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Supporting Information for Proteomics DOI 10.1002/Pmic.200400942

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Supporting Information for Proteomics DOI 10.1002/pmic.200400942 Wei-Jun Qian, Jon M. Jacobs, David G. Camp II, Matthew E. Monroe, Ronald J. Moore, Marina A. Gritsenko, Steve E. Calvano, Stephen F. Lowry, Wenzhong Xiao, Lyle L. Moldawer, Ronald W. Davis, Ronald G. Tompkins and Richard D. Smith Comparative proteome analyses of human plasma following in vivo lipopolysaccharide administration using multidimensional separations coupled with tandem mass spectrometry ã 2004 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.proteomics-journal.de Supplemental Table 1: List of 804 identified plasma proteins. Note: Reference IDs correspond to either SwissProt, NCBI, or PIR database entries. For each protein, one representive peptide sequence and the peptide charge_state, SEQUEST Xcorr, and Delcn are listed. The number of different peptides identifying each specific protein is also indicated. To facilitate comparison of protein abundances between the untreated and treated samples, the numbers of peptide hit, the protein abundance ratio (treated/untreated) calculated from peptide peak area ratios, and the standard deviation of peptide peak area ratios for each protein are also listed. No abundance ratio is shown if the protein has no common peptide identified in the two samples. Whether the same protein ID was reported in reference 16 and reference 27 (195 proteins observed from two different sources) is also indicated. Reference Description # of different Representitive peptide Charge_state Xcorr DelCn peptides Peptide Hits Peptide Protein Standard ID overlapped with ID overlapped with reference (untreated) hits abundance ratio deviation reference [16]-- Shen et al. [27]-- Anderson et al. SW:ALBU_HUMAN serum albumin precursor 360 K.EFNAETFTFHADICTLSEK.E 1 6.942 1 7858 7141 1.23 0.29 YES YES SW:CO3_HUMAN complement c3 precursor 224 R.IFTVNHK.L 1 6.929 0.597 [contains: c3a anaphylatoxin] 916 848 0.91 0.19 YES YES SW:APB_HUMAN apolipoprotein b-100 precursor 219 K.KLTISEQNIQR.A 1 6.975 1 (apo b-100) [contains: 574 525 1.03 0.44 YES YES SW:A2MG_HUMAN alpha-2-macroglobulin precursor 211 K.KDNSVHWERPQKPK.A 1 5.715 0.526 (alpha-2-m) 1030 959 1.09 0.24 YES YES SW:CO4_HUMAN complement c4 precursor 160 R.NVNFQK.A 1 7.054 0.574 [contains: c4a anaphylatoxin] 532 492 1.06 0.36 YES YES SW:TRFE_HUMAN serotransferrin precursor 150 R.AIAANEADAVTLDAGLVYDAYLAPNN 3 7.436 0.563 (siderophilin) (beta-1-metal 979 998 1.14 0.42 YES YES Reference Description # of different Representitive peptide Charge_state Xcorr DelCn peptides Peptide Hits Peptide Protein Standard ID overlapped with ID overlapped with reference (untreated) hits abundance ratio deviation reference [16]-- Shen et al. [27]-- Anderson et al. SW:FINC_HUMAN fibronectin precursor (fn) (cold- 100 R.TKTETITGFQVDAVPANGQTPIQR.T 1 5.206 0.517 insoluble globulin) (cig) 328 343 1.17 0.45 YES YES SW:A1AT_HUMAN alpha-1-antitrypsin precursor 92 K.LSITGTYDLK.S 1 6.618 0.617 (alpha-1 protease inhibitor) 504 516 1.11 0.46 YES YES SW:CERU_HUMAN ceruloplasmin precursor (ec 1 89 R.SVPPSASHVAPTETFTYEWTVPK.E 1 6.884 0.58 275 307 1.05 0.38 YES YES SW:FIBA_HUMAN fibrinogen alpha/alpha-e chain 83 R.GDFSSANNR.D 1 6.430 0.583 precursor 285 325 1.34 0.37 YES YES SW:FIBG_HUMAN fibrinogen gamma chain 81 K.FFTSHNGMQFSTWDNDNDKFEGN 1 5.993 0.616 precursor 277 276 1.17 0.51 YES SW:FIBB_HUMAN fibrinogen beta chain precursor 81 R.TPCTVSCNIPVVSGK.E 1 6.520 0.565 327 345 1.23 0.43 YES YES SW:VTDB_HUMAN vitamin d-binding protein 68 R.VCSQYAAYGEK.K 1 5.895 0.587 precursor (dbp) (group-specific 188 180 1.28 0.4 YES YES SW:CFAH_HUMAN complement factor h precursor (h 65 K.SPPEISHGVVAHMSDSYQYGEEVTY 1 6.001 0.578 factor 1) 168 166 1.29 0.38 YES YES Reference Description # of different Representitive peptide Charge_state Xcorr DelCn peptides Peptide Hits Peptide Protein Standard ID overlapped with ID overlapped with reference (untreated) hits abundance ratio deviation reference [16]-- Shen et al. [27]-- Anderson et al. SW:APA1_HUMAN apolipoprotein a-i precursor (apo- 63 R.AHVDALR.T 1 3.407 0.429 ai) 282 269 1.12 0.43 YES YES SW:PLMN_HUMAN plasminogen precursor (ec 3 57 K.LSSPAVITDK.V 1 6.902 0.537 106 107 1.19 0.44 YES YES SW:HPTR_HUMAN haptoglobin-related protein 57 K.KQLVEIEK.V 1 5.728 1 precursor 222 216 1.27 0.48 YES SW:HEMO_HUMAN hemopexin precursor (beta-1b- 54 R.GECQAEGVLFFQGDR.E 1 4.730 0.419 glycoprotein) 169 161 1.23 0.33 YES YES SW:ITH4_HUMAN inter-alpha-trypsin inhibitor heavy 53 K.VRPQQLVK.H 1 5.178 0.526 chain h4 precursor 147 127 1.14 0.59 YES YES SW:CFAB_HUMAN complement factor b precursor 53 R.DLLYIGK.D 1 6.242 0.676 (ec 3 127 127 1.12 0.33 YES YES SW:HPT2_HUMAN haptoglobin-2 precursor 52 K.DYAEVGR.V 1 6.203 0.564 337 301 1.64 0.41 YES YES SW:CO5_HUMAN complement c5 precursor 46 K.TLLPVSKPEIR.S 1 5.604 0.525 [contains: c5a anaphylatoxin] 134 107 0.88 0.37 YES YES Reference Description # of different Representitive peptide Charge_state Xcorr DelCn peptides Peptide Hits Peptide Protein Standard ID overlapped with ID overlapped with reference (untreated) hits abundance ratio deviation reference [16]-- Shen et al. [27]-- Anderson et al. SW:ITH2_HUMAN inter-alpha-trypsin inhibitor heavy 41 K.TQVADAK.R 1 2.081 0.302 chain h2 precursor 146 133 0.94 0.33 YES YES SW:C4BP_HUMAN c4b-binding protein alpha chain 40 R.GSSVIHCDADSK.W 1 7.339 0.589 precursor (c4bp) (proline-rich 94 90 1.35 0.48 YES YES SW:A2HS_HUMAN alpha-2-hs-glycoprotein 39 K.AALAAFNAQNNGSNFQLEEISR.A 1 4.231 0.513 precursor (fetuin-a) (alpha-2-z- 155 150 1.18 0.47 YES YES SW:KNG_HUMAN kininogen precursor (alpha-2-thiol 38 K.KYNSQNQSNNQFVLYR.I 1 5.150 0.572 proteinase inhibitor) [contains: 86 83 0.9 0.32 YES YES SW:A1AH_HUMAN alpha-1-acid glycoprotein 2 38 K.SDVVYTDWK.K 1 5.890 0.565 precursor (agp 2) (orosomucoid 2) 163 150 0.95 0.45 YES SW:TTHY_HUMAN transthyretin precursor 37 R.GSPAINVAVHVFR.K 1 5.968 0.52 (prealbumin) (tbpa) (ttr) (attr) 199 190 1.33 0.33 YES YES SW:ITH1_HUMAN inter-alpha-trypsin inhibitor heavy 36 K.QLVHHFEIDVDIFEPQGISK.L 1 6.657 0.536 chain h1 precursor 120 108 1 0.34 YES YES SW:VTNC_HUMAN vitronectin precursor (serum 36 K.PFDAFTDLK.N 1 4.306 0.482 spreading factor) (s-protein) 61 57 0.98 0.28 YES YES Reference Description # of different Representitive peptide Charge_state Xcorr DelCn peptides Peptide Hits Peptide Protein Standard ID overlapped with ID overlapped with reference (untreated) hits abundance ratio deviation reference [16]-- Shen et al. [27]-- Anderson et al. SW:A1BG_HUMAN alpha-1b-glycoprotein 34 R.LETPDFQLFK.N 1 5.732 0.531 126 112 1.19 0.53 YES YES SW:THRB_HUMAN prothrombin precursor (ec 3 34 K.GQPSVLQVVNLPIVER.P 1 6.745 0.595 64 75 1.42 0.32 YES YES SW:GELS_HUMAN gelsolin precursor, plasma (actin- 33 K.FDLVPVPTNLYGDFFTGDAYVILK.T 2 4.156 0.543 depolymerizing factor) (adf) 127 126 0.96 0.33 YES YES SW:APOH_HUMAN beta-2-glycoprotein i precursor 32 K.ATVVYQGER.V 1 5.582 0.514 (apolipoprotein h) (apo-h) (b2gpi) 80 71 1.36 0.4 YES YES SW:HRG_HUMAN histidine-rich glycoprotein 29 K.NLVINCEVFDPQEHENINGVPPHLGH 1 6.094 0.512 precursor (histidine-proline rich 82 85 1.03 0.42 YES YES SW:ANT3_HUMAN antithrombin-iii precursor (atiii) 28 K.ANRPFLVFIR.E 2 3.688 0.213 106 98 0.91 0.31 YES YES SW:AACT_HUMAN alpha-1-antichymotrypsin 27 K.ITLLSALVETR.T 1 7.016 0.587 precursor (act) 94 98 1.19 0.49 YES YES SW:APA4_HUMAN apolipoprotein a-iv precursor 26 K.SLAELGGHLDQQVEEFR.R 1 6.241 0.507 (apo-aiv) 69 49 0.95 0.34 YES YES Reference Description # of different Representitive peptide Charge_state Xcorr DelCn peptides Peptide Hits Peptide Protein Standard ID overlapped with ID overlapped with reference (untreated) hits abundance ratio deviation reference [16]-- Shen et al. [27]-- Anderson et al. SW:IC1_HUMAN plasma protease c1 inhibitor 26 K.YPVAHFIDQTLK.A 1 4.724 0.481 precursor (c1 inh) (c1inh) 70 79 0.95 0.33 YES YES SW:AFAM_HUMAN afamin precursor (alpha-albumin) 25 R.RHPDLSIPELLR.I 1 7.072 0.555 (alpha-alb) 131 100 1.02 0.4 YES YES SW:CO6_HUMAN complement component c6 23 K.IEEADCK.N 1 5.490 0.437 precursor 37 34 1.36 0.18 YES YES SW:APL1_HUMAN apolipoprotein l1 precursor 23 R.ANLQSVPHASASRPR.V 1 5.635 0.613 (apolipoprotein l-i) (apolipoprotein 68 52 1.18 0.38 YES YES PIR1:I38344 titin, cardiac muscle [validated] - 23 K.RVDLIQDLPRVELQIK.E 1 2.584 0.145 human 22 15 0.5 0.31 YES SW:APA2_HUMAN apolipoprotein a-ii precursor 23 K.AGTELVNFLSYFVELGTQPAT.Q 2 5.268 0.407 (apo-aii) (apoa-ii) 184 175 0.75 0.27 YES YES SW:CLUS_HUMAN clusterin precursor (complement- 22 R.IDSLLENDR.Q 1 5.611 0.541 associated protein sp-40,40) 82 80 0.82 0.23 YES YES GP:AF384856_1 Homo sapiens peptidoglycan 19 R.GSQTQSHPDLGTEGCWDQLSAPR.T 1 5.812 0.574 recognition protein L precursor 62 64 1.05 0.32 YES Reference Description # of different Representitive peptide Charge_state Xcorr DelCn peptides Peptide Hits Peptide Protein Standard ID overlapped with ID overlapped with reference (untreated) hits abundance ratio deviation reference [16]-- Shen et al.
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    ARTICLE https://doi.org/10.1038/s41467-020-19177-y OPEN Systematic elucidation of neuron-astrocyte interaction in models of amyotrophic lateral sclerosis using multi-modal integrated bioinformatics workflow Vartika Mishra et al.# 1234567890():,; Cell-to-cell communications are critical determinants of pathophysiological phenotypes, but methodologies for their systematic elucidation are lacking. Herein, we propose an approach for the Systematic Elucidation and Assessment of Regulatory Cell-to-cell Interaction Net- works (SEARCHIN) to identify ligand-mediated interactions between distinct cellular com- partments. To test this approach, we selected a model of amyotrophic lateral sclerosis (ALS), in which astrocytes expressing mutant superoxide dismutase-1 (mutSOD1) kill wild-type motor neurons (MNs) by an unknown mechanism. Our integrative analysis that combines proteomics and regulatory network analysis infers the interaction between astrocyte-released amyloid precursor protein (APP) and death receptor-6 (DR6) on MNs as the top predicted ligand-receptor pair. The inferred deleterious role of APP and DR6 is confirmed in vitro in models of ALS. Moreover, the DR6 knockdown in MNs of transgenic mutSOD1 mice attenuates the ALS-like phenotype. Our results support the usefulness of integrative, systems biology approach to gain insights into complex neurobiological disease processes as in ALS and posit that the proposed methodology is not restricted to this biological context and could be used in a variety of other non-cell-autonomous communication
  • Ultrarare Heterozygous Pathogenic Variants of Genes Causing Dominant Forms of Early-Onset Deafness Underlie Severe Presbycusis

    Ultrarare Heterozygous Pathogenic Variants of Genes Causing Dominant Forms of Early-Onset Deafness Underlie Severe Presbycusis

    Ultrarare heterozygous pathogenic variants of genes causing dominant forms of early-onset deafness underlie severe presbycusis Sophie Bouchera,b,c,d, Fabienne Wong Jun Taia, Sedigheh Delmaghania, Andrea Lellia, Amrit Singh-Estivaleta,b, Typhaine Duponta, Magali Niasme-Grarea,e, Vincent Michela, Nicolas Wolfff, Amel Bahloula, Yosra Bouyacouba, Didier Bouccarag, Bernard Fraysseh, Olivier Deguineh, Lionel Colleti, Hung Thai-Vana,j,k, Eugen Ionescuj, Jean-Louis Kemenyl, Fabrice Giraudetm,n, Jean-Pierre Lavieilleo, Arnaud Devèzeo, Anne-Laure Roudevitch-Pujolp, Christophe Vincentq, Christian Renardr, Valérie Franco-Vidals, Claire Thibult-Apts, Vincent Darrouzets, Eric Bizaguett, Arnaud Coezt,u,v, Hugues Aschardw, Nicolas Michalskia, Gaëlle M. Lefevrea, Anne Auboisp, Paul Avana,m,n,x,1, Crystel Bonneta,b,1, and Christine Petita,y,1,2 aInstitut de l’Audition, Institut Pasteur, INSERM, 75012 Paris, France; bComplexité du Vivant, Sorbonne Universités, Université Pierre et Marie Curie, Université Paris 06, 75005 Paris, France; cCentre Hospitalier Universitaire, Service d’Oto-Rhino-Laryngologie et Chirurgie Cervico-Faciale, 49100 Angers, France; dFaculté de Médecine, Unité de Formation et de Recherche Santé, Université d’Angers, 49100 Angers, France; eService de Biochimie et Biologie Moléculaire, Hôpital d’Enfants Armand-Trousseau, Assistance Publique-Hôpitaux de Paris (AP-HP), 75012 Paris, France; fUnité Récepteurs-Canaux, Institut Pasteur, 75015 Paris, France; gHôpital Beaujon, Hôpitaux Universitaires Paris Nord val-de-Seine, AP-HP, 92110 Clichy,
  • Expansion, Folding, and Abnormal Lamination of the Chick Optic Tectum After Intraventricular Injections of FGF2

    Expansion, Folding, and Abnormal Lamination of the Chick Optic Tectum After Intraventricular Injections of FGF2

    Expansion, folding, and abnormal lamination of the chick optic tectum after intraventricular injections of FGF2 Luke D. McGowan1, Roula A. Alaama, Amanda C. Freise, Johnny C. Huang, Christine J. Charvet, and Georg F. Striedter Department of Neurobiology and Behavior, University of California, Irvine, CA 92697 Edited by John C. Avise, University of California, Irvine, Irvine, CA, and approved May 3, 2012 (received for review February 21, 2012) Comparative research has shown that evolutionary increases in human cortical evolution and expansion in terms of delayed and brain region volumes often involve delays in neurogenesis. How- prolonged precursor proliferation (15, 16). ever, little is known about the influence of such changes on The present study began as an attempt to phenocopy natural subsequent development. To get at this question, we injected variation in telencephalon size among birds. Specifically, we rea- FGF2—which delays cell cycle exit in mammalian neocortex—into soned that FGF2 injections into ventricles of embryonic chicks the cerebral ventricles of chicks at embryonic day (ED) 4. This ma- should, by analogy to the work in mammals (14), increase telen- nipulation alters the development of the optic tectum dramatically. cephalon volume, effectively creating chickens with a telencepha- By ED7, the tectum of FGF2-treated birds is abnormally thin and has lon as large as that of parrots and songbirds (7, 9). However, our a reduced postmitotic layer, consistent with a delay in neurogenesis. FGF2 injections did not significantly alter telencephalon de- FGF2 treatment also increases tectal volume and ventricular surface velopment. Instead, they increased the size of the optic tectum, area, disturbs tectal lamination, and creates small discontinuities disrupted tectal lamination, and created tectal gyri and sulci.