Conditional Knockout Mouse Catalog (Last Update: January 2018)

Total Page:16

File Type:pdf, Size:1020Kb

Conditional Knockout Mouse Catalog (Last Update: January 2018) Conditional Knockout Mouse Catalog (Last Update: January 2018) Personalized Genome Engineering Service Conditional Knockout Mouse Catalog Access to the Largest Repository of Mouse Models • Today, more than 1900 off-the-shelf strains are available • Live mice, frozen embryos and/or sperm are delivered in as quick as 4 weeks • Systematic broad-based phenotyping is performed on most strains • High versatility of these models allows access to conditional, constitutive, and tissue-specific Knockout, and/or reporter mice Conditional or constitutive Knockouts: Reporter mouse lines: - Safety studies - Gene expression patterns - Target validation - Cell trafficking - Gene function studies - Monitoring of biomarker - Screening of transcriptional regulators Guaranteed Rights of Use / Freedom to Operate (FTO) We have acquired all necessary intellectual property rights, most of them exclusively, so that we can provide our customers the FTO they need. Animals genOway provides you with cohorts of VAFelite/SOPF certified animals together with phenotyping data. This package is a major timesaving advantage for your research program. EUCOMM and genOway Have Combined Forces to Create That Service • EUCOMM - The European Conditional Mouse Mutagenesis Program is a founding member and European cornerstone of the International Knockout Mouse Consortium (IKMC). • EUCOMM’s main objective is the generation and archiving of conditional mutations across the mouse genome. Personalized Genome Engineering Service www.genoway.com Targeted Genes GENE ACCN GENE ACCN GENE ACCN GENE ACCN Acp2 MGI:87882 Grb2 MGI:95805 Pdgfrb MGI:97531 Cntfr MGI:99605 Chrnb2 MGI:87891 Grin1 MGI:95819 Pfkl MGI:97547 Ryr1 MGI:99659 Aspa MGI:87914 Grin2d MGI:95823 Pfn1 MGI:97549 Syt1 MGI:99667 Plin2 MGI:87920 Hoxa2 MGI:96174 Prkcz MGI:97602 Adcy3 MGI:99675 Adh5 MGI:87929 Hprt MGI:96217 Prps1 MGI:97775 Adcy1 MGI:99677 Agtr2 MGI:87966 Hspa1l MGI:96231 Psph MGI:97788 Cttn MGI:99695 Areg MGI:88068 Trmt2a MGI:96270 Pth MGI:97799 Chrna7 MGI:99779 Atp1a3 MGI:88107 Id2 MGI:96397 Pth1r MGI:97801 Rab23 MGI:99833 Atp2a2 MGI:88110 Ide MGI:96412 Ptpn2 MGI:97806 Gdi2 MGI:99845 Atp5a1 MGI:88115 Ido1 MGI:96416 Slc20a2 MGI:97851 Ppm1a MGI:99878 Avp MGI:88121 Il12a MGI:96539 Rel MGI:97897 Lama1 MGI:99892 Tff1 MGI:88135 Il1r2 MGI:96546 Rlbp1 MGI:97930 Gja8 MGI:99953 Tspo MGI:88222 Irf1 MGI:96590 Rpe65 MGI:98001 Traf2 MGI:101835 C8b MGI:88236 Itga2 MGI:96600 Rpl32 MGI:98038 Usp15 MGI:101857 Anxa6 MGI:88255 Kcnb1 MGI:96666 Rpn2 MGI:98085 Ap2a2 MGI:101920 Cd28 MGI:88327 Ldha MGI:96759 S100b MGI:98217 Cpe MGI:101932 Cdh1 MGI:88354 Ldlr MGI:96765 Sag MGI:98227 Ppp5c MGI:102666 F2 MGI:88380 Lgals3 MGI:96778 Sell MGI:98279 Grb7 MGI:102683 Cfh MGI:88385 Lifr MGI:96788 Shh MGI:98297 Nelfe MGI:102744 Clu MGI:88423 Lmnb1 MGI:96795 Pmel MGI:98301 Trim25 MGI:102749 Cnp MGI:88437 Klrb1 MGI:96877 Sparc MGI:98373 Rph3a MGI:102788 Col9a2 MGI:88466 Lyn MGI:96892 Sptbn1 MGI:98388 Prph2 MGI:102791 Comt MGI:88470 Golga3 MGI:96958 Src MGI:98397 Entpd1 MGI:102805 Cryab MGI:88516 Mgat1 MGI:96973 Med22 MGI:98446 Mybpc3 MGI:102844 Cyp11a1 MGI:88582 Mmp12 MGI:97005 Tap1 MGI:98483 Klkb1 MGI:102849 Csde1 MGI:92356 Mpg MGI:97073 Tcf4 MGI:98506 Elk4 MGI:102853 Adipor2 MGI:93830 Mpi MGI:97075 Tcp11 MGI:98544 Epb41l5 MGI:103006 Oaf MGI:94852 Mx1 MGI:97243 Timp1 MGI:98752 Il15 MGI:103014 Egfr MGI:95294 Myl4 MGI:97267 Tpi1 MGI:98797 Ecm1 MGI:103060 Ercc2 MGI:95413 Myl2 MGI:97272 Tpm1 MGI:98809 Pdpn MGI:103098 Fbp2 MGI:95491 Ncf2 MGI:97284 Ucp1 MGI:98894 F10 MGI:103107 Fcgr3 MGI:95500 Nedd4 MGI:97297 Usp4 MGI:98905 Uchl1 MGI:103149 Fgf2 MGI:95516 Ngfr MGI:97323 Uros MGI:98917 Aqp1 MGI:103201 Fgf7 MGI:95521 Nodal MGI:97359 Ezr MGI:98931 Fdx1 MGI:103224 Fyn MGI:95602 Notch1 MGI:97363 Wnt3 MGI:98955 Efna1 MGI:103236 Gad2 MGI:95634 Nras MGI:97376 Rapsn MGI:99422 Cyb561 MGI:103253 Gap43 MGI:95639 Ntrk1 MGI:97383 Hira MGI:99430 Nfatc3 MGI:103296 Gfap MGI:95697 Ntrk2 MGI:97384 Arf3 MGI:99432 Rbl1 MGI:103300 Gfpt1 MGI:95698 Ocm MGI:97401 Abhd16a MGI:99476 Bmp7 MGI:103302 Ggt1 MGI:95706 Pax5 MGI:97489 Syk MGI:99515 Myo7a MGI:104510 Gnao1 MGI:95775 Pbx3 MGI:97496 Aldh2 MGI:99600 Rcn1 MGI:104559 Gnb3 MGI:95785 Pcx MGI:97520 Acan MGI:99602 Wars MGI:104630 Personalized Genome Engineering Service www.genoway.com GENE ACCN GENE ACCN GENE ACCN GENE ACCN Pdcd2 MGI:104643 Sgsm1 MGI:107320 Epas1 MGI:109169 Tmc6 MGI:1098686 Capzb MGI:104652 Gfm1 MGI:107339 Tead3 MGI:109241 Esyt3 MGI:1098699 Rora MGI:104661 Gstt1 MGI:107379 Sema4d MGI:109244 Sgol2a MGI:1098767 Tfap2b MGI:104672 Irak1 MGI:107420 Sqle MGI:109296 Lbp MGI:1098776 Hgs MGI:104681 Efna5 MGI:107444 Mapkapk2 MGI:109298 Coq4 MGI:1098826 Col4a3 MGI:104688 Myl12b MGI:107494 F7 MGI:109325 Fgf10 MGI:1099809 Scnn1g MGI:104695 Kcnj11 MGI:107501 Bnip2 MGI:109327 Atp5f1 MGI:1100495 Wbp2 MGI:104709 Sipa1 MGI:107576 Nxn MGI:109331 Myt1l MGI:1100511 Cdkn2a MGI:104738 Npat MGI:107605 Ctr9 MGI:109345 Twf1 MGI:1100520 Pls3 MGI:104807 Ifnar1 MGI:107658 Snap23 MGI:109356 Capn5 MGI:1100859 Pdia4 MGI:104864 Plxna2 MGI:107684 Hp1bp3 MGI:109369 Frs2 MGI:1100860 Rest MGI:104897 Kif3b MGI:107688 Cbx5 MGI:109372 Rbbp7 MGI:1194910 Nup88 MGI:104900 Myh9 MGI:107717 Hmox2 MGI:109373 Per2 MGI:1195265 Tnfaip1 MGI:104961 Myo9a MGI:107735 Atf3 MGI:109384 Tcaim MGI:1196217 Gclc MGI:104990 Dctn1 MGI:107745 Abca4 MGI:109424 Casz1 MGI:1196251 Lepr MGI:104993 Dync1i2 MGI:107750 Raet1c MGI:109431 Spice1 MGI:1196252 Slc9a4 MGI:105074 Zfp69 MGI:107794 Oaz1 MGI:109433 Ccpg1 MGI:1196419 Cxcr2 MGI:105303 Akr7a5 MGI:107796 Ctcf MGI:109447 Atpif1 MGI:1196457 Rab5c MGI:105306 Prmt1 MGI:107846 Sms MGI:109490 Mrpl23 MGI:1196612 Cbx1 MGI:105369 D6Wsu163e MGI:107893 Trpc2 MGI:109527 Pitpnm1 MGI:1197524 Cfi MGI:105937 Tial1 MGI:107913 Il4i1 MGI:109552 Anxa3 MGI:1201378 Txlna MGI:105968 Lrig1 MGI:107935 Psmc2 MGI:109555 Blzf1 MGI:1201607 Cyp7a1 MGI:106091 Ezh2 MGI:107940 Enc1 MGI:109610 Synj2 MGI:1201671 Etfdh MGI:106100 Klc2 MGI:107953 Barx2 MGI:109617 Dennd5a MGI:1201681 Mybbp1a MGI:106181 Myd88 MGI:108005 Arvcf MGI:109620 Kif20a MGI:1201682 Hells MGI:106209 Kcnj9 MGI:108007 Ostf1 MGI:700012 Eomes MGI:1201683 Cdc42 MGI:106211 Cited1 MGI:108023 Prdx6 MGI:894320 Nmt2 MGI:1202298 Slx4 MGI:106299 Laptm5 MGI:108046 Bach2 MGI:894679 Itch MGI:1202301 Fam104a MGI:106351 Smyd5 MGI:108048 Pa2g4 MGI:894684 Vps72 MGI:1202305 Rbfox3 MGI:106368 Traf6 MGI:108072 Ywhae MGI:894689 Chrna9 MGI:1202403 Rnasek MGI:106369 Frrs1 MGI:108076 Kdm6a MGI:1095419 Tcf7l1 MGI:1202876 Grsf1 MGI:106479 Nptn MGI:108077 Adam17 MGI:1096335 Tcf7l2 MGI:1202879 Chpf MGI:106576 Cep250 MGI:108084 Sema3f MGI:1096347 Rhd MGI:1202882 Pla2g2c MGI:106638 Hdac1 MGI:108086 Car4 MGI:1096574 Bap1 MGI:1206586 Pon2 MGI:106687 Rgs16 MGI:108407 Tex261 MGI:1096575 Naga MGI:1261422 Vdac1 MGI:106919 Lrmp MGI:108424 Npc1 MGI:1097712 Myo15 MGI:1261811 Aff3 MGI:106927 Adcy9 MGI:108450 Cenpe MGI:1098230 Usp12 MGI:1270128 Ppp3cc MGI:107162 Fzd6 MGI:108474 Kif13b MGI:1098265 Alox12e MGI:1274790 Ppp3ca MGI:107164 Fzd3 MGI:108476 Gse1 MGI:1098275 Mmp16 MGI:1276107 Tfdp2 MGI:107167 Kcnj12 MGI:108495 Rgs5 MGI:1098434 Ncoa3 MGI:1276535 Cbr2 MGI:107200 Hnf4a MGI:109128 Ift81 MGI:1098597 Gfi1b MGI:1276578 Nsun2 MGI:107252 Ltbp1 MGI:109151 Anapc4 MGI:1098673 Gpr33 MGI:1277106 Personalized Genome Engineering Service www.genoway.com GENE ACCN GENE ACCN GENE ACCN GENE ACCN Pde8a MGI:1277116 Slc31a2 MGI:1333844 Car14 MGI:1344341 Cstf3 MGI:1351825 Ldlrad4 MGI:1277150 Rfxank MGI:1333865 Dlg2 MGI:1344351 Pdxk MGI:1351869 Parl MGI:1277152 Bre MGI:1333875 Nek3 MGI:1344371 Cxcl9 MGI:1352449 Dcx MGI:1277171 Prkaa2 MGI:1336173 Natd1 MGI:1344388 Capn11 MGI:1352490 Ddx56 MGI:1277172 Prkab2 MGI:1336185 Oasl2 MGI:1344390 Bag3 MGI:1352493 Ifi27 MGI:1277180 Agpat3 MGI:1336186 Adam23 MGI:1345162 Stau2 MGI:1352508 Il13ra2 MGI:1277954 Mocs2 MGI:1336894 Zfp119a MGI:1345189 Cabp1 MGI:1352750 Pycr2 MGI:1277956 Ap3s1 MGI:1337062 Gtf2h2 MGI:1345669 Reg3d MGI:1353426 Dlg4 MGI:1277959 Ap4m1 MGI:1337063 Arhgef28 MGI:1346016 Timm9 MGI:1353436 Epc2 MGI:1278321 Rnf7 MGI:1337096 Gpc6 MGI:1346322 Fkbp3 MGI:1353460 Epc1 MGI:1278322 P2rx6 MGI:1337113 Fyb MGI:1346327 Slc25a4 MGI:1353495 Dnpep MGI:1278328 Sort1 MGI:1338015 Def6 MGI:1346328 Arhgef1 MGI:1353510 Nipsnap1 MGI:1278344 Bex2 MGI:1338017 Mapk1 MGI:1346858 Sspn MGI:1353511 Ncaph2 MGI:1289164 Mapk11 MGI:1338024 Mapk10 MGI:1346863 Pik3cg MGI:1353576 Itgae MGI:1298377 Ikbkb MGI:1338071 Map2k2 MGI:1346867 Siva1 MGI:1353606 Sh3pxd2a MGI:1298393 Sec22b MGI:1338759 Map2k7 MGI:1346871 Tor3a MGI:1353652 Ccl22 MGI:1306779 Cyfip1 MGI:1338801 Map3k7 MGI:1346877 Usp21 MGI:1353665 Gstm6 MGI:1309467 Celf2 MGI:1338822 Map3k10 MGI:1346879 Sirt6 MGI:1354161 Gsta4 MGI:1309515 P2rx4 MGI:1338859 Mapkbp1 MGI:1347004 Acsl4 MGI:1354713 Marco MGI:1309998 Gfpt2 MGI:1338883 Orc5 MGI:1347044 Orc3 MGI:1354944 Sptbn2 MGI:1313261 Uhrf1 MGI:1338889 Decr2 MGI:1347059 Polg2 MGI:1354947 Eif2b3 MGI:1313286 Smc3 MGI:1339795 Creb3l1 MGI:1347062 Synj1 MGI:1354961 Khdrbs3 MGI:1313312 P2rx7 MGI:1339957 Nubp2 MGI:1347072 Exosc9 MGI:1355319 Hipk3 MGI:1314882 Cth MGI:1339968 Fto MGI:1347093 Atp5e MGI:1855697 Tnfrsf1a MGI:1314884 Pak1 MGI:1339975 Usp5 MGI:1347343 Usp2 MGI:1858178 Lrrc23 MGI:1315192 Zfp207 MGI:1340045 Hunk MGI:1347352 Ccnc MGI:1858199 Slc40a1 MGI:1315204 Chil4 MGI:1341098 Pla2g10 MGI:1347522 Ech1 MGI:1858208 Prmt2 MGI:1316652 Gldc MGI:1341155 Abcd1 MGI:1349215 Zranb2 MGI:1858211 Cyba MGI:1316658 Aqp6 MGI:1341204 Abcd4 MGI:1349217 Clpp MGI:1858213 Lgals7 MGI:1316742 Dapk2 MGI:1341297 Polr2f MGI:1349393 Pkd2l2 MGI:1858231 Hint1 MGI:1321133 Ggps1 MGI:1341724 Mecr MGI:1349441 Caprin1 MGI:1858234 Vamp3 MGI:1321389 Ehd1 MGI:1341878
Recommended publications
  • Supplemental Information
    Supplemental information Dissection of the genomic structure of the miR-183/96/182 gene. Previously, we showed that the miR-183/96/182 cluster is an intergenic miRNA cluster, located in a ~60-kb interval between the genes encoding nuclear respiratory factor-1 (Nrf1) and ubiquitin-conjugating enzyme E2H (Ube2h) on mouse chr6qA3.3 (1). To start to uncover the genomic structure of the miR- 183/96/182 gene, we first studied genomic features around miR-183/96/182 in the UCSC genome browser (http://genome.UCSC.edu/), and identified two CpG islands 3.4-6.5 kb 5’ of pre-miR-183, the most 5’ miRNA of the cluster (Fig. 1A; Fig. S1 and Seq. S1). A cDNA clone, AK044220, located at 3.2-4.6 kb 5’ to pre-miR-183, encompasses the second CpG island (Fig. 1A; Fig. S1). We hypothesized that this cDNA clone was derived from 5’ exon(s) of the primary transcript of the miR-183/96/182 gene, as CpG islands are often associated with promoters (2). Supporting this hypothesis, multiple expressed sequences detected by gene-trap clones, including clone D016D06 (3, 4), were co-localized with the cDNA clone AK044220 (Fig. 1A; Fig. S1). Clone D016D06, deposited by the German GeneTrap Consortium (GGTC) (http://tikus.gsf.de) (3, 4), was derived from insertion of a retroviral construct, rFlpROSAβgeo in 129S2 ES cells (Fig. 1A and C). The rFlpROSAβgeo construct carries a promoterless reporter gene, the β−geo cassette - an in-frame fusion of the β-galactosidase and neomycin resistance (Neor) gene (5), with a splicing acceptor (SA) immediately upstream, and a polyA signal downstream of the β−geo cassette (Fig.
    [Show full text]
  • The Discovery and Regulation of Modes of Exocytosis Through the Lens of Computer Vision
    THE DISCOVERY AND REGULATION OF MODES OF EXOCYTOSIS THROUGH THE LENS OF COMPUTER VISION Fabio Urbina A thesis submitted to the faculty at the University of North Carolina at Chapel Hill in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the department of Cell Biology and Physiology in the School of Medicine. Chapel Hill 2020 Approved by: Stephanie Gupton Patrick Brennwald Doug Cyr Keith Burridge Shawn Gomez © 2020 Fabio Urbina ALL RIGHTS RESERVED ii ABSTRACT Fabio Urbina: Discovery and Regulation of the Modes of Exocytosis through the lens of computer vision (Under the direction of Stephanie Gupton) The formation of the nervous system involves establishing complex networks of synaptic connections between proper partners, which requires the rapid expansion of the plasma membrane surface area as neurons grow. Critical to the expansion of the plasma membrane is exocytic vesicle fusion, a regulated mechanism driven by soluble N-ethylmaleimide-sensitive factor attachment proteins receptors (SNAREs). Multiple modes of exocytosis have been proposed, with full-vesicle fusion (FVF) and kiss-and-run (KNR) being the best described. The basis of SNARE-mediated fusion, the opening of a fusion pore, and its contribution to plasma membrane expansion remains enigmatic, as vesicle fusion is spatially small and temporally fast. We exploited TIRF microscopy to image VAMP-pHluorin mediated exocytosis in murine embryonic cortical neurons and developed computer-vision software and statistical tools to perform unbiased, efficient identification of exocytic events and uncover spatiotemporal aspects of exocytosis during neuron development. We further developed novel classification algorithms to describe. and classify individual exocytic events.
    [Show full text]
  • Supplementary Table S4. FGA Co-Expressed Gene List in LUAD
    Supplementary Table S4. FGA co-expressed gene list in LUAD tumors Symbol R Locus Description FGG 0.919 4q28 fibrinogen gamma chain FGL1 0.635 8p22 fibrinogen-like 1 SLC7A2 0.536 8p22 solute carrier family 7 (cationic amino acid transporter, y+ system), member 2 DUSP4 0.521 8p12-p11 dual specificity phosphatase 4 HAL 0.51 12q22-q24.1histidine ammonia-lyase PDE4D 0.499 5q12 phosphodiesterase 4D, cAMP-specific FURIN 0.497 15q26.1 furin (paired basic amino acid cleaving enzyme) CPS1 0.49 2q35 carbamoyl-phosphate synthase 1, mitochondrial TESC 0.478 12q24.22 tescalcin INHA 0.465 2q35 inhibin, alpha S100P 0.461 4p16 S100 calcium binding protein P VPS37A 0.447 8p22 vacuolar protein sorting 37 homolog A (S. cerevisiae) SLC16A14 0.447 2q36.3 solute carrier family 16, member 14 PPARGC1A 0.443 4p15.1 peroxisome proliferator-activated receptor gamma, coactivator 1 alpha SIK1 0.435 21q22.3 salt-inducible kinase 1 IRS2 0.434 13q34 insulin receptor substrate 2 RND1 0.433 12q12 Rho family GTPase 1 HGD 0.433 3q13.33 homogentisate 1,2-dioxygenase PTP4A1 0.432 6q12 protein tyrosine phosphatase type IVA, member 1 C8orf4 0.428 8p11.2 chromosome 8 open reading frame 4 DDC 0.427 7p12.2 dopa decarboxylase (aromatic L-amino acid decarboxylase) TACC2 0.427 10q26 transforming, acidic coiled-coil containing protein 2 MUC13 0.422 3q21.2 mucin 13, cell surface associated C5 0.412 9q33-q34 complement component 5 NR4A2 0.412 2q22-q23 nuclear receptor subfamily 4, group A, member 2 EYS 0.411 6q12 eyes shut homolog (Drosophila) GPX2 0.406 14q24.1 glutathione peroxidase
    [Show full text]
  • Time-Resolved Systems Analysis of Virus Infection Fate Regulation
    Time-resolved systems analysis of virus infection fate regulation Mireia Pedragosa Marín TESI DOCTORAL UPF / 2018 DIRECTORS DE LA TESI Dr. Andreas Meyerhans i Dr. Jordi Argilaguet DEPARTAMENT DE CIÈNCIES EXPERIMENTALS I DE LA SALUT Als que estimo, i a les “Surullotes”, ACKNOWLEDGEMENTS Sembla mentida però per fi ha arribat el moment d’entregar i defensar la tesi. No m’ho puc ni creure… Així que toca agraïr a tots i totes els/les que han fet que això hagi estat posible. To start with, I want to thank my supervisor Dr. Andreas Meyerhans, not only for providing a lab and money for the experiments, but also for his help during the thesis. I know I am not always easy and that I have still lots of things to learn… but I enjoyed (and will continue enjoying) the process. Jordi, coneixent-me saps que, de tota la tesi, el que més m’està costant és aquest apartat… així que seré breu com sempre. INFINITES GRÀCIES PER TOT. Necessito una tesi sencera per poder agraïr-te tot el que has fet (I segur que hauràs de seguir fent, ho sento). Gràcies pel suport moral, mental i físic. I per cert, no m’oblido de la paella… To all my labmates from the past and from the present. Gracielita (gracias por enseñarme Paraguayo Y por hacer del lab una fiesta), Vale, Eva, Kat, Mie, Javier, and the people from Juana’s lab. You make from everyday a different and happy day, really. A l’Eva, l’Erika, l’Òscar i a l’Àlex per la seva ajuda en els projectes de flow, que no sempre surt tot com una vol i per les xerrades “no tècniques” que fan les hores de flow més curtes.
    [Show full text]
  • SNAP47 (D-11): Sc-514428
    SAN TA C RUZ BI OTEC HNOL OG Y, INC . SNAP47 (D-11): sc-514428 BACKGROUND APPLICATIONS In eukaryotic cells, the Golgi apparatus receives newly synthesized proteins SNAP47 (D-11) is recommended for detection of SNAP47 of human origin from the endoplasmic reticulum and delivers them after covalent modifica tion by Western Blotting (starting dilution 1:100, dilution range 1:100-1:1000), to their destination in the cell. For membrane-directed proteins, this process immunoprecipitation [1-2 µg per 100-500 µg of total protein (1 ml of cell is believed to be carried out via vesicular transport. Correct vesicular trans port lysate)], immunofluorescence (starting dilution 1:50, dilution range 1:50- is determined by specific pairing of vesicle-associated SNAREs (v-SNAREs) 1:500) and solid phase ELISA (starting dilution 1:30, dilution range 1:30- with those on the target membrane (t-SNAREs). This complex then recruits 1:3000). soluble NSF attachment proteins (SNAPs) and N-ethylmaleimide-sensitive Suitable for use as control antibody for SNAP47 siRNA (h): sc-88350, SNAP47 factor (NSF) to form the highly stable SNAP receptor (SNARE) complex. The shRNA Plasmid (h): sc-88350-SH and SNAP47 shRNA (h) Lentiviral Particles: formation of a SNARE complex pulls the vesicle and target membrane together sc-88350-V. and may provide the energy to drive fusion of the lipid bilayers. SNAP47 (synaptosomal-associated protein 47), also known as epididymis luminal Molecular Weight of SNAP47 isoforms 1-4: 53/50/23/25 kDa. protein 170, is a 464 amino acid protein that is ubiquitously expressed with Positive Controls: Jurkat whole cell lysate: sc-2204, COLO 205 whole cell highest levels found in nervous tissue.
    [Show full text]
  • Downloaded Per Proteome Cohort Via the Web- Site Links of Table 1, Also Providing Information on the Deposited Spectral Datasets
    www.nature.com/scientificreports OPEN Assessment of a complete and classifed platelet proteome from genome‑wide transcripts of human platelets and megakaryocytes covering platelet functions Jingnan Huang1,2*, Frauke Swieringa1,2,9, Fiorella A. Solari2,9, Isabella Provenzale1, Luigi Grassi3, Ilaria De Simone1, Constance C. F. M. J. Baaten1,4, Rachel Cavill5, Albert Sickmann2,6,7,9, Mattia Frontini3,8,9 & Johan W. M. Heemskerk1,9* Novel platelet and megakaryocyte transcriptome analysis allows prediction of the full or theoretical proteome of a representative human platelet. Here, we integrated the established platelet proteomes from six cohorts of healthy subjects, encompassing 5.2 k proteins, with two novel genome‑wide transcriptomes (57.8 k mRNAs). For 14.8 k protein‑coding transcripts, we assigned the proteins to 21 UniProt‑based classes, based on their preferential intracellular localization and presumed function. This classifed transcriptome‑proteome profle of platelets revealed: (i) Absence of 37.2 k genome‑ wide transcripts. (ii) High quantitative similarity of platelet and megakaryocyte transcriptomes (R = 0.75) for 14.8 k protein‑coding genes, but not for 3.8 k RNA genes or 1.9 k pseudogenes (R = 0.43–0.54), suggesting redistribution of mRNAs upon platelet shedding from megakaryocytes. (iii) Copy numbers of 3.5 k proteins that were restricted in size by the corresponding transcript levels (iv) Near complete coverage of identifed proteins in the relevant transcriptome (log2fpkm > 0.20) except for plasma‑derived secretory proteins, pointing to adhesion and uptake of such proteins. (v) Underrepresentation in the identifed proteome of nuclear‑related, membrane and signaling proteins, as well proteins with low‑level transcripts.
    [Show full text]
  • Curriculum Vitae
    The Roles of Autophagic SNARE proteins SNAP29 and SNAP47 in Autophagy and Enterovirus D68 Replication Item Type dissertation Authors Corona, Abigail Publication Date 2019 Abstract Enterovirus-D68 (EV-D68) is a positive-sense, single-stranded RNA virus of the Picornaviridae family that causes respiratory disease in children and has been implicated in recent outbreaks of acute flaccid myelitis, a severe paralysis syndrome. We ha... Keywords Virology; Cellular biology; amphisome; picornavirus; SNAP29; SNAP47; Autophagy; Enterovirus D, Human; Picornaviridae Download date 04/10/2021 22:18:40 Link to Item http://hdl.handle.net/10713/11615 Curriculum Vitae Abigail Kristen Corona Formerly: Abigail Kristen McGillivray [email protected] Education Doctor of Philosophy* to be conferred - 2019 Degree in Molecular Microbiology and Immunology University of Maryland-Baltimore; Baltimore, Maryland 21201 Advisor: William T. Jackson, PhD Bachelor of Science 2014 Degree in Biochemistry Carroll University; Waukesha, Wisconsin 53186 Publications Corona AK and Jackson WT. “Finding the middle ground for autophagic fusion requirements.” Trends in Cell Biology 2018. 28 (11): 869-881. Corona AK, Mohamud Y, Jackson WT, Luo H. “Oh, SNAP! How enteroviruses redirect autophagic traffic away from degradation.” Autophagy 2018. 14 (8): 1469-1471. Corona Velazquez AF, Corona AK, Klein KA, Jackson WT. “Poliovirus induces autophagic signaling independent of the ULK1 complex.” Autophagy 2018. 14 (7):1201-1213. Corona AK, Saulsbery HM, Corona Velazquez AF, Jackson WT. “Enteroviruses remodel autophagic trafficking through regulation of host SNARE proteins to promote virus replication and cell exit.” Cell Reports 2018. 22 (12): 3304-3314. Singh RK, Lall N, Leedahl TS, McGillivray A, Mandal T, Haldar M, Mallik S, Cook G, Srivastava DK.
    [Show full text]
  • Identification of Key Mirna‑Mrna Pairs in Septic Mice by Bioinformatics Analysis
    3858 MOLECULAR MEDICINE REPORTS 20: 3858-3866, 2019 Identification of key miRNA‑mRNA pairs in septic mice by bioinformatics analysis JIANXIN CHEN1,2, MIN LIN3 and SEN ZHANG1 1Department of Colorectal Surgery, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi 530021; 2The First Department of Gastrointestinal Surgery, The Affiliated Hospital of Putian University; 3School of Information Engineering, Putian University, Putian, Fujian 351100, P.R. China Received April 11, 2019; Accepted July 26, 2019 DOI: 10.3892/mmr.2019.10594 Abstract. Sepsis is one of the most common causes of death Introduction among critically ill patients in intensive care units worldwide; however, the microRNAs (miRNAs/miRs) involved in the Sepsis is defined as a life‑threatening organ dysfunction caused sepsis process (and their target genes) are largely unknown. by a dysregulated host response to an infection (1). Sepsis is The present study integrated miRNA and mRNA datasets particularly lethal as it often follows a linear continuum from to elucidate key sepsis-related miRNA‑mRNA pairs. The systemic inflammatory response syndrome through to septic datasets, GSE74952 and GSE55238 were downloaded from shock and organ function failure (2-4). Despite advancements the Gene Expression Omnibus. By performing bioinformatics in antibiotic therapy, immunotherapy and resuscitative strate- analysis such as GEO2R, miRNA target gene prediction, Gene gies, sepsis remains the leading cause of death in intensive Ontology analysis, Kyoto Encyclopedia of Genes and Genomes care units (5). pathway analysis and miRNA‑mRNA network analysis, a total In the pathophysiological process of sepsis, certain gene of four sepsis-related miRNA‑mRNA pairs were successfully expression levels markedly change in vivo and contribute to obtained.
    [Show full text]
  • The H2BG53D Oncohistone Directly Upregulates ANXA3 Transcription and Enhances Cell Migration in Pancreatic Ductal Adenocarcinoma
    Signal Transduction and Targeted Therapy www.nature.com/sigtrans LETTER OPEN The H2BG53D oncohistone directly upregulates ANXA3 transcription and enhances cell migration in pancreatic ductal adenocarcinoma Signal Transduction and Targeted Therapy (2020) 5:106; https://doi.org/10.1038/s41392-020-00219-2 Dear Editor, when compared with the randomly shuffled peaks with the same Histones are essential proteins in compacting genomic DNA length of G53D peaks (Fig. 1f). A significant number of the and regulating gene expression. Previous studies on histone H3 promoter-bound G53D peaks co-localized with open chromatin oncohistones in pediatric brain cancers1,2 and chondroblastoma3, regions (Fig. 1g) as revealed by ATAC-seq (Fig. 1e), suggesting that documented the transcriptomic reprogramming through the these G53D-H2B enriched regions might impact gene transcrip- alterations of histone modifications. We recently reported the tion. However, the majority of the G53D peaks at intergenic region identification of a novel cancer associated mutation, the H2BG53- and gene bodies are not located at open chromatin regions, to-D in pancreatic ductal adenocarcinoma (PDAC)4. We showed indicating that the G53D mutant H2B might have additional that the H2BG53D mutation weakens the interaction between effects on the chromatin. When correlating the genomic distribu- nucleosomal DNA and histone octamer, subsequently enhances tion of G53D peaks (Fig. 1e–g) to gene expression changes 1234567890();,: transcription in vitro. We further showed that cells expressing the (Fig. 1a–d), we found that only a small proportion of the genes G53D mutant H2B acquired oncogenic phenotypes in our CRISPR- with promoter enrichment of G53D had increased gene expres- Cas9 knock-in model.
    [Show full text]
  • High Functioning Autism with Missense
    International Journal of Molecular Sciences Article High Functioning Autism with Missense Mutations in Synaptotagmin-Like Protein 4 (SYTL4) and Transmembrane Protein 187 (TMEM187) Genes: SYTL4- Protein Modeling, Protein-Protein Interaction, Expression Profiling and MicroRNA Studies Syed K. Rafi 1,* , Alberto Fernández-Jaén 2 , Sara Álvarez 3, Owen W. Nadeau 4 and Merlin G. Butler 1,* 1 Departments of Psychiatry & Behavioral Sciences and Pediatrics, University of Kansas Medical Center, Kansas City, KS 66160, USA 2 Department of Pediatric Neurology, Hospital Universitario Quirón, 28223 Madrid, Spain 3 Genomics and Medicine, NIM Genetics, 28108 Madrid, Spain 4 Department of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, KS 66160, USA * Correspondence: rafi[email protected] (S.K.R.); [email protected] (M.G.B.); Tel.: +816-787-4366 (S.K.R.); +913-588-1800 (M.G.B.) Received: 25 March 2019; Accepted: 17 June 2019; Published: 9 July 2019 Abstract: We describe a 7-year-old male with high functioning autism spectrum disorder (ASD) and maternally-inherited rare missense variant of Synaptotagmin-like protein 4 (SYTL4) gene (Xq22.1; c.835C>T; p.Arg279Cys) and an unknown missense variant of Transmembrane protein 187 (TMEM187) gene (Xq28; c.708G>T; p. Gln236His). Multiple in-silico predictions described in our study indicate a potentially damaging status for both X-linked genes. Analysis of predicted atomic threading models of the mutant and the native SYTL4 proteins suggest a potential structural change induced by the R279C variant which eliminates the stabilizing Arg279-Asp60 salt bridge in the N-terminal half of the SYTL4, affecting the functionality of the protein’s critical RAB-Binding Domain.
    [Show full text]
  • 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.
    [Show full text]
  • Distinct Localization of SNAP47 Protein in Gabaergic and Glutamatergic Neurons in the Mouse and the Rat Hippocampus
    ORIGINAL RESEARCH published: 13 July 2017 doi: 10.3389/fnana.2017.00056 Distinct Localization of SNAP47 Protein in GABAergic and Glutamatergic Neurons in the Mouse and the Rat Hippocampus Agnieszka Münster-Wandowski 1*, Heike Heilmann 1, Felix Bolduan 1, Thorsten Trimbuch 2, Yuchio Yanagawa 3 and Imre Vida 1,4* 1Institute of Integrative Neuroanatomy, Charité—Universitätsmedizin Berlin, Berlin, Germany, 2Institute of Neurophysiology, Charité—Universitätsmedizin Berlin, Berlin, Germany, 3Departments of Genetic and Behavioral Neuroscience, Gunma University, Graduate School of Medicine, Maebashi City, Japan, 4Neurocure Cluster of Excellence, Charité—Universitätsmedizin Berlin, Berlin, Germany Synaptosomal-associated protein of 47 kDa (SNAP47) isoform is an atypical member of the SNAP family, which does not contribute directly to exocytosis and synaptic vesicle (SV) recycling. Initial characterization of SNAP47 revealed a widespread expression in nervous tissue, but little is known about its cellular and subcellular localization in hippocampal neurons. Therefore, in the present study we applied multiple- immunofluorescence labeling, immuno-electron microscopy and in situ hybridization (ISH) and analyzed the localization of SNAP47 in pre- and postsynaptic compartments of glutamatergic and GABAergic neurons in the mouse and rat hippocampus. While the immunofluorescence signal for SNAP47 showed a widespread distribution in both mouse and rat, the labeling pattern was complementary in the two species: in the mouse the immunolabeling was higher over the CA3 stratum radiatum, oriens and cell body Edited by: Jackson Cioni Bittencourt, layer. In contrast, in the rat the labeling was stronger over the CA1 neuropil and in the University of São Paulo, Brazil CA3 stratum lucidum. Furthermore, in the mouse high somatic labeling for SNAP47 was Reviewed by: observed in GABAergic interneurons (INs).
    [Show full text]