10 FBXO18 FBXO24 FBXO25 FBXO27 FBXO28 FBXO3 FBXO33 FBXO34 FBXO38 FBXO4 FBXO40 FBXO6 FBXO9 FBXW11 FBXW2 FBXW5 FBXW7 FCHSD2 FER FES FGFR1 FGFR3 FGR FKBP4 FKBP5 FKBP6 FKBP8 FKBPL FLNA FLT4 FOXD4L6 FOXM1 FOXP2 FRK FYN G2E3 GABARAP GABARAPL1 GABARAPL2 GAN GAPDH GNAI2 GRB2 GRK4 GRK6 GRK7 GSG2 GSK3A GTF2IRD2 HCK HECTD3 HERC4 HERC6 HES4 HGH1 HIF1A HIPK4 HMGA1 HP1BP3 HSP90AA1 HSP90AB1 HSPA1A HSPA1B HSPB1 HSPH1 IARS2 ICK IFIT1 IGF1R IKBKB IKBKE IKBKG ILK INSRR IQGAP1 IRAK2 IRAK3 IRF2 IRF3 ISX ITGB1BP2 ITK JAK1 JUN KAT5 KBTBD4 KBTBD7 KCNA5 KCNA6 KCNG1 KCNS3 KCTD8 KLHL1 KLHL10 KLHL13 KLHL14 KLHL15 KLHL22 KLHL23 KLHL25 KLHL26 KLHL29 KLHL32 KLHL34 KLHL36 KLHL38 KLHL6 KSR1 KSR2 LARP4B LCK LDHA LGALS3BP LIMK1 LIMK2 LNX1 LRRK1 LRRK2 LRSAM1 LYN MAFG MAP1LC3A MAP1LC3B MAP2K5 MAP2K7 MAP3K1 MAP3K12 MAP3K14 MAP3K15 MAP3K2 MAP3K3 MAP3K5 MAP3K6 MAP3K7 MAP3K8 MAP3K9 MAP4K1 MAP4K2 MAP4K4 MAPK15 MAPK4 MAPK6 MAPK7 MAPRE1 MAPT MARCH9 MAST2 MATK MAX MCM7 MDH1 MDM4 MERTK MINK1 MKNK1 MKX MOS MTHFD1 MUSK MYH9 MYLK2 MYLK3 MYLK4 MYO19 MYO3B NANS NEK11 NEK8 NEK9 NELFE NFIC NFKB1 NFKB2 NFKBIB NFKBIE NFRKB NHLRC1 NPHP4 NPR2 NR1H3 NR1I2 NR1I3 NR2C2 NR3C2 NR4A1 NTRK1 NTRK2 NTRK3 NUAK2 NUMA1 PAK6 PARK2 PASK PCGF1 PCGF3 PCGF6 PDGFRB PDIK1L PGK1 PHB PIM1 PIM2 PIM3 PINK1 PKM PKN1 PKN2 POGK PPARD PPARG PPID PPP5C PRDM1 PREB PRKAA1 PRKAA2 PRKACA PRKACB PRKCA PRKCB PRKCE PRKCG PRKCH PRKCI PRKCQ PRKCZ PRKD1 PRKD2 PRKDC PRKG2 PRKX PRKY PRPF19 PSAT1 PSKH1 PSKH2 PSMB5 PSMD1 PTGES3 PTK2 PTK2B PTK6 RAB40A RAF1 RAG1 RAPSN RCBTB1 RCBTB2 RELA RET RFWD3 RGS11 RGS6 RGS7 RGS9 RHOBTB1 RIPK1 RIPK3 RNF10 RNF111 RNF19B RNF40 ROCK1 ROR2 RPL5 RPL7 RPLP0 RPS3A RPS4X RPS6 RPS6KA1 RPS6KA2 RPS6KA3 RPS6KA5 RPS6KA6 RPS6KB1 RPS6KC1 RPS6KL1 RPSA SARS2 SETDB1 SF3B3 SGK1 SGK2 SGK223 SGK3 SGTA SH3RF2 SIM2 SKP1 SKP2 SLC33A1 SLFN11 SNW1 SOCS6 SPSB1 SPSB3 SPTAN1 SREBF1 SRPK1 SRPK3 STARD13 STAT1 STAT2 STIP1 STK11 STK32B STK32C STK38 STK38L STUB1 STYK1 SUGT1 TAB1 TADA2A TAF1D TAOK3 TBK1 TBX22 TCF25 TCP1 TEAD2 TESK1 TESK2 TFDP3 THAP4 TIE1 TMOD4 TNFAIP3 TNK1 TNK2 TNNI3K TNNT1 TOMM34 TP53 TP53RK TP63 TPM3 TRADD TRAF2 TRAF3IP1 TRIM10 TRIM17 TRIM2 TRIM32 TRIM36 TRIM37 TRIM41 TRIM49 TRIM56 TRIM7 TRIM73 TRIM74 TSSK1B TSSK2 TSSK3 TSSK6 TTC4 TTI2 TUBA1A TUBA1C TUBG1 TYK2 TYRO3 UBA1 UNC45A UNC45B VCAM1 VPS18 VPS41 WNK4 WSB2 WWP1 XPO1 XRCC3 YES1 YWHAB YWHAZ ZBED4 ZBTB17 ZBTB20 ZBTB49 ZC3H7B ZNF215 ZNF74 Development and MT3 TTR differentiation Development and TFAP4 TRAF1 differentiation EXOSC8 PRDM5 GOLGA2 FBXW11 AIM2 FOXA1 RBPJ FOXK2 FOXE1 Development and CAMK2A ACTN1 differentiation DLG3 GRIN2B RCHY1 PPM1F CAMK2D CAMK2A ZMYM1 CAMK2G SMAD2 HSP90AB1 CAMK2B CHMP5 NR2F6 CALM1 GRIA4 Development and CAMK2B POP5 differentiation RBPMS ACOT7 KRTAP10-11 SEMA4G SMYD3 CAMK2A MRPL11 PHKB MORF4L1 RBFOX2 FAM171A2 MED18 SPRYD7 KRTAP19-5 KRTAP19-7 MAD2L2 RPL11 RAP2B AP5B1 PKM CAMK2B HSP90AB1 TTC5 ATXN1 NINL Development and CAMK2D FXR2 differentiation FKBP1B FNDC3B EPHA10 TNPO2 HSP90AB1 CAMK2A HNMT IFNGR2 DNAL4 WASF3 BANP MOAP1 IKBKG MRPL11 EIF4B CAMK2D SRPK1 CYLD SPATA24 RPS4X ARL2BP FAM171B TTC5 AIM2 GRB2 NIN CEP170 ARRB2 MYC JUN STIP1 Development and HSP90AA1 STUB1 differentiation HIF1A RAD51 FKBP8 DARS EPRS LCK ZAP70 HSPA1A HSPA1B CHORDC1 PRKCZ PAK1 JUN EGFR ERBB4 NDRG1 HSPB1 ERBB2 LRP1 TAB2 TAB1 RIPK3 RIPK2 RIPK1 NFKB2 TRADD MAP3K14 TRAF2 TRAF1 AHSA1 NFKBIE NFKBIB MAP3K8 MAP3K7 TBK1 MAP3K1 MAP3K3 IKBKE IKBKG CHUK IKBKB LSM1 RPS3A CDK9 CDC37L1 STK11 NLRP12 PTGES3 HSP90AB1 FBXO25 CCDC117 TSSK6 ARAF HP1BP3 CDC37 HIG-1 DYRK4 AKT3 STIP1 HSP90AB1 PPP2R1A HSPA8 RPAP3 FASN FKBP5 FKBP4 DNAJA2 PDRG1 TOMM34 GIGYF2 DNAJA1 IRS4 TUBB4B POLR2E HSPA4 TUBB2B TUBB TUBA1A HSP90AA1 TUBAL3 SSBP1 TTC4 SIRT1 COBLL1 U2AF2 WDR20 VARS CDC37L1 TTC1 FAM103A1 HK2 TERF1 SKIV2L2 PRPF4B FLII PRR14L EDRF1 FAM83H ZMYM1 NUDCD3 TTC9C PPP5C PLCE1 SUGT1 UNC45A CSNK1A1 MYLK2 TFIP11 USP19 CNOT6 PRPF8 BAG2 URI1 EFTUD2 DYNC1H1 CALD1 CDK11A CEP97 NUDC SCRIB SNRNP200 CACYBP ST13 UBE2N ACTB FYN MARS AGO2 QARS CDH1 USP49 FBXW2 KLHL38 RAF1 SKP2 PIWIL2 RELA AP3D1 NR3C1 MOS YWHAZ ITGB1BP2 NFKB2 PIWIL4 UNC45B AGO3 KSR2 CDK15 PSKH2 PIWIL1 PKN2 FBXO24 MAP3K8 AMHR2 LCK MUSK ZBED4 TRIM56 TESK2 CDK13 NOD1 KLHL1 PRKACB MMP2 CERS2 H2AFX GABARAPL1 ATF2 APP GABARAP IQCB1 PPP2R2B MAP1LC3A LRRK2 NPHP4 AGO3 AGO4 ARRB1 NES PRKACA PRKACB CDK5 STK4 MCM7 TRAF3IP1 GABARAPL2 AICDA SNW1 PTBP3 CDC5L PPID CDK2 RPS6KA1 CDKN2A PRKCI PRKAA1 CDK4 BRMS1 ERBB3 GZMA IFIT1 ADRBK1 ALKBH8 GATA3 NUAK2 Development and PPP2R1A PHB2 differentiation PPP2R5E CSNK2B EIF1B NME2 BCAR3 IKBKE TRAF6 MCC TAB1 PPP4C PPP2CA PPP2R1B NFKB2 PLA2G16 MAP3K3 ARIH2 STK24 TNIK EIF6 FTSJ1 PPP2R3A PPP2R2A PPP5C CFTR GNA12 SMAD2 PRR14 S100A9 SKIV2L2 PPP2R2D SGOL1 ZCCHC8 SERTAD4 RBM7 FOXO3 CDK1 STRN3 RAP1A CDK4 INTS6 NCAPH2 PRR14L SIKE1 LPP PPP2R3C ATP6V1C1 PPME1 PPP2R5D EIF4A1 STRN RAB11A PARK7 PRDX1 MCM3 TRADD ANAPC10 RAB18 EEF2 PRDX2 RAB7A TBCCD1 FBXL16 INTS3 DYNLL1 LIMD1 C1QBP FOXC2 SET FGFR1OP ABCF3 FECH PPFIA1 PPP2R5C PPP2R5B PPP2R5A STRIP1 PPP2R3B STRN4 SGOL2 FAM13A SOGA1 INTS2 CPSF3L CCDC6 INTS4 PPFIBP1 INTS9 PPP2R2B INTS1 PRR14 PLEKHA5 CDCA4 ARHGEF2 MTCL1 ANKLE2 CTTNBP2NL INTS12 FGFR1OP2 PPP2CB FOXC1 FAM122A PPFIA2 SLMAP MOB4 KIAA1524 HSPD1 TP53 CCNG1 AIMP2 MAPK6 RELA BHLHE40 SMAD3 AKT1 CTNNBIP1 RORC ZFYVE9 ERBB2 FN1 GABARAPL1 VCAM1 GABARAP MAP1LC3B HSP90AA1 AHI1 MARK4 MARK2 ARRB2 GABARAPL2 LRFN4 SNW1 CDC5L JUN NKD1 DOCK5 PPP4R1 SAMHD1 PPP2R2C TRAF3IP3 CTTNBP2 PDCD10 VWA9 ABI1 NABP1 STK26 STK25 Development and YWHAG EPB41L3 differentiation LRRK2 STK4 MARK2 MARK3 SAMD4B MPRIP SH3BP5L SMARCD1 LTB4R ATP6V0B YWHAE BAD MAP3K3 HDAC4 RAB11A EPB41L2 HIVEP2 FAM13B DDX27 TERF1 WNK1 PTPN3 SH3BP4 NDEL1 SIMC1 FAM53C FRYL CHEK1 MDM4 RAB11FIP2 KIF1B PAK4 EDC3 CCNY AKAP13 RAI14 TIAM1 PIK3R1 PABPC1 DDX39B USP8 PUF60 LUC7L2 PRPF4B TSC2 SRSF10 TJP2 YAP1 GSK3A ZBTB21 PI4KB MFAP1 TRA2A RMDN3 LUC7L3 ATP5B C1QBP TUBA1A VIM BAIAP2 RALGPS2 TSC1 DENND4A LSR MAGOHB HDAC7 HSPA1A HSPA1B SRRM2 EEF1G CFAP20 ARHGEF2 DFFA DOCK7 SAMD4A MIEF1 KIAA0930 THRAP3 TRIM21 ERC1 SRRM1 STK11 PRPF19 TUBB PIK3C3 SRGAP2 ARHGEF7 KANK1 YWHAG HSPB6 CBL RAF1 TP53 KIF1C GP1BA ING1 NDRG1 ALB DCAF7 TBC1D1 SAMD4B NEFL PRPF40A PARD3B CLK1 FRY SFN CSE1L DACT1 CRTC3 RACGAP1 HSPA9 FAM65B CDK16 ARAF RNPS1 PLA2G12A DHX15 SAP18 PNN ZC3H18 KIAA0408 HNRNPH1 KRTAP19-5 BRAF WWTR1 MARK1 KRT38 SRPK1 SYNPO KRT31 CYFIP1 EIF4A3 MAGOH CDKN1B CENPJ COPS5 EPB41 ACIN1 CHAF1A SNRNP200 EFTUD2 KIF5C KLC2 SRSF3 CDC5L PPFIBP1 PANK2 RSRC1 CLASP1 PRPF38B LRP1 ARHGEF16 ZC3HC1 TMEM102 SF3B1 HSU53209 KIF23 KRT37 SF3B3 MICALL1 RPL3 ZNF638 HNRNPCL1 PFKFB2 FRMD6 LRFN1 NOLC1 KLC1 CASP3 HOXC10 MAP3K2 CGNL1 ZAK NCBP1 SRSF1 SHTN1 LBR CTPS1 PIK3R4 NELFE DYRK1A KRT85 NCKIPSD MAPKAP1 PARD3 PPIG RABGEF1 KIF5B SRSF6 NCKAP1 MLLT4 IRS2 WEE1 VANGL2 GBF1 MPHOSPH9 MYH10 KRT18 ANKHD1 SSFA2 SYNPO2 NEDD4L MSL2 CEP95 TNFAIP3 CLK2 ANKS1A NADK CDK17 CGN KMT5B TRA2B IGF1R KRT35 KRT34 OSBPL3 EML3 BCLAF1 SHCBP1 SRSF11 SON KRT33B RASAL2 MYCBP2 KLC4 CAMSAP2 TBC1D1 RABEP1 LARP1 CLK3 KRT82 SRSF4 CRTC2 PAK1 PRKDC UBC DDX5 CFL1 ATP5A1 PPP1R3D SKIV2L2 RASSF8 FN1 VCAM1 ATF2 HTT GRB2 CDC25B WWC1 YWHAH YWHAB LCA5 CEP89 IRS4 ABL1 YWHAZ ARRB1 ARRB2 RASSF2 OPTN PYHIN1 LRFN4 CBX4 MAP3K5 MAP3K6 GAB2 TH TET2 NEDD8 RBM7 TNK1 WDR62 KDR HDAC5 FRMD5 Development and FLT1 PTPRB differentiation CRKL VEGFA CTNNB1 NRP1 HCK PIK3R1 PTK2 PTPRJ CBL LDLR EEA1 CRK PTPN11 PLCG1 PGF LGALS1 SRPK1 PKM Development and MAPK1 ARHGAP9 differentiation STAT5A TP53 RPS6KA3 ARRB2 PTPN7 PXN ETS1 MAPK14 ID2 GAPDH IFI35 PACSIN3 DUSP1 MTIF3 SUPT20H CRP TNIP1 HLA-B TNIK CTSD PEA15 BCL2 PTPRR DUSP9 MAP2K1 DUSP7 ACPP PTPRB DUSP3 YBX1 PPP2CA YBX3 IER3 PPP2R5C PTPRJ HMGB1 PDCD6IP MAPK12 MAPK3 RPS6KA2 CEP350 NAV1 ELK1 PPM1A DUSP6 DUSP5 DUSP4 RET FGF5 MAPKAPK5 MTPN EGLN3 GNPTAB TNIP2 SHANK3 ENAH PRPSAP1 CRKL SMAD3 CASP8 LCK VCAM1 MBP MAP3K3 DUSP2 JUN PPP1CA RARA DCC RPS6KA1 Development and RAP1B PDHB differentiation KMT2B FAF1 DDAH2 RALGDS TP53 TLE1 SDF4 APLP1 ALAS1 A2M RAP1GAP UBC RAPGEF3 MAP3K14 MCC PAK2 RGS2 NRBP2 KIAA1191 NCKAP5L TSEN2 KLC1 USP32 AP3M1 MAP3K4 DICER1 DMXL1 AARS2 MRPS35 UBR4 GAR1 WRAP53 UNC119 ZNF135 LRIF1 CHGB CSAD SMURF2 PKM RASSF5 RAB7B RGL2 CCT7 ZDHHC17 FN1 VCAM1 ATP6AP2 XRCC1 LIMA1 Development and UCHL1 NCAM1 differentiation KRT4 MCC TNIK EIF1B VHL EIF6 RANBP9 COPS5 NEDD8 CBX1 CCDC14 KRT17 EGFR UBB IKBKE
Recommended publications
  • 4-6 Weeks Old Female C57BL/6 Mice Obtained from Jackson Labs Were Used for Cell Isolation
    Methods Mice: 4-6 weeks old female C57BL/6 mice obtained from Jackson labs were used for cell isolation. Female Foxp3-IRES-GFP reporter mice (1), backcrossed to B6/C57 background for 10 generations, were used for the isolation of naïve CD4 and naïve CD8 cells for the RNAseq experiments. The mice were housed in pathogen-free animal facility in the La Jolla Institute for Allergy and Immunology and were used according to protocols approved by the Institutional Animal Care and use Committee. Preparation of cells: Subsets of thymocytes were isolated by cell sorting as previously described (2), after cell surface staining using CD4 (GK1.5), CD8 (53-6.7), CD3ε (145- 2C11), CD24 (M1/69) (all from Biolegend). DP cells: CD4+CD8 int/hi; CD4 SP cells: CD4CD3 hi, CD24 int/lo; CD8 SP cells: CD8 int/hi CD4 CD3 hi, CD24 int/lo (Fig S2). Peripheral subsets were isolated after pooling spleen and lymph nodes. T cells were enriched by negative isolation using Dynabeads (Dynabeads untouched mouse T cells, 11413D, Invitrogen). After surface staining for CD4 (GK1.5), CD8 (53-6.7), CD62L (MEL-14), CD25 (PC61) and CD44 (IM7), naïve CD4+CD62L hiCD25-CD44lo and naïve CD8+CD62L hiCD25-CD44lo were obtained by sorting (BD FACS Aria). Additionally, for the RNAseq experiments, CD4 and CD8 naïve cells were isolated by sorting T cells from the Foxp3- IRES-GFP mice: CD4+CD62LhiCD25–CD44lo GFP(FOXP3)– and CD8+CD62LhiCD25– CD44lo GFP(FOXP3)– (antibodies were from Biolegend). In some cases, naïve CD4 cells were cultured in vitro under Th1 or Th2 polarizing conditions (3, 4).
    [Show full text]
  • Anti-Inflammatory Role of Curcumin in LPS Treated A549 Cells at Global Proteome Level and on Mycobacterial Infection
    Anti-inflammatory Role of Curcumin in LPS Treated A549 cells at Global Proteome level and on Mycobacterial infection. Suchita Singh1,+, Rakesh Arya2,3,+, Rhishikesh R Bargaje1, Mrinal Kumar Das2,4, Subia Akram2, Hossain Md. Faruquee2,5, Rajendra Kumar Behera3, Ranjan Kumar Nanda2,*, Anurag Agrawal1 1Center of Excellence for Translational Research in Asthma and Lung Disease, CSIR- Institute of Genomics and Integrative Biology, New Delhi, 110025, India. 2Translational Health Group, International Centre for Genetic Engineering and Biotechnology, New Delhi, 110067, India. 3School of Life Sciences, Sambalpur University, Jyoti Vihar, Sambalpur, Orissa, 768019, India. 4Department of Respiratory Sciences, #211, Maurice Shock Building, University of Leicester, LE1 9HN 5Department of Biotechnology and Genetic Engineering, Islamic University, Kushtia- 7003, Bangladesh. +Contributed equally for this work. S-1 70 G1 S 60 G2/M 50 40 30 % of cells 20 10 0 CURI LPSI LPSCUR Figure S1: Effect of curcumin and/or LPS treatment on A549 cell viability A549 cells were treated with curcumin (10 µM) and/or LPS or 1 µg/ml for the indicated times and after fixation were stained with propidium iodide and Annexin V-FITC. The DNA contents were determined by flow cytometry to calculate percentage of cells present in each phase of the cell cycle (G1, S and G2/M) using Flowing analysis software. S-2 Figure S2: Total proteins identified in all the three experiments and their distribution betwee curcumin and/or LPS treated conditions. The proteins showing differential expressions (log2 fold change≥2) in these experiments were presented in the venn diagram and certain number of proteins are common in all three experiments.
    [Show full text]
  • Tumor Growth and Cancer Treatment
    Molecular Cochaperones: Tumor Growth and Cancer Treatment The Harvard community has made this article openly available. Please share how this access benefits you. Your story matters Citation Calderwood, Stuart K. 2013. “Molecular Cochaperones: Tumor Growth and Cancer Treatment.” Scientifica 2013 (1): 217513. doi:10.1155/2013/217513. http://dx.doi.org/10.1155/2013/217513. Published Version doi:10.1155/2013/217513 Citable link http://nrs.harvard.edu/urn-3:HUL.InstRepos:11879066 Terms of Use This article was downloaded from Harvard University’s DASH repository, and is made available under the terms and conditions applicable to Other Posted Material, as set forth at http:// nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of- use#LAA Hindawi Publishing Corporation Scientifica Volume 2013, Article ID 217513, 13 pages http://dx.doi.org/10.1155/2013/217513 Review Article Molecular Cochaperones: Tumor Growth and Cancer Treatment Stuart K. Calderwood Division of Molecular and Cellular Biology, Department of Radiation Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, 99 Brookline Avenue, Boston, MA 02215, USA Correspondence should be addressed to Stuart K. Calderwood; [email protected] Received 11 February 2013; Accepted 1 April 2013 Academic Editors: M. H. Manjili and Y. Oji Copyright © 2013 Stuart K. Calderwood. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Molecular chaperones play important roles in all cellular organisms by maintaining the proteome in an optimally folded state. They appear to be at a premium in cancer cells whose evolution along the malignant pathways requires the fostering of cohorts of mutant proteins that are employed to overcome tumor suppressive regulation.
    [Show full text]
  • Identification of Bleomycin and Radiation-Induced Pulmonary Fibrosis Susceptibility Genes in Mice Anne-Marie Lemay Department Of
    Identification of bleomycin and radiation-induced pulmonary fibrosis susceptibility genes in mice Anne-Marie Lemay Department of Human Genetics McGill University, Montréal February 4th, 2010 A thesis submitted to McGill University in partial fulfilment of the requirements of the degree of Doctor of Philosophy © Anne-Marie Lemay 2010 Comme il est profond, ce mystère de l’Invisible ! Nous ne pouvons le sonder avec nos sens misérables, avec nos yeux qui ne savent apercevoir ni le trop petit, ni le trop grand, ni le trop près, ni le trop loin, ni les habitants d’une étoile, ni les habitants d’une goutte d’eau… Guy de Maupassant Le Horla ii Table of contents Table of contents ................................................................................................... iii Abstract...................................................................................................................vi Résumé ................................................................................................................ viii Acknowledgments................................................................................................... x Abbreviations........................................................................................................ xii Original contributions to knowledge...................................................................xiv Author contribution to research...........................................................................xv List of figures ........................................................................................................
    [Show full text]
  • Bioinformatic and Modelling Approaches for a System-Level Understanding of Oxidative Stress Toxicity Elias Zgheib
    Bioinformatic and modelling approaches for a system-level understanding of oxidative stress toxicity Elias Zgheib To cite this version: Elias Zgheib. Bioinformatic and modelling approaches for a system-level understanding of oxidative stress toxicity. Quantitative Methods [q-bio.QM]. Université de Technologie de Compiègne, 2018. English. NNT : 2018COMP2464. tel-02088169 HAL Id: tel-02088169 https://tel.archives-ouvertes.fr/tel-02088169 Submitted on 2 Apr 2019 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Par Elias ZGHEIB Bioinformatic and modelling approaches for a system- level understanding of oxidative stress toxicity Thèse présentée pour l’obtention du grade de Docteur de l’UTC Soutenue le 18 décembre 2018 Spécialité : Bio-ingénierie et Mathématiques Appliquées : Unité de Recherche Biomécanique et Bio-ingénierie (UMR-7338) D2464 BIOINFORMATIC AND MODELLING APPROACHES FOR A SYSTEM-LEVEL UNDERSTANDING OF OXIDATIVE STRESS TOXICITY A THESIS SUBMITTED TO THE UNIVERSITE DE TECHNOLOGIE DE COMPIEGNE SORBONNE UNIVERSITES LABORATOIRE DE BIO-MECANIQUE ET BIOINGENIERIE UMR CNRS 7338 – BMBI 18TH OF DECEMBER 2018 For the degree of Doctor Spécialité : Bio-ingénierie et Mathématiques Appliquées Elias ZGHEIB SUPERVISED BY Prof. Frédéric Y. BOIS JURY MEMBERS Mme. Karine AUDOUZE Rapporteur Mr.
    [Show full text]
  • Senescence Inhibits the Chaperone Response to Thermal Stress
    SUPPLEMENTAL INFORMATION Senescence inhibits the chaperone response to thermal stress Jack Llewellyn1, 2, Venkatesh Mallikarjun1, 2, 3, Ellen Appleton1, 2, Maria Osipova1, 2, Hamish TJ Gilbert1, 2, Stephen M Richardson2, Simon J Hubbard4, 5 and Joe Swift1, 2, 5 (1) Wellcome Centre for Cell-Matrix Research, Oxford Road, Manchester, M13 9PT, UK. (2) Division of Cell Matrix Biology and Regenerative Medicine, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, M13 9PL, UK. (3) Current address: Department of Biomedical Engineering, University of Virginia, Box 800759, Health System, Charlottesville, VA, 22903, USA. (4) Division of Evolution and Genomic Sciences, School of Biological Sciences, Faculty of Biology, Medicine and Health, Manchester Academic Health Science Centre, University of Manchester, Manchester, M13 9PL, UK. (5) Correspondence to SJH ([email protected]) or JS ([email protected]). Page 1 of 11 Supplemental Information: Llewellyn et al. Chaperone stress response in senescence CONTENTS Supplemental figures S1 – S5 … … … … … … … … 3 Supplemental table S6 … … … … … … … … 10 Supplemental references … … … … … … … … 11 Page 2 of 11 Supplemental Information: Llewellyn et al. Chaperone stress response in senescence SUPPLEMENTAL FIGURES Figure S1. A EP (passage 3) LP (passage 16) 200 µm 200 µm 1.5 3 B Mass spectrometry proteomics (n = 4) C mRNA (n = 4) D 100k EP 1.0 2 p < 0.0001 p < 0.0001 LP p < 0.0001 p < 0.0001 ) 0.5 1 2 p < 0.0001 p < 0.0001 10k 0.0 0 -0.5 -1 Cell area (µm Cell area fold change vs. EP fold change vs.
    [Show full text]
  • Here in Liverpool, Both As a Physiologist and a Tourist
    Contents Welcome 2 Programme Tuesday, 17 December 4 Wednesday, 18 December 8 Poster Communications 11 General Information 35 Abstracts Symposia 38 Oral Communications 45 Poster Communications 70 Future Physiology 2019: Translating Cellular Mechanisms into Lifelong Health Strategies 17–18 December 2019 Liverpool John Moores University, UK Organised by: Katie Hesketh and Mark Viggars Liverpool John Moores University, UK Welcome As co-organisers of Future Physiology 2019 and on behalf of Liverpool John Moores University and The Physiological Society, we would like to warmly welcome you to Liverpool as guests to attend the second Future Physiology conference. A conference dedicated to the development of early career researchers, which has been organised by early career researchers. The two day meeting will take place at Liverpool John Moores University, on the edge of Liverpool city centre, known worldwide for its culture and heritage in music, sport and art. Across the two days, we are delighted to offer four diverse sessions, eight keynote talks, 20 selected oral presentations and over 90 posters showcasing international experts and current early career researchers supporting the conference’s theme of ‘Translating Cellular Mechanisms into Lifelong Health Strategies’. We hope this conference will inspire you to engage in research and will help you feel a part of a wider community of physiologists. We are also offering four professional development sessions aimed specifically at early career researchers, along with an exciting evening social programme with a Beatles theme at the Hard Days Night Hotel, just a stone’s throw away from the iconic Cavern Club which will provide plenty of chance to network and meet other like-minded physiologists.
    [Show full text]
  • Combinatorial Immune and Stress Response, Cytoskeleton and Signal
    Journal of Hazardous Materials 378 (2019) 120778 Contents lists available at ScienceDirect Journal of Hazardous Materials journal homepage: www.elsevier.com/locate/jhazmat Combinatorial immune and stress response, cytoskeleton and signal transduction effects of graphene and triphenyl phosphate (TPP) in mussel T Mytilus galloprovincialis ⁎ ⁎ Xiangjing Menga,c, Fei Lia, , Xiaoqing Wanga,c, Jialin Liua, Chenglong Jia,b, Huifeng Wua,b, a CAS Key Laboratory of Coastal Environmental Processes and Ecological Remediation, Yantai Institute of Coastal Zone Research (YIC), Chinese Academy of Sciences (CAS), Shandong Key Laboratory of Coastal Environmental Processes, YICCAS, Yantai 264003, PR China b Laboratory for Marine Fisheries Science and Food Production Processes, Qingdao National Laboratory for Marine Science and Technology, Qingdao 266237, PR China c University of Chinese Academy of Sciences, Beijing 100049, PR China GRAPHICAL ABSTRACT ARTICLE INFO ABSTRACT Keywords: Owing to its unique surface properties, graphene can absorb environmental pollutants, thereby affecting their Joint effects environmental behavior. Triphenyl phosphate (TPP) is a highly produced flame retardant. However, the toxi- Graphene cities of graphene and its combinations with contaminants remain largely unexplored. In this work, we in- Triphenyl phosphate (TPP) vestigated the toxicological effects of graphene and TPP to mussel Mytilus galloprovincialis. Results indicated that Toxicity graphene could damage the digestive gland tissues, but no significant changes were found in
    [Show full text]
  • FKBPL and FKBP8 Regulate DLK Degradation and Neuronal Responses to Axon Injury
    bioRxiv preprint doi: https://doi.org/10.1101/2021.08.20.457064; this version posted August 20, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 FKBPL and FKBP8 regulate DLK degradation and neuronal responses to axon injury 2 3 Bohm Lee1, Yeonsoo Oh1, Eunhye Cho1, Aaron DiAntonio2, Valeria Cavalli3, Jung Eun 4 Shin4,5 and Yongcheol Cho1* 5 6 1 Department of Life Sciences, Korea University, Seoul 02841, Republic of Korea. 7 2 Department of Developmental Biology, Washington University School of Medicine in Saint 8 Louis, St. Louis, MO, USA; Needleman Center for Neurometabolism and Axonal Therapeutics, 9 Washington University School of Medicine in Saint Louis, St. Louis, MO, USA. 10 3 Department of Neuroscience, Washington University School of Medicine, St. Louis, MO 63110, 11 USA; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, 12 MO 63110, USA; Hope Center for Neurological Disorders, Washington University School of 13 Medicine, St. Louis, MO 63110, USA 14 4 Department of Molecular Neuroscience, Dong-A University College of Medicine, Busan 49201, 15 Republic of Korea 16 5 Department of Translational Biomedical Sciences, Graduate School of Dong-A University, 17 Busan 49201, Republic of Korea 18 19 *Correspondence to Yongcheol Cho ([email protected]) 20 21 22 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.08.20.457064; this version posted August 20, 2021.
    [Show full text]
  • FKBPL and FKBP8 Regulate DLK Degradation and Neuronal Responses to Axon Injury
    bioRxiv preprint doi: https://doi.org/10.1101/2021.08.20.457064; this version posted August 20, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY-NC-ND 4.0 International license. 1 FKBPL and FKBP8 regulate DLK degradation and neuronal responses to axon injury 2 3 Bohm Lee1, Yeonsoo Oh1, Eunhye Cho1, Aaron DiAntonio2, Valeria Cavalli3, Jung Eun 4 Shin4,5 and Yongcheol Cho1* 5 6 1 Department of Life Sciences, Korea University, Seoul 02841, Republic of Korea. 7 2 Department of Developmental Biology, Washington University School of Medicine in Saint 8 Louis, St. Louis, MO, USA; Needleman Center for Neurometabolism and Axonal Therapeutics, 9 Washington University School of Medicine in Saint Louis, St. Louis, MO, USA. 10 3 Department of Neuroscience, Washington University School of Medicine, St. Louis, MO 63110, 11 USA; Center of Regenerative Medicine, Washington University School of Medicine, St. Louis, 12 MO 63110, USA; Hope Center for Neurological Disorders, Washington University School of 13 Medicine, St. Louis, MO 63110, USA 14 4 Department of Molecular Neuroscience, Dong-A University College of Medicine, Busan 49201, 15 Republic of Korea 16 5 Department of Translational Biomedical Sciences, Graduate School of Dong-A University, 17 Busan 49201, Republic of Korea 18 19 *Correspondence to Yongcheol Cho ([email protected]) 20 21 22 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.08.20.457064; this version posted August 20, 2021.
    [Show full text]
  • Supplementary Table S1 Shrna ID Accession Number Gene Symbol
    Supplementary Table S1 shRNAs that deplete in vivo and in vitro. shRNAs targeting annotated genes, predicted genes, and predicted proteins that deplete an average of four-fold in vivo and in vitro are listed. The average fold change of each shRNA in vitro and in vivo was normalized to the median fold change of all shRNAs in that setting. accession shRNA ID number gene symbol gene name V2MM_235925 NM_026914 1500032L24Rik hypothetical protein LOC69029 V2MM_68910 NM_029639 1600029D21Rik placenta expressed transcript 1 V2MM_105037 NM_029309 1700010A17Rik hypothetical protein LOC75495 V2MM_104257 NM_029336.1 1700022P22Rik RIKEN cDNA 1700022P22 gene V2MM_99656 NM_001163521.1 1700034F02Rik RIKEN cDNA 1700034F02 gene V2MM_75928 NM_029697 1700128F08Rik V2MM_34899 NM_024249 1810073N04Rik hypothetical protein LOC72055 V2MM_108828 NM_026961 2200002J24Rik hypothetical protein LOC69147 V2MM_38299 NM_172280 2210018M11Rik EMSY protein V2MM_204483 NM_027155.1 2310061N02Rik RIKEN cDNA 2310061N02 gene V2MM_206017 NM_029741 2410127E16Rik hypothetical protein LOC76787 V2MM_262492 NM_183119 2410141K09Rik hypothetical protein LOC76803 V2MM_162618 NM_029366.2 2810422J05Rik RIKEN cDNA 2810422J05 gene V2MM_78039 NM_026063 2900010M23Rik hypothetical protein LOC67267 V2MM_46523 NM_028455 3110043J09Rik Rho GTPase activating protein 8 V2MM_12203 NM_026486 4432405B04Rik tectonic 2 V2MM_73397 NM_030069 4432416J03Rik hypothetical protein LOC78252 phosphatidic acid phosphatase V2MM_106261 NM_029425 4833424O15Rik type 2d V2MM_77999 NM_025724 4921510H08Rik hypothetical protein
    [Show full text]
  • Autocrine IFN Signaling Inducing Profibrotic Fibroblast Responses By
    Downloaded from http://www.jimmunol.org/ by guest on September 23, 2021 Inducing is online at: average * The Journal of Immunology , 11 of which you can access for free at: 2013; 191:2956-2966; Prepublished online 16 from submission to initial decision 4 weeks from acceptance to publication August 2013; doi: 10.4049/jimmunol.1300376 http://www.jimmunol.org/content/191/6/2956 A Synthetic TLR3 Ligand Mitigates Profibrotic Fibroblast Responses by Autocrine IFN Signaling Feng Fang, Kohtaro Ooka, Xiaoyong Sun, Ruchi Shah, Swati Bhattacharyya, Jun Wei and John Varga J Immunol cites 49 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2013/08/20/jimmunol.130037 6.DC1 This article http://www.jimmunol.org/content/191/6/2956.full#ref-list-1 Information about subscribing to The JI No Triage! Fast Publication! Rapid Reviews! 30 days* Why • • • Material References Permissions Email Alerts Subscription Supplementary The Journal of Immunology The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2013 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. This information is current as of September 23, 2021. The Journal of Immunology A Synthetic TLR3 Ligand Mitigates Profibrotic Fibroblast Responses by Inducing Autocrine IFN Signaling Feng Fang,* Kohtaro Ooka,* Xiaoyong Sun,† Ruchi Shah,* Swati Bhattacharyya,* Jun Wei,* and John Varga* Activation of TLR3 by exogenous microbial ligands or endogenous injury-associated ligands leads to production of type I IFN.
    [Show full text]