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Supplementary Table 1: Differentially expressed genes in L group versus vehicle-treated group (1004 genes) Upregulated genes Downregulated genes Il33 4930438A08Rik Etv4 Mcoln2 Gpr18 Cyth3 Mad2l1 Ttc38 Rab19 Gpd1 Klhl6 Ccl5 Nlrp3 Clec4e Ddx58 Bcl2a1d Sh3pxd2b Map3k6 Rab39 Calr3 Ptger4 Fndc10 Serpinb2 Pfkfb3 Dgkh Spata13 Ptger2 Itgav Ckb Hist1h1c Gm12522 Susd3 Pard6g Lif Ccl2 Dusp1 Vgf Gm14286 Spred1 Brca2 Ncapd2 Tle2 Sorbs1 4933431G14Rik Il6 Oasl2 Smim3 Gm12059 Rnf186 Maml2 Gm16576 Brip1 Lfng Smc1b Morn5 Akap12 Gdnf Furin Vegfa Fgr Samsn1 Bag2 Mtfp1 Aurkb Sorbs3 Fam13c Edn1 Styk1 Csrnp1 6030443J06Rik Samd9l Nod2 Tmem218 Plk1 Neurl1b Tmem79 Sarm1 U90926 Gm26675 Sema3e Ifi202b Il10ra Clic4 Tsc22d3 Ttc28 Oip5 Dixdc1 Rarb Il1b Gbp2 Dtx2 Gm7609 Trim25 Gm17275 Fut10 Bmf Knstrn Zfp108 Gm13710 Tpbg Peli1 Gm11496 Adamts7 Slfn4 Ksr1 Zfp760 H2-T10 6430548M08Rik Olfml2b AC159314.1 Cxcl10 Zfp36 Nfkbie Gm9774 Irf9 Gstt1 Kcnn1 Rnasel Pax6 Tbc1d8 9930111J21Rik2 Csf2 Trim30b Tmem171 Lta Ccr1 Hck Chst12 Nfia Cerkl Kcnab3 Fam171a2 Sox30 Lix1 Gm20219 Gja1 Pmp22 Tnfsf13b Tmem43 Casp3 Lrrc56 Coq8a Mtl5 Sprr2d Hmx3 Klk9 Ptch1 Zc3h12a Pdlim7 Gm16675 Foxm1 Cdon Myo7b Gdf9 Rsad2 Cxcl11 Kdm6b Junb Procr Hcls1 Pdcd4 Agmo Catsperg1 Fbxo5 Speer9-ps1 Rtp4 Col5a3 Sema4c Eid3 Micall2 6230400D17Rik Ak1 Col4a6 4930558J18Rik Daglb BC037032 Ttc39c Fam46c Oaf Tnip1 Fam214b Tgfb1 Il6ra Rab3d Nav2 Rnf144b Mkln1os Ifit1 Fam110c Glrx Sod2 Pilra Dusp10 Hist2h2be Lpar5 Arrb1 Fam46b AC153365.1 Isg15 Hist2h2aa2 Dusp2 Arhgef3 Itga5 Casp6 Brca1 Racgap1 Depdc1b Ppp1r1a Snhg7os Oasl1 Kctd12 Rab20 Gm4961 Plcxd1 Mir22hg D3Ertd751e Fbxo48 Gpr155 Mgst1 Rflnb Gbp5 Ahr Slc15a3 Cd274 Asb6 Gch1 Tert Kif20a Prnp Adgre5 Gm17383 Rgs16 Met Adam33 Rtn2 Gm14275 Smarcd3 Napepld Gm21982 E130317F20Rik Eya4 Gm4804 Ifit1bl2 Slc7a2 A530032D15Rik Myadm Slc7a11 Gm28048 Zfp41 Pald1 Igfbp4 Kank3 Angptl4 Gm43079 Tnf Tnfrsf8 Osgin2 4933430I17Rik Gm45837 Gamt Knl1 Cela1 Mblac2 Socs2 Il10 Xcr1 Src Gm26902 Slc25a37 A530040E14Rik Cdkn2c Clec4n Itga4 Gpr183 Scd4 Dpep3 Zbp1 Cd83 Spred3 Rps6ka2 Cdk18 2310015A10Rik Pbk Pcyox1 Shpk H2-DMb2 Il1f6 Fas Stx11 Lrrc25 Stat3 Hip1r Gemin4 Cdca2 9230114K14Rik Kbtbd11 Gm15482 Gbp2b Gm9260 Gm9887 Agpat4 Jak2 Clic1 Fam105a Sgol2a Birc5 Mastl Ranbp3l Csf3 Hrc Gm12840 Birc3 Gm16861 Ptpn23 Slc25a45 E2f7 Noxo1 Bcas1 Gm996 Ccl22 Mxd1 Dusp16 Hmga2 Bcl2a1a Plekhh1 Gm14327 Hexim2 Ndc80 Gm27029 Angpt2 Sprr2e Socs3 Gm19026 Best1 Adgrl2 Zfhx2 Fut11 Shtn1 Pth1r C130050O18Rik Gm45736 Sprr2g 2310034G01Rik Rgcc Rhbdf2 Egr1 Fam129b Pidd1 Spc25 Dnajc28 Gm45808 Icos Tnn Pde4b Ankrd33b Bcl6 Ptafr Gm14005 Acss2 Tmtc4 Adrb2 Aqp11 Fbxo32 Mmp3 Fabp4 Sh2d2a Slc28a2 Adamts1 Lasp1 Paqr4 Rasgrp3 Gpr19 Cldn11 Nacad Marcks Gm17017 Plagl2 Dhrs3 Cav1 Gbp7 Cenpi Cdca3 Aph1c Ccdc18 3110067C02Rik Gm18445 Dusp8 Serpine1 Ddit4 Wnt6 Galnt3 Rab3a Fam198b Zfp862-ps Tnfrsf14 Abcd2 Il1a Gadd45b Hbegf Gm21986 Bcl2a1b Rhebl1 Nsl1 Tns4 Lrguk Prss42 Hdc Mmp13 Gm29284 Arg2 B630019K06Rik Kifc3 Zrsr1 Hcn2 Tgfbi Wasf1 Thbs1 Fbxo15 Itpkb Prrt1 Hivep3 Psd3 Ckap2l Cpt1a Fam26f C8g Il11 Ntng2 Jdp2 Rab11fip1 Iffo2 Slc25a42 Kif2c 2010110K18Rik Nrm Pcdhb20 Phlda1 Tmc3 Gm15491 Cd40 Xylt2 Bub1 Cenpf Ndrg2 Slc13a3 Mapkapk3 Ifih1 Gdf15 Gm26819 Gm28913 Anxa7 Fzd7 Trp53cor1 Traf3ip3 Tlr4 A730071L15Rik Tm4sf1 Saa3 Nfkbia Cfb Creb5 L3hypdh Lrr1 Dlx1 Tk1 9930111J21Rik1 Tnc Gipr Tbc1d9 Nfkbib Nnat Endod1 Ska1 1190005I06Rik Gm14308 Klhl33 Ptgs2 Pdpn Plpp3 Olr1 Plpp1 Rmi2 Msh2 Kif11 Gm11131 Gm9949 Pdgfb Ccbe1 Cdk5r1 4930486L24Rik Acvr1b Cenpn Kif14 Rin2 D030055H07Rik Syt12 Dusp5 Gm20517 Gm26586 Perm1 Mt1 Hspb6 Sgol1 Trim7 Myh11 Gm16181 Scimp Myo10 Gk Sbno2 D330050G23Rik Osbpl3 Dscc1 Map1a E230029C05Rik Fry Urah Bcar3 Srcin1 Dcbld2 Tnfrsf9 Mr1 Deptor Dbp Zfp985 Xkr5 Adora2a Trem1 Nfkb2 March11 Id2 Trim65 Melk Rad54l Oit3 Bpifb9b Acod1 Tnfsf9 Mt2 Ltb Fzd5 Hpdl Gmnn Tfdp2 Esco2 Aox1 Thbd Tcp10b Capns2 Irak2 Gpr84 Dnajc9 Idh1 Steap3 Sash3 Gm7889 Ccl4 Cyp27b1 Dusp14 Sik3 Gm15753 Rwdd2a Psmb9 Gm4117 Cysltr1 Hist1h3g Tnfrsf1b Nfkbiz Oas2 Pim1 Fpr1 Rbl2 Cenpp Sesn1 Zfp493 B430212C06Rik Gm13822 Arrdc4 Nfkb1 Ell2 Ets2 Eno4 Prc1 Bmyc Tspan10 Gm28845 Sema6d Mir155hg Atf3 Nr1d1 Stap1 Rad51 Tcf19 Slc7a4 Neil3 CT030159.2 Flrt3 St3gal1 Pim2 Slfn5 Il7r Crot Zfp324 Gm16537 Peg12 Tdo2 Fst Rbfox1 Mndal Plek Cd44 Ttk Cenph Ptpro Prrt2 Scel Gfpt2 Clcf1 BC049352 C5ar1 Rhoc Mgst2 Kifc5b Pcyox1l Abcc3 Gcom1 Il27 Hilpda Lilr4b Ifi211 Zbtb32 Gm10658 Mki67 Itgb5 Ankle1 Tppp Ccrl2 Shroom4 Sema3c P3h2 Gramd1a Frmd4b Cep128 Pdk2 Fam64a Hist2h3b Il1rn Calcrl Cd300lf Cpd Dtwd1 Zfp362 Kifc1 Ttc39aos1 Myh7b Gm45729 Adamts4 Notch1 Ptprj Isg20 Tgif1 E2f8 Mettl7a1 Angptl2 Ssbp2 Hist1h2ag 9130230L23Rik Maff Cdc42ep2 Lcn2 Noct 9930012K11Rik Nemp2 Kif15 2310001K24Rik 2700016F22Rik Ccl7 Rsbn1 Ikbke Ptpre Adora2b Tbc1d32 Rubcnl Fancd2 Gm26634 Gm26690 Cxcl3 Odc1 Steap1 Rabgef1 Myo1e Kank2 Gbp8 Tlr8 Sema3f A930018M24Rik Bcl6b Prokr1 Gm29094 Ccl9 Daam1 Zwilch Rogdi Tnfsf13 Gm6225 Gm43738 Il13ra2 Cd93 Cebpd Lilrb4a_1 Znrf1 Vmac Syt11 Bdh2 Gm10269 Gm20186 Gm15512 Ier3 Gpat3 Gm16028 Ppm1k Gtse1 Ccna2 Slc37a2 B230208H11Rik Ccl3 Gm6377 Gm16026 Tgm2 Hlx Kdelc2 Tmem220 Fanci Gm12205 Acpp Stfa3 Gm14636 Ehd1 Ptges Cd72 Bach2os A630052C17Rik Rgs12 Ddx60 Rnd1 Parp14 Actg1 Rnf149 Kif20b Abcd1 Ttc7 Gm10069 Slpi Ifit3 Ppfia3 Rnf19b Pla2g5 Cx3cr1 Nudt13 Tmem25 Cyp2u1 Usp18 Ercc1 Sh2d3c Fosl1 Slc4a8 Cbx8 Cenpk Chek2 Fer1l5 Cxcl2 Plaur Metrnl Spp1 Mfap3l Nusap1 Lpin1 2210408F21Rik Kmo Gm5416 Gm26841 Mreg Mmp9 Slc2a1 Spag5 Efna1 Eml6 Pbx1 Il1f9 Osm Slamf7 Malt1 Sash1 Traip Slc25a10 Sec16b Zfpm2 Csf1 Gadd45a Gm45713 Gm20559 Cers4 Sapcd2 Cenpu 1700025G04Rik Fam186b Krt23 Gm6264 Vegfc Trim13 Srgn Tmem8b Pif1 Odf3l1 Fstl1 Upp1 Gm12184 Bcl3 Psd Hvcn1 Gm10143 Zbtb8a Cnr2 Matn3 Traf1 Hcar2 Fosl2 Gm26674 Lims2 Slc22a18 Abcg1 Rgs18 Fgd2 Gm5483 E230013L22Rik Slc39a14 Cd14 Mtmr10 Asap2 Cep72 AC112265.1 Ptgs1 Cmpk2 Tmem2 Nos2 Carmil1 Snx18 Trp53inp1 Shcbp1 Tmem119 AA465934 Timp1 Gm10634 Spryd7 Ugcg Slc4a7 Zdhhc14 Tbc1d4 Txnip Opcml S100a8 Ppbp Gm20548 Rpl37rt Mybpc3 Anln Aspm Zfand4 Pdzd9 Efnb3 Slc5a1 Kcng3 Cebpb Txlnb Gm20507 Spata33 Gm2260 Ttc39a Foxp3 Irf7 Gm35339 Dhrs9 Lancl3 Apitd1 Zfp873 Cdca5 Abhd15 Mtmr7 6530402F18Rik Sp110 Jarid2 Mmp2 Rad51ap1 Rasa3 Mns1 CT030159.3 Gm26809 Stk40 C130026I21Rik Ccl12 Rmdn2 Kif4 Kbtbd3 Dact3 Asb13 Marcksl1 Sptbn2 Lcp2 Gsap Slc6a4 Ccnf 2900052L18Rik Cxcr3 Nanp Gbp3 Ralgds Ifi204 Rdh11 Notch2 Rin1 Arhgef39 4930524J08Rik Strip2 Gm26778 Sdc4 Fam71f2 P2ry2 Optn Rad54b Chst1 Them6 Nlrp10 AC117226.2 Fosb Nabp1 Gm14085 Ppard Dck Zfp30 Mab21l3 Gm26737 Rdh12 Prkg2 Abca1 Bcl2l1 Adat3_1 Kif22 Sept3 Smco3 Cort Gprc5a Plek2 Gm15832 Xaf1 Prdx5 Fam212b Fam78a Fcgr1 Gm3550 Gpx3 Gpr17 Tnfaip2 Relb Helz2 Fgd4 D630023F18Rik Eldr Gm28869 Plet1 Batf Pear1 Styx Soga1 Hmmr G430095P16Rik Efcab11 Nqo1 Tnfaip3 Gm10073 Slfn2 Ptgs2os2 Carhsp1 Tifab Haus4 Mxd3 Zfp354b Il23a Dhx58 Sp140 Etv3 Plk3 Wdr90 Nuf2 Ccdc125 Itpka Ccdc189 Zfp811 5830432E09Rik Stk10 2810002D19Rik Rab27a Iqgap3 2310040G24Rik Matn1 6XSSOHPHQWDU\7DEOH/LVWRIGLIIHUHQWLDOO\H[SUHVVHGJHQHVLQ/JURXSYHUVXVYHKLFOH WUHDWHGJURXS JHQHV Supplementary Table 2: Differentially expressed genes in L + S groups versus L group L + S 1 h versus L group (64 genes) L + S 3 h versus L group (78 genes) L + S 4 h versus L group (78 genes) Upregulated genes Downregulated genes Upregulated genes Downregulated genes Upregulated genes Downregulated genes Gm43738 Glcci1 Gm7334 Zfp965 CT030159.2 Synpo 2700016F22Rik Gm6594 Gm26649 Gm6741 Gm43738 Hspa1l Gm26611 6030443J06Rik Apoo-ps Gm6793 Pakap Rsc1a1 Gm14401 Gm21887 Pakap Tlr8 Gm45736 Gm21985 Trpc5os Prx Gm15247 Rgs18 Gm14820 Cdh24 Btbd8_1 Gm16534 Ugt1a5 Dnd1 3110035E14Rik Tlr8 Xkr5 Gm10131 2700016F22Rik U90926 Alms1-ps2 Zfp607b Wisp3 Gm28035 Gm19410 A330023F24Rik Gm26669 Gm45713 Zfp784 Ccdc65 Hspa1a Gm5601 2700016F22Rik Gm26541 Slc3a1 Gm5601 Gm13610 Pagr1a Gprc5b AC166358.2 Lbp Asap2 Gm11175 Gm20503 Frem1 Gm14168 Cxadr B230398E01Rik CT030159.2 Gm28047 B4galnt2 Gm19719 Trim15 Hist2h2aa2 Itih1 Gm26920 Gm26965 Evl Rasd1 Hist1h2af Hist2h2aa2 C8g Gm15501 Pagr1b Gm45736 Gm10645 Gm14435 Gm18192 Sumo3_2 CT009754.1 Gm26668 Mroh6 C8g Gm13610 2310002F09Rik Gm45736 Gp9 Scd3 Hist2h2aa2 Hoxb3os 2600006K01Rik B430218F22Rik Gm29609 Gm28308 Papln Spns3 2700033N17Rik Inhbe Gm13684 Abhd11os Hmx3 Gm42417 Susd2 Pagr1b Pla2g4b Abhd11os Dzip1 Gdf9 Nanp Sdk2 Hist1h3g Sap30bpos Pla2g2d Fam89a Gm17111 Gm28845 Gm42791 Ccdc142 Mroh6 Cdh23 Gm26675 Gm15983 Gm2245 Pdzk1ip1 Gm42836 Gm15645 Hist2h2ac Gm13963 Pagr1a 5033417F24Rik Scd4 AC118476.2 Gm28539 Podxl Gm15628 Ifitm1 Klkb1 Rragd 1700109K24Rik Tmem236 Gm12867 Crtam 4930448A20Rik Amy1 1700060J05Rik Tnfrsf14 Gm28845 Gm614 Tfpi AC118476.2 Bspry Opcml 4930505N22Rik a Ypel1 Gm1972 Serpinb9b Gm14387 Gm26635 Adig Gabrb1 Ppp1r1a Ttll11 Gm45808 Gm42743 Gm12867 Tnfsf13 D130007C19Rik Fabp3 Clec11a Rapgef3 Triqk 2310001H17Rik Gm17383 AC154552.2 Gm28119 Cxcr4 A430078G23Rik Zfp647 Crtam Cxcl10 6330549D23Rik B430219N15Rik Gm26534 Zbtb46 Htr2b Gm527 1700113A16Rik Gm12764 Catsperg1 Capn3 Ccdc142 Shpk Sirpb1c Gm45808 Kank3 Gm13147 Gm16094 Cldn11 Rell1 Gm10382 Tnfrsf14 Zfp647 Slc17a7 Fjx1 Fam171a2 Bcl6b Cxcl10 Ldhd Ifit1 6XSSOHPHQWDU\7DEOH/LVWRIGLIIHUHQWLDOO\H[SUHVVHGJHQHVLQ/6JURXSVYHUVXV/JURXS.
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  • Minus End–Directed Motor KIFC3 Suppresses E-Cadherin Degradation by Recruiting USP47 to Adherens Junctions

    Minus End–Directed Motor KIFC3 Suppresses E-Cadherin Degradation by Recruiting USP47 to Adherens Junctions

    M BoC | ARTICLE Minus end–directed motor KIFC3 suppresses E-cadherin degradation by recruiting USP47 to adherens junctions Kyoko Sako-Kubotaa, Nobutoshi Tanakaa, Shigenori Nagaea, Wenxiang Menga,b, and Masatoshi Takeichia aRIKEN Center for Developmental Biology, Kobe 650-0047, Japan; bState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China ABSTRACT The adherens junction (AJ) plays a crucial role in maintaining cell–cell adhesion in Monitoring Editor epithelial tissues. Previous studies show that KIFC3, a minus end–directed kinesin motor, Kozo Kaibuchi moves into AJs via microtubules that grow from clusters of CAMSAP3 (also known as Nezha), Nagoya University a protein that binds microtubule minus ends. The function of junction-associated KIFC3, how- Received: Jul 30, 2014 ever, remains to be elucidated. Here we find that KIFC3 binds the ubiquitin-specific protease Revised: Sep 17, 2014 USP47, a protease that removes ubiquitin chains from substrates and hence inhibits protea- Accepted: Sep 18, 2014 some-mediated proteolysis, and recruits it to AJs. Depletion of KIFC3 or USP47 promotes cleavage of E-cadherin at a juxtamembrane region of the cytoplasmic domain, resulting in the production of a 90-kDa fragment and the internalization of E-cadherin. This cleavage de- pends on the E3 ubiquitin protein ligase Hakai and is inhibited by proteasome inhibitors. E- cadherin ubiquitination consistently increases after depletion of KIFC3 or USP47. These find- ings suggest that KIFC3 suppresses the ubiquitination and resultant degradation of E-cadherin by recruiting USP47 to AJs, a process that may be involved in maintaining stable cell–cell adhesion in epithelial sheets.
  • The Pdx1 Bound Swi/Snf Chromatin Remodeling Complex Regulates Pancreatic Progenitor Cell Proliferation and Mature Islet Β Cell

    The Pdx1 Bound Swi/Snf Chromatin Remodeling Complex Regulates Pancreatic Progenitor Cell Proliferation and Mature Islet Β Cell

    Page 1 of 125 Diabetes The Pdx1 bound Swi/Snf chromatin remodeling complex regulates pancreatic progenitor cell proliferation and mature islet β cell function Jason M. Spaeth1,2, Jin-Hua Liu1, Daniel Peters3, Min Guo1, Anna B. Osipovich1, Fardin Mohammadi3, Nilotpal Roy4, Anil Bhushan4, Mark A. Magnuson1, Matthias Hebrok4, Christopher V. E. Wright3, Roland Stein1,5 1 Department of Molecular Physiology and Biophysics, Vanderbilt University, Nashville, TN 2 Present address: Department of Pediatrics, Indiana University School of Medicine, Indianapolis, IN 3 Department of Cell and Developmental Biology, Vanderbilt University, Nashville, TN 4 Diabetes Center, Department of Medicine, UCSF, San Francisco, California 5 Corresponding author: [email protected]; (615)322-7026 1 Diabetes Publish Ahead of Print, published online June 14, 2019 Diabetes Page 2 of 125 Abstract Transcription factors positively and/or negatively impact gene expression by recruiting coregulatory factors, which interact through protein-protein binding. Here we demonstrate that mouse pancreas size and islet β cell function are controlled by the ATP-dependent Swi/Snf chromatin remodeling coregulatory complex that physically associates with Pdx1, a diabetes- linked transcription factor essential to pancreatic morphogenesis and adult islet-cell function and maintenance. Early embryonic deletion of just the Swi/Snf Brg1 ATPase subunit reduced multipotent pancreatic progenitor cell proliferation and resulted in pancreas hypoplasia. In contrast, removal of both Swi/Snf ATPase subunits, Brg1 and Brm, was necessary to compromise adult islet β cell activity, which included whole animal glucose intolerance, hyperglycemia and impaired insulin secretion. Notably, lineage-tracing analysis revealed Swi/Snf-deficient β cells lost the ability to produce the mRNAs for insulin and other key metabolic genes without effecting the expression of many essential islet-enriched transcription factors.
  • Lineage-Specific Effector Signatures of Invariant NKT Cells Are Shared Amongst Δγ T, Innate Lymphoid, and Th Cells

    Lineage-Specific Effector Signatures of Invariant NKT Cells Are Shared Amongst Δγ T, Innate Lymphoid, and Th Cells

    Downloaded from http://www.jimmunol.org/ by guest on September 26, 2021 δγ is online at: average * The Journal of Immunology , 10 of which you can access for free at: 2016; 197:1460-1470; Prepublished online 6 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600643 http://www.jimmunol.org/content/197/4/1460 Lineage-Specific Effector Signatures of Invariant NKT Cells Are Shared amongst T, Innate Lymphoid, and Th Cells You Jeong Lee, Gabriel J. Starrett, Seungeun Thera Lee, Rendong Yang, Christine M. Henzler, Stephen C. Jameson and Kristin A. Hogquist J Immunol cites 41 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription http://www.jimmunol.org/content/suppl/2016/07/06/jimmunol.160064 3.DCSupplemental This article http://www.jimmunol.org/content/197/4/1460.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 © 2016 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 26, 2021. The Journal of Immunology Lineage-Specific Effector Signatures of Invariant NKT Cells Are Shared amongst gd T, Innate Lymphoid, and Th Cells You Jeong Lee,* Gabriel J.
  • Murine Perinatal Beta Cell Proliferation and the Differentiation of Human Stem Cell Derived Insulin Expressing Cells Require NEUROD1

    Murine Perinatal Beta Cell Proliferation and the Differentiation of Human Stem Cell Derived Insulin Expressing Cells Require NEUROD1

    Page 1 of 105 Diabetes Murine perinatal beta cell proliferation and the differentiation of human stem cell derived insulin expressing cells require NEUROD1 Anthony I. Romer,1,2 Ruth A. Singer1,3, Lina Sui2, Dieter Egli,2* and Lori Sussel1,4* 1Department of Genetics and Development, Columbia University, New York, NY 10032, USA 2Department of Pediatrics, Columbia University, New York, NY 10032, USA 3Integrated Program in Cellular, Molecular and Biomedical Studies, Columbia University, New York, NY 10032, USA 4Department of Pediatrics, University of Colorado Denver School of Medicine, Denver, CO 80045, USA *Co-Corresponding Authors Dieter Egli 1150 St. Nicholas Avenue New York, NY 10032 [email protected] Lori Sussel 1775 Aurora Ct. Aurora, CO 80045 [email protected] Word Count: Abstract= 149; Body= 4773 Total Paper Figures= 7, Total Supplemental Tables= 4, Total Supplemental Figures= 5 Diabetes Publish Ahead of Print, published online September 13, 2019 Diabetes Page 2 of 105 Abstract Inactivation of the β cell transcription factor NEUROD1 causes diabetes in mice and humans. In this study, we uncovered novel functions of Neurod1 during murine islet cell development and during the differentiation of human embryonic stem cells (HESCs) into insulin-producing cells. In mice, we determined that Neurod1 is required for perinatal proliferation of alpha and beta cells. Surprisingly, apoptosis only makes a minor contribution to beta cell loss when Neurod1 is deleted. Inactivation of NEUROD1 in HESCs severely impaired their differentiation from pancreatic progenitors into insulin expressing (HESC-beta) cells; however survival or proliferation was not affected at the time points analyzed. NEUROD1 was also required in HESC-beta cells for the full activation of an essential beta cell transcription factor network.
  • Comparative Analysis of Two C-Terminal Kinesin Motor Proteins: KIFC1 and KIFC5A

    Comparative Analysis of Two C-Terminal Kinesin Motor Proteins: KIFC1 and KIFC5A

    Cell Motility and the Cytoskeleton 58:213–230 (2004) Comparative Analysis of Two C-Terminal Kinesin Motor Proteins: KIFC1 and KIFC5A Yuguo Zhang and Ann O. Sperry* Department of Anatomy and Cell Biology, Brody School of Medicine at East Carolina University, Greenville, North Carolina We have taken advantage of the close structural relationship between two C- terminal motors, KIFC5A and KIFC1, to examine the sequence requirements for targeting of these two motors within the cell. Although KIFC5A and KIFC1 are almost identical in their motor and stalk domains, they differ in well-defined regions of their tail domains. Specific antisera to these motors were used to determine their localization to distinct subcellular compartments, the spindle for KIFC5A or membranous organelles for KIFC1. In addition to defining the intracellular localization of KIFC1, the reactivity of the KIFC1 antibody demon- strates that this motor contains a frame shift with respect to KIFC5A and is likely the product of a separate gene. The divergent tail domains of these motors are predicted to harbor specific information that directs them to their correct intra- cellular targets. In order to define the sequences responsible for the differential localization of these two motors, GFP was fused to motors with various tail deletions and their localization visualized after transfection. We were able to identify distinct sequences in each motor responsible for its unique cellular localization. The KIFC5A tail contains a 43 amino acid sequence with both nuclear localization and microtubule binding activity while KIFC1 contains a 19 amino acid sequence sufficient to target this motor to membrane-bounded or- ganelles.
  • UC Irvine Electronic Theses and Dissertations

    UC Irvine Electronic Theses and Dissertations

    UC Irvine UC Irvine Electronic Theses and Dissertations Title Contribution of C5aR1 to Neuroinflammation and Neuronal Dysfunction in Alzheimer’s Disease Permalink https://escholarship.org/uc/item/7s66m6tf Author Hernandez, Michael Publication Date 2017 Peer reviewed|Thesis/dissertation eScholarship.org Powered by the California Digital Library University of California UNIVERSITY OF CALIFORNIA, IRVINE Contribution of C5aR1 to Neuroinflammation and Neuronal Dysfunction in Alzheimer’s Disease DISSERTATION submitted in partial satisfaCtion of the requirements for the degree of DOCTOR OF PHILOSOPHY in BiomediCal Sciences by MiChael Hernandez Dissertation Committee: Professor Andrea J. Tenner, Chair Professor Edwin S. Monuki AssoCiate Professor Kim Green 2017 © 2017 MiChael Hernandez DEDICATION To My sister, Jennifer, who has been there for me the entire way, and my friends, old and new. Thank you for your support and the many adventures we’ve shared. ii TABLE OF CONTENTS Page LIST OF FIGURES iv LIST OF TABLES viii ACKNOWLEDGMENTS x CURRICULUM VITAE xi ABSTRACT OF THE DISSERTATION xv CHAPTER 1: IntroduCtion 1 CHAPTER 2: C5a Increases the Injury to Primary Neurons EliCited by 20 Fibrillar Amyloid Beta CHAPTER 3: Prevention of C5aR1 Signaling Delays Microglial 47 Inflammatory Polarization, Favors Clearance Pathways and Suppresses Cognitive Loss CHAPTER 4: Comparing SurfaCe Expression of Proteins on MiCroglia 130 in vitro vs in vivo and MiCroglial Changes in AD CHAPTER 5: Summary and Future DireCtions 172 iii LIST OF FIGURES Page Figure 1.1. SChematiC diagram of Complement aCtivation by 6 fibrillar β-amyloid. Figure 1.2. C5aR1 inhibition maintains benefiCial response of 14 Complement aCtivation and inhibits detrimental response. Figure 2.1.