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Supplementary Table 8. Cpcp PPI Network Details for Significantly Changed Proteins, As Identified in 3.2, Underlying Each of the Five Functional Domains

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Supplementary Table 8. cPCP 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 Park7 Rack1 differentiation Kcnma1 Atp6v1a Ywhae Ywhaz Pgls Hsd3b7 Development and Prdx6 Ncoa3 differentiation Pla2g4a Sufu Ncf2 Gstp1 Grin2b Ywhae Pgls Hsd3b7 Development and Atp1a2 Kcnma1 differentiation Vamp2 Development and Cntn1 Prnp differentiation Ywhaz Clstn1 Dlg4 App Ywhae Ywhab Development and Rac1 Pak1 differentiation Cdc42 Rhoa Dlg4 Ctnnb1 Mapk9 Mapk8 Pik3cb Sod1 Rrad Epb41l2 Nono Ltbp1 Evi5 Rbm39 Aplp2 Smurf2 Grin1 Grin2b Xiap Chn2 Cav1 Cybb Pgls Ywhae Development and Hbb-b1 Atp5b differentiation Hba Kcnma1 Got1 Aldoa Ywhaz Pgls Hsd3b4 Hsd3b7 Ywhae Development and Myh6 Mybpc3 differentiation Prkce Ywhae Development and Amph Capn2 differentiation Ap2a2 Dnm1 Dnm3 Dnm2 Atp6v1a Ywhab Development and Dnm3 Bin1 differentiation Amph Pacsin1 Grb2 Ywhae Bsn Development and Eef2 Ywhaz differentiation Rpgrip1l Atp6v1a Nphp1 Iqcb1 Ezh2 Ywhae Ywhab Pgls Hsd3b7 Hsd3b4 Development and Gnai1 Dlg4 differentiation Development and Gnao1 Dlg4 differentiation Vamp2 App Ywhae Ywhab Development and Psmd3 Rpgrip1l differentiation Psmd4 Hmga2 Development and Thy1 Syp differentiation Atp6v1a App Ywhae Ywhaz Ywhab Hsd3b7 Hsd3b4 Development and Tubb2a Ywhaz differentiation Nphp4 Dlg4 Snap25 Trpm7 Ywhae Development and Atp1a3 Kcnma1 differentiation Grin1 Grin2b Clstn1 Vamp2 Ywhab Development and Atp5b Ppif differentiation Prdx2 Prdx1 Alad Naca Arhgdia Ftl1 Pdpk1 P4hb Hspa4 Prdx4 Hbb-b1 Hspa2 Stip1 Hist1h3b H3f3a Hist1h3a Ywhaz Kcnma1 Dlg4 Invs Prkce Rab31 Ywhah Fbp1 Ezh2 Ywhab Hsd3b4 Hsd3b7 Ywhae Development and Canx Sgip1 differentiation Mcl1 Rpn2 Hmox1 Ywhaz App Ezh2 Ywhae Ywhab Pgls Bax Tnfrsf1a Hsd3b7 Hsd3b4 Development and Dpysl2 Kcnma1 differentiation Grin2b Rpgrip1l Ywhah Ywhae Ywhab Development and Pacsin1 Mapt differentiation Dnm2 Dnm1 Dnm3 Ywhaz Dlg4 Ywhae Development and Syp Thy1 differentiation Gnat2 Actg1 Snap25 Calm1 Vamp2 Tubb4b Slc1a2 Syt1 Tuba1c Atp6v0a1 Fbxl20 Ap1g1 Clstn1 Dlg4 Ywhae Ywhab Development and Cnp Ywhaz differentiation Dlg4 Cask Gria2 Grid2 Ywhae Ywhab Ybx3 Development and Mapt Pacsin1 differentiation Ppp1ca Bin1 Ywhae Ywhab Vac14 Development and Uchl1 Ncam1 differentiation Kcnma1 Rpgrip1l Ywhae Development and Hsp90aa1 Akt1 differentiation Ahr Sim1 Cdk9 Eed Ago2 Ywhaz Rpgrip1l Nphp4 Nphp1 Ahi1 Iqcb1 Gdi1 Stra8 Ezh2 Ilk Chordc1 Slc34a1 Map3k7 Itgb1bp2 Pgls Hsd3b4 Hsd3b7 Ywhae Development and Actc1 Pdpk1 differentiation Btk Mybpc3 Development and Hspd1 Hsp90b1 differentiation Sirt5 Uox Kcnma1 Nphp4 Dlg4 Nphp1 Prkce Crkl Nphp1 Ilk Ywhaz Ywhab Pgls Hsd3b4 Mcl1 Hsd3b7 Ywhae Development and Clta Ywhab differentiation Development and Napb Clstn1 differentiation Dlg4 Nphp4 Vamp2 Ywhae Ywhab Development and Ncam1 Fgfr2 differentiation Prnp Ywhaz App Ywhae Uchl1 Ywhab Development and Rab6b Irs1 differentiation Ywhae Ccdc64 Apba1 Development and Stx1b Dlg4 differentiation Vamp2 Ywhae Cltc Development and Ywhaz Vdac2 differentiation Pacsin1 Atp5h Cnp Tubb2a Cntn1 Ncam1 Eno2 Ppp2r1a Lrrk2 Hsp90aa1 Hspa8 Canx Atp5b Eef2 Hspa5 Aldoa Amhr2 Actn2 Aldh1l1 Actg1 Actn1 Aco2 Blnk Wwp1 Tubb4a Vcp Tkt Tln2 Atp6v1b2 Atp6v1c1 Atp6v1e1 Vps35 Sphk2 Sptan1 Sertad4 Stxbp1 Synj1 Syt1 Tuba1a Tubb3 Uqcrc2 Plcb1 Mok Adam22 Sh3gl2 Sept7 Rtn1 Hormad1 Lcat Wnt10a Actg1 Actr3 Idh3a Tnr Ywhae Hba-a1 Atp6v0d1 Atp1a3 Sfxn3 Sptbn2 Ap2a2 Syn2 Dnajc6 Dync1h1 Clta Nr1h5 Aak1 Papln Vdac1 Syce1l Phb Pfkm Ppia Pink1 Snap25 Pfkl Ppp3ca Gdf7 Gnao1 Pdhb Mbp Ap2a1 Hk1 Syn1 Dlat Pdha1 Ndufb4 Ndufs3 Nfasc Nsf Lrrc47 Mdh2 Ndufa2 Ndufa10 L1cam Prkcg Ckmt1 Ckb Kcnab2 Mapk8ip3 Eif5a Hsp90ab1 Golph3 Gnai2 Gna13 Glul Gphn Fh Fam208b Fam189b Hadhb Exoc4 Dlg3 Dnm1 Dctn2 Glud1 Slc25a12 Csrp1 Cs Cltc Atp5a1 Cdh2 Ap1b1 Arpc2 Ank2 Anxa6 Mlf1 Rrad Hist1h3a Lrpap1 Aldh3a2 Aldh8a1 Aldob Akr1b1 Amacr Amn Anpep Acy1 Acy3 Adh1 Slc25a5 Aifm1 Akr1a1 Akr1c18 Rps7 Rpsa Rtcb Slc12a1 Slc12a3 Slc22a12 Slc27a2 Slc4a4 Ahcy Psap Selenbp2 Sec23a Scfd1 Oxct1 Scarb2 Sdf2l1 Rpn2 Rplp2 Rps12 Rrbp1 Rps15 Rps14 Rps19 Rps15a Rps23 Rps20 Rps2 Rps28 Rps3 Fau Rps6 Rps4x Sult1d1 Stt3b Sorbs2 Cttn Farsa Rars Stx16 Susd2 Tubb4b Cct5 Tagln2 Tuba4a Tgm1 Acaa1a Cct6a Sh3bgrl3 Sf1 Eefsec Sdha Napa Snrpd1 Slc3a1 Sigirr Pipox Sod1 Snx4 Snd1 Sptbn1 Sptb Usp10 Ugt1a1 Ugdh Ugp2 Txndc12 Txndc5 Ube2l3 Ubc Rps27a Uba52 Ubb Atp6v1d Atp6v1e2 Hrsp12 Plau Ush1c Atp6v1a Tkfc Tm9sf3 Tln1 Acat1 Acaa1b Mpst Acaa2 Tpp1 Tpi1 Ttc39c Tf Tmed10 Tmed4 Tor1aip2 Tmem27 Acads Ace2 Abhd14b Abi1 Got1 Abcg2 Serpina1a App Actn4 Acta2 Actb Acly Acsl1 Ace Atp6v0a4 Vim Vil1 Hdlbp Atp6v1h Atp6v1g1 Atp6v1f Nt5e Slc3a2 Epb41 Znfx1 Ybx1 Xpnpep1 Wdr61 Vps45 Uggt1 Ppp2r1a Lpl Cat Dnajc13 Rps17 Ddx5 Serpinh1 Ket90 Myh10 Ndufa12 Rpn1 Adsl Pc Nnt Vapb Gna11 Ces1f Atp6v1b1 Slc22a19 Abcd3 Rps5 Cltc Alpl Pls1 Csad NA Tm9sf2 Calb1 Tln2 Pon2 Naprt Podxl Pcbd1 Plvap Pah Ptgs1 Pgk1 Pdia4 Pdzd9 P4hb Pdia3 Pcm1 Pcyox1 Ptrh2 Pter Ptbp1 Psmd7 Psmc5 Prpf4b Prosc Prodh Prkra Prdx5 Prdx4 Prdx2 Prdx1 Ppm1h Ppic Ppib Rpl15 Rpl17 Rpl18a Rpl19 Rpl22 Rpl23 Rpl23a Rpl24 Rhoa Rpl10 Rpl10a Rpl11 Rpl12 Rpl13 Rpl13a Rpl5 Rpl4 Rpl7 Rpl6 Rpl8 Rpl7a Rplp1 Rpl9 Rpl27a Rpl26 Rpl31 Rpl29 Rpl37a Rpl36 Rpl3 Rpl38 Mccc2 Hao2 Anxa2 Rps3 Stau1 Wdr1 Atp5c1 Pdia6 Stxbp2 Enpp3 Rps13 Ddx1 Pabpc4 NA Bcam Plxnb2 Rdx Rab35 Rab1A Rab14 Rab11fip5 Reps1 Rbm47 Rbbp9 Slc15a2 NA Cox6a1 Hspa5 Cryz Uqcrc1 Eif6 Kcnn3 Pklr Khk Itpa Itih4 Ivd Itpr1 Lman1 Lin7b Lpp Lman2 Ssb Llgl2 Glo1 Lactb2 Lamtor5 Luzp2 Mtdh Gstz1 Lrrc59 Lrp1 Lrp2 Lamtor3 Mccc1 Abcb1a Abcb1b Mep1a Manf Me1 Metap1 Marc2 Gstp2 Gstm1 Gsta2 Glg1 Grk5 Grhpr Gpx3 Gpx1 Syncrip Hnrnpk Hgd Alad Hadh Hbb-b2 H3f3a Hist1h2ab; Idh1 Idi1 Hyi Hyou1 Ephx2 Hook3 Hspa1b Isg15 Itgb1 Inadl Iqgap1 Ifitm3 Ilvbl Ifi203 Ndufa5 Ndufa8 Ndufs1 Ndufc2 Ndufs2 Mme Ndufv1 Pdzk1 Slc9a3r1 Nomo1 Carkd Nsdhl Nptn Nucb1 Ncl Nudt19 Crot Ogdh Opa1 Ddost Pm20d1 P4ha1 Pycrl Pa2g4 Pabpc1 Serbp1 Papss2 Mif Immt Mettl7b Mep1b Msn Aldh6a1 Mmel1 Mlec Msra Msi2 Mpp6 Mpp5 Myh11 Myo18a Mvp Mup1 Myl9 Myo1c Myh9 Myl6 Qprt Amdhd2 Myo6 Myo7b Ncald Nceh1 Nampt Napsa Nme2 Ndrg1 Ncln Por Dld Sord Qdpr Hsd11b2 Hsd17b4 Hsd17b12 Hsd17b11 Ddx6 Ddx3x Dctn1 Dync1i2 Cycs Cacybp Cyb5b Cyb5a Cyc1 Ctnna1 Ctnnd1 Cask Ctage5 Crip2 Csnk2a1 Cyp4a14 Cyp4b1 Cyp2d26 Cyp2j5 Mtco2 Cox8a Copb1 Coro1c Cobll1 Cfl1 Cnpy2 NA C3 Cnpy3 Clic1 Clic5 Clic4 Cp Cdc42 Clcn5 Ces1d Ccdc22 Cbr1 Cd81 Cd36 Calm1 Calr Caprin1 Capzb Mthfd1 Cdh16 Ca12 Ca2 Blvra Bloc1s6 Bphl Btf3l4 Atp5o Slc4a1 Bsg Baiap2l1 Galnt11 Gk Hagh Gpm6a Gpd1 Gnas Prkcsh Ganab Gapdh G3bp1 Fxr1 Ggt1 Rack1 Gng5 Gnb1 Fkbp2 Fkbp3 Fcgrt Ahsg Fmo1 Flii Flna Fbp1 Fam46b FAM120A Fam151a Fahd1 Fasn Fah Zmpste24 Clint1 Hsp90b1 Erlin2 Eps8 Ces2c Erp44 St13 Ezr Eif3e Eif3b Eif3h Eif3f Emc1 Mpp1 Eno1 Emc9 Echdc2 Ehhadh Eef1a1 Eef1a2 Tufm Ehd1 Ehd3 Eif3a Dnaja1 Dnm1l Dpep1 Dpp4 Dync1h1 Dysf Epb41l1 Hadha Actr2 Actr3 Aqp4 Arl8a Asph Ass1 Asah2 Aspdh Atp1a4 Atp1b1 Atp11a Atp1a1 Atp5d Atp2a2 Atad1 Ank1 Hap1 Anxa3 Anxa1 Kap Ano6 Ap1m1 Aoc3 Anxa4 Apoa2 Apmap Ap2b1 Ap2a2 Park7 Pgam1 Gpi Alb Hspd1 Hbb-b1 Pkm Thy1 Crk Gab2 Kcnma1 Grin2b Rpgrip1l Invs Snn Gfap Gem Krt18 Ksr1 Ndel1 Rem2 Arhgef28 Rem1 Ywhab Ywhae Development and Atp6v1g2 Atp6v1a differentiation Ywhae Development and Hspa8 Klc1 differentiation Ckb Rnf2 Nphp3 Hist1h3b H3f3a Hist1h3a Bag5 Ywhaz Kcnma1 Irs1 Rpgrip1l Nphp4 Dlg4 Nphp1 Invs Cep290 Ahi1 Mks1 Iqcb1 Ezh2 Ilk Ftl1 Sult2b1 Ywhab Pgls Hsd3b4 Hsd3b7 Ywhae Development and Ak1 Kcnma1 differentiation Csf1 Ywhae Development and Atp5h Ywhaz differentiation Ywhae Hsd3b7 Hsd3b4 Development and Ldhb Kcnma1 differentiation Grin2b Dlg4 Atp6v1a Cep290 Ywhae Development and Pgam1 Kcnma1 differentiation Rpgrip1l Ywhae Ywhaz Pgls Hsd3b7 Hsd3b4 Development and Pkm Pou5f1 differentiation Casp3 Dlg4 Nphp1 Invs Htt Ywhaz Pgls Hsd3b4 Hsd3b7 Ywhae Casp7 Development and Umps Hmga2 differentiation Ywhae Pgls Development and Ppp3ca Grin1 differentiation Grin2b Dlg4 Neurl1 Ywhae Ywhab Development and Hspa5 Ywhaz differentiation Kcnma1 Rpgrip1l Nphp4 Nphp1 App Invs Ahi1 Mks1 Iqcb1 Prnp Ezh2 Ywhae Ywhab Papolb Gsg1 Hsd3b7 Development and Rab12 Ccdc64 differentiation Ccdc64b Ywhab Slc36a4 Development and Kctd10 Hmga2 differentiation Ywhah B9d1 Development and Vdac2 Bak1 differentiation Grin2b Ywhaz Dlg4 Invs Ywhah Fbp1 Ywhae Ywhab Hsd3b4 Intracellular signalling Myh6 Mybpc3 and regulation Prkce Ywhae Intracellular signalling Atp1a2 Kcnma1 and regulation Vamp2 Intracellular signalling Atp1a3 Kcnma1 and regulation Grin1 Grin2b Clstn1 Vamp2 Ywhab Intracellular signalling Mapt Pacsin1 and regulation Ppp1ca Bin1 Ywhae Ywhab Vac14 Intracellular signalling Park7 Rack1 and regulation Kcnma1 Atp6v1a Ywhae Ywhaz Pgls Hsd3b7 Intracellular signalling Prdx6 Ncoa3 and regulation Pla2g4a Sufu Ncf2 Gstp1 Grin2b Ywhae Pgls Hsd3b7 Intracellular signalling Cnp Ywhaz and regulation Dlg4 Cask Gria2 Grid2 Ywhae Ywhab Ybx3 Intracellular signalling Hsp90aa1 Akt1 and regulation Ahr Sim1 Cdk9 Eed Ago2 Ywhaz Rpgrip1l Nphp4 Nphp1 Ahi1 Iqcb1 Gdi1 Stra8 Ezh2 Ilk Chordc1 Slc34a1 Map3k7 Itgb1bp2 Pgls Hsd3b4 Hsd3b7 Ywhae Intracellular signalling Amph Capn2 and regulation Ap2a2 Dnm1 Dnm3 Dnm2 Atp6v1a Ywhab Intracellular signalling Canx Sgip1 and regulation Mcl1 Rpn2 Hmox1 Ywhaz App Ezh2 Ywhae Ywhab Pgls Bax Tnfrsf1a Hsd3b7 Hsd3b4 Intracellular signalling Dpysl2 Kcnma1 and regulation Grin2b Rpgrip1l Ywhah Ywhae Ywhab Intracellular signalling
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    International Journal of Molecular Sciences Article Neural Stem Cell-Derived Exosomes Revert HFD-Dependent Memory Impairment via CREB-BDNF Signalling Matteo Spinelli 1, Francesca Natale 1,2, Marco Rinaudo 1, Lucia Leone 1,2, Daniele Mezzogori 1, Salvatore Fusco 1,2,* and Claudio Grassi 1,2 1 Department of Neuroscience, Università Cattolica del Sacro Cuore, 00168 Rome, Italy; [email protected] (M.S.); [email protected] (F.N.); [email protected] (M.R.); [email protected] (L.L.); [email protected] (D.M.); [email protected] (C.G.) 2 Fondazione Policlinico Universitario Agostino Gemelli IRCCS, 00168 Rome, Italy * Correspondence: [email protected] Received: 6 October 2020; Accepted: 25 November 2020; Published: 26 November 2020 Abstract: Overnutrition and metabolic disorders impair cognitive functions through molecular mechanisms still poorly understood. In mice fed with a high fat diet (HFD) we analysed the expression of synaptic plasticity-related genes and the activation of cAMP response element-binding protein (CREB)-brain-derived neurotrophic factor (BDNF)-tropomyosin receptor kinase B (TrkB) signalling. We found that a HFD inhibited both CREB phosphorylation and the expression of a set of CREB target genes in the hippocampus. The intranasal administration of neural stem cell (NSC)-derived exosomes (exo-NSC) epigenetically restored the transcription of Bdnf, nNOS, Sirt1, Egr3, and RelA genes by inducing the recruitment of CREB on their regulatory sequences. Finally, exo-NSC administration rescued both BDNF signalling and memory in HFD mice. Collectively, our findings highlight novel mechanisms underlying HFD-related memory impairment and provide evidence of the potential therapeutic effect of exo-NSC against metabolic disease-related cognitive decline.
  • Merlin Is a Potent Inhibitor of Glioma Growth

    Merlin Is a Potent Inhibitor of Glioma Growth

    Research Article Merlin Is a Potent Inhibitor of Glioma Growth Ying-Ka Ingar Lau,1 Lucas B. Murray,1 Sean S. Houshmandi,2 Yin Xu,1 David H. Gutmann,2 and Qin Yu1 1Department of Oncological Sciences, Mount Sinai School of Medicine, New York, New York and 2Department of Neurology, Washington University School of Medicine, St. Louis, Missouri Abstract The NF2 gene shares sequence similarity with the members of Neurofibromatosis 2 (NF2) is an inherited cancer syndrome in Band 4.1 superfamily (4, 5). In particular, the NF2 protein, merlin (or schwannomin), most closely resembles proteins of the ezrin- which affected individuals develop nervous system tumors, including schwannomas, meningiomas, and ependymomas. radixin-moesin (ERM) subfamily. Similar to the ERM proteins, The NF2 protein merlin (or schwannomin) is a member of the merlin serves as a linker between transmembrane proteins and the Band 4.1superfamily of proteins, which serve as linkers actin cytoskeleton and regulates cytoskeleton remodeling and cell between transmembrane proteins and the actin cytoskeleton. motility (6–8). Unlike ERM proteins, merlin functions as a negative In addition to mutational inactivation of the NF2 gene in NF2- growth regulator or tumor suppressor. In this regard, mutational associated tumors, mutations and loss of merlin expression inactivation of the NF2 gene is sufficient to result in the have also been reported in other types of cancers. In the development of NF2-associated nervous system tumors. Moreover, present study, we show that merlin expression is dramatically NF2 mutations have also been reported in other tumor types, reduced in human malignant gliomas and that reexpression of including melanoma and mesothelioma (9), suggesting that merlin plays an important role, not only in NF2-associated tumors but also functional merlin dramatically inhibits both subcutaneous and intracranial growth of human glioma cells in mice.
  • Simultaneously Inhibiting BCL2 and MCL1 Is a Therapeutic Option for Patients with Advanced Melanoma

    Simultaneously Inhibiting BCL2 and MCL1 Is a Therapeutic Option for Patients with Advanced Melanoma

    cancers Article Simultaneously Inhibiting BCL2 and MCL1 Is a Therapeutic Option for Patients with Advanced Melanoma Nabanita Mukherjee 1, Carol M. Amato 2 , Jenette Skees 1, Kaleb J. Todd 1, Karoline A. Lambert 1, William A. Robinson 2, Robert Van Gulick 2, Ryan M. Weight 2, Chiara R. Dart 2, Richard P. Tobin 3, Martin D. McCarter 3, Mayumi Fujita 1,4,5 , David A. Norris 1,4 and Yiqun G. Shellman 1,5,* 1 Department of Dermatology, School of Medicine, University of Colorado Anschutz Medical Campus, Mail Stop 8127, Aurora, CO 80045, USA; [email protected] (N.M.); [email protected] (J.S.); [email protected] (K.J.T.); [email protected] (K.A.L.); [email protected] (M.F.); [email protected] (D.A.N.) 2 Division of Medical Oncology, School of Medicine, University of Colorado Anschutz Medical Campus, Mail Stop 8117, Aurora, CO 80045, USA; [email protected] (C.M.A.); [email protected] (W.A.R.); [email protected] (R.V.G.); [email protected] (R.M.W.); [email protected] (C.R.D.) 3 Division of Surgical Oncology, Department of Surgery, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA; [email protected] (R.P.T.); [email protected] (M.D.M.) 4 Dermatology Section, Department of Veterans Affairs Medical Center, Denver, CO 80220, USA 5 Gates Center for Regenerative Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA * Correspondence: [email protected]; Tel.: +1-303-724-4034; Fax: +1-303-724-4048 Received: 30 June 2020; Accepted: 31 July 2020; Published: 5 August 2020 Abstract: There is an urgent need to develop treatments for patients with melanoma who are refractory to or ineligible for immune checkpoint blockade, including patients who lack BRAF-V600E/K mutations.
  • A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus

    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.
  • A Multistep Bioinformatic Approach Detects Putative Regulatory

    A Multistep Bioinformatic Approach Detects Putative Regulatory

    BMC Bioinformatics BioMed Central Research article Open Access A multistep bioinformatic approach detects putative regulatory elements in gene promoters Stefania Bortoluzzi1, Alessandro Coppe1, Andrea Bisognin1, Cinzia Pizzi2 and Gian Antonio Danieli*1 Address: 1Department of Biology, University of Padova – Via Bassi 58/B, 35131, Padova, Italy and 2Department of Information Engineering, University of Padova – Via Gradenigo 6/B, 35131, Padova, Italy Email: Stefania Bortoluzzi - [email protected]; Alessandro Coppe - [email protected]; Andrea Bisognin - [email protected]; Cinzia Pizzi - [email protected]; Gian Antonio Danieli* - [email protected] * Corresponding author Published: 18 May 2005 Received: 12 November 2004 Accepted: 18 May 2005 BMC Bioinformatics 2005, 6:121 doi:10.1186/1471-2105-6-121 This article is available from: http://www.biomedcentral.com/1471-2105/6/121 © 2005 Bortoluzzi et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: Searching for approximate patterns in large promoter sequences frequently produces an exceedingly high numbers of results. Our aim was to exploit biological knowledge for definition of a sheltered search space and of appropriate search parameters, in order to develop a method for identification of a tractable number of sequence motifs. Results: Novel software (COOP) was developed for extraction of sequence motifs, based on clustering of exact or approximate patterns according to the frequency of their overlapping occurrences.