DOCSLIB.ORG

Supplementary Data

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Supplementary Data Figure 2S 4 7 A - C 080125 CSCs 080418 CSCs - + IFN-a 48 h + IFN-a 48 h + IFN-a 72 h 6 + IFN-a 72 h 3 5 MRFI 4 2 3 2 1 1 0 0 MHC I MHC II MICA MICB ULBP-1 ULBP-2 ULBP-3 ULBP-4 MHC I MHC II MICA MICB ULBP-1 ULBP-2 ULBP-3 ULBP-4 7 B 13 080125 FBS - D 080418 FBS - + IFN-a 48 h 12 + IFN-a 48 h + IFN-a 72 h + IFN-a 72 h 6 080125 FBS 11 10 5 9 8 4 7 6 3 MRFI 5 4 2 3 2 1 1 0 0 MHC I MHC II MICA MICB ULBP-1 ULBP-2 ULBP-3 ULBP-4 MHC I MHC II MICA MICB ULBP-1 ULBP-2 ULBP-3 ULBP-4 Molecule Molecule FIGURE 4S FIGURE 5S Panel A Panel B FIGURE 6S A B C D Supplemental Results Table 1S. Modulation by IFN-α of APM in GBM CSC and FBS tumor cell lines. Molecule * Cell line IFN-α‡ HLA β2-m# HLA LMP TAP1 TAP2 class II A A HC§ 2 7 10 080125 CSCs - 1∞ (1) 3 (65) 2 (91) 1 (2) 6 (47) 2 (61) 1 (3) 1 (2) 1 (3) + 2 (81) 11 (80) 13 (99) 1 (3) 8 (88) 4 (91) 1 (2) 1 (3) 2 (68) 080125 FBS - 2 (81) 4 (63) 4 (83) 1 (3) 6 (80) 3 (67) 2 (86) 1 (3) 2 (75) + 2 (99) 14 (90) 7 (97) 5 (75) 7 (100) 6 (98) 2 (90) 1 (4) 3 (87) 080418 CSCs - 2 (51) 1 (1) 1 (3) 2 (47) 2 (83) 2 (54) 1 (4) 1 (2) 1 (3) + 2 (81) 3 (76) 5 (75) 2 (50) 2 (83) 3 (71) 1 (3) 2 (87) 1 (2) 080418 FBS - 1 (3) 3 (70) 2 (88) 1 (4) 3 (87) 2 (76) 1 (3) 1 (3) 1 (2) + 2 (78) 7 (98) 5 (99) 2 (94) 5 (100) 3 (100) 1 (4) 2 (100) 1 (2) 070104 CSCs - 1 (2) 1 (3) 1 (3) 2 (78) 1 (3) 1 (2) 1 (3) 1 (3) 1 (2) + 2 (98) 8 (100) 10 (88) 4 (89) 3 (98) 3 (94) 1 (4) 2 (86) 2 (79) * expression of APM molecules was evaluated by intracellular staining and cytofluorimetric analysis; ‡ cells were treatead or not (+/-) for 72 h with 1000 IU/ml of IFN-α; # β-2 microglobulin; § β-2 microglobulin-free HLA-A heavy chain; ∞ values are indicated as ratio between the mean of fluorescence intensity of cells stained with the selected mAb and that of the negative control; bold values indicate significant MRFI (≥ 2). The numbers in parenthesis represent the percentage of positive cells. The experiment has been repeated three times; SD for each value ≥ 0.8 ≤ 4. Table 2S . Expression of proteasome and APM-associated chaperon molecules in GBM CSC and FBS tumor cell lines. Cell line Molecule * Delta MB1 Z Calnexin Calreticulin ERp57 Tapasin 0627 CSCs 7 ‡ (100) 1 (3) 1 (5) 20 (100) 2 (92) 2 (67) 2 (86) 0627 FBS 1 (1) 1 (2) 1 (3) 3 (99) 1 (3) 1 (2) 1 (2) 080125 CSCs 16 (85) 1 (2) 1 (2) 49 (99) 2 (85) 1 (3) 2 (99) 080125 FBS 1 (5) 1 (4) 1 (5) 28 (100) 3 (95) 1 (2) 1 (3) 080418 CSCs 8 (100) 1 (5) 1 (4) 13 (100) 2 (99) 1 (5) 1 (4) 080418 FBS 7 (89) 1 (5) 1 (4) 16 (98) 3 (98) 1 (3) 1 (5) 080201 CSCs 36 (99) 3 (98) 3 (98) 55 (100) 10 (98) 3 (98) 7 (97) 080201 FBS 16 (98) 3 (98) 6 (98) 80 (100) 9 (98) 2 (97) 5 (98) 071011 CSCs 17 (98) 3 (87) 3 (75) 100 (100) 15 (98) 3 (87) 7 (76) 071011 FBS 16 (100) 1 (4) 2 (87) 20 (100) 4 (87) 1 (3) 2 (98) 080325 CSCs 10 (98) 3 (98) 4 (98) 200 (100) 5 (99) 2 (95) 5 (98) 070104 CSCs 1 (3) 2 (93) 1 (4) 52 (100) 2 (88) 1 (4) 1 (3) 1869 EBV-B 2 (99) 3 (89) 2 (82) 100 (91) 2 (94) 2 (81) 2 (70) * expression of APM molecules was evaluated by immunofluorescence on permeabilized cells and cytofluorimetric analysis; ‡ values are indicated as ratio between the mean of fluorescence intensity of cells stained with the selected mAb and that of the negative control; bold values indicate significant MRFI (≥ 2). The numbers in parenthesis represent the percentage of positive cells. The experiment has been repeated three times; SD for each value ≥ 1.2 ≤ 4. Table 3S . Modulation by IFN-α of the expression of proteasome and APM-associated chaperon molecules in GBM CSC and FBS tumor cell lines. Molecule * Cell line IFN-α ‡ Delta MB1 Z Calnexin Calreticulin ERp57 Tapasin 080125 CSCs - 16# (85) 1 (2) 1 (5) 49 (100) 2 (95) 1 (2) 2 (3) + 22 (100) 1 (3) 1 (4) 73 (100) 2 (100) 1 (2) 2 (2) 080125 FBS - 1 (5) 1 (4) 1 (5) 28 (100) 3 (95) 1 (2) 1 (3) + 10 (99) 1 (2) 2 (99) 30 (100) 3 (98) 2 (89) 1 (2) 080418 CSCs - 8 (100) 1 (5) 1 (4) 13 (100) 2 (99) 1 (5) 1 (4) + 8 (100) 1 (4) 1 (3) 13 (100) 3 (100) 8 (99) 1 (3) 080418 FBS - 7 (89) 1 (5) 1 (4) 16 (98) 3 (98) 1 (3) 1 (5) + 9 (100) 1 (3) 1 (3) 26 (100) 3 (99) 1 (2) 1 (3) 070104 CSCs - 1 (3) 2 (93) 1 (4) 52 (100) 2 (88) 1 (4) 1 (3) + 13 (99) 1 (3) 1 (4) 27 (100) 3 (98) 1 (3) 1 (3) * expression of APM molecules was evaluated by immunofluorescence on permeabilized cells and cytofluorimetric analysis; ‡ cells were treatead or not (+/-) for 72 h with 1000 IU/ml of IFN-α; # values are indicated as ratio between the mean of fluorescence intensity of cells stained with the selected mAb and that of the negative control; bold values indicate significant MRFI (≥ 2). The numbers in parenthesis represent the percentage of positive cells. The experiment has been repeated three times; SD for each value ≥ 1 ≤ 4. Table 4S. Modulation of MHC and APM molecules by 5-Aza CdR treatment of GBM and FBS tumor cell lines Cell line 5-Aza-CdR * Molecule ‡ MHC II MICA MB1 LMP10 TAP1 080125 CSCs - 1# (2) 1 (4) 1 (2) 1 (3) 1 (2) + 1 (2) 1 (3) 2 (98) 1 (3) 1 (3) 080125 FBS - 1 (2) 3 (95) 1 (3) 1 (4) 1 (2) + 1 (3) 3 (98) 3 (90) 2 (80) 2 (88) 080418 CSCs - 1 (2) 1 (2) 1 (5) 1 (4) 1 (3) + 1 (3) 1 (3) 1 (3) 1 (3) 1 (2) 080418 FBS - 1 (3) 3 (95) 3 (98) 4 (97) 1 (3) + 1 (3) 4 (99) 6 (100) 6 (100) 6 (99) 070104 - 2 (18) 1 (3) 2 (93) 1 (3) 1 (3) + 5 (87) 1 (4) 2 (97) 1 (2) 1 (3) 1869 EBV-B - 12 (96) 1 (3) 3 (89) 3 (91) 4 (95) + 20 (100) 1 (3) 5 (100) 4 (100) 8 (100) * 5-Aza-2'-deoxycytidine (5μM) was added to culture medium for 4 days; ‡ molecule expression was assessed by surface (MHC II and MICA) or intracellular staining (MIB, LMP10 and TAP1) of cells with specific antibodies (see Material and Methods) and cytofluorimetric analysis. # values are indicated as ratio between the mean of fluorescence intensity of cells stained with the selected mAb and that of the negative control; bold values indicate significant MRFI (≥ 2). The numbers in parenthesis represent the percentage of positive cells. The experiment has been repeated three times; SD for each value ≥ 1 ≤ 4. Table 5S. Expression of immune response inhibitory molecules by GBM CSC or FBS tumor cell lines Cell line Molecule* CTLA-4 PD-1 PD-L1 PD-L2 070104 CSC 2‡ (69) 5 (95) 12 (98) 1 (4) 080125 CSCs 2 (81) 2 (94) 10 (99) 1 (3) 080125 FBS 2 (65) 3 (96) 19 (99) 2 (70) 080418 CSCs 2 (55) 2 (85) 7 (99) 1 (2) 080418 FBS 1 (5) 1 (2) 9 (98) 1 (3) 080201 CSCs 2 (77) 3 (95) 11 (99) 1 (3) 080201 FBS 2 (95) 2 (97) 31 (98) 2 (93) 071011 CSCs 2 (42) 2 (59) 4 (97) 1 (2) 071011 FBS 1 (5) 1 (4) 2 (50) 1 (3) 080325 CSCs 2 (62) 2 (56) 4 (94) 1 (3) SW480 col 2 (59) 2 (80) 6 (98) 1 (1) 1061 mel 2 (54) 1 (1) 6 (99) 1 (2) 1869 EBV-B 1 (1) 2 (83) 5 (97) 1 (2) * expression of the indicated molecules was evaluated by immunofluorescence and cytofluorimetric analysis; ‡ values are indicated as ratio between the mean of fluorescence intensity of cells stained with the selected mAb and that of the negative control (MRFI); bold values indicate significant MRFI (≥ 2). The numbers in parenthesis represent the percentage of positive cells. The experiment has been repeated three times with SD for each value ≥ 0.6 ≤ 4. SW480 col and 1061 mel, that are a colorectal and a melanoma cell lines, respectively, were used in the experiment as not GBM tumor cells. Table 6S. Genes differentially expressed between CSC and FBS, p<0.005. Genes are ranked according to fold change. Fold- Paramet Permutati change Gene symbol Description UG cluster ric p- on p-value (CSC/FB value S) oligodendrocyte transcription OLIG1 factor 1 (OLIG1), mRNA.
Load more

Recommended publications
  • Supplementary Materials: Evaluation of Cytotoxicity and Α-Glucosidase Inhibitory Activity of Amide and Polyamino-Derivatives of Lupane Triterpenoids
    Supplementary Materials: Evaluation of cytotoxicity and α-glucosidase inhibitory activity of amide and polyamino-derivatives of lupane triterpenoids Oxana B. Kazakova1*, Gul'nara V. Giniyatullina1, Akhat G. Mustafin1, Denis A. Babkov2, Elena V. Sokolova2, Alexander A. Spasov2* 1Ufa Institute of Chemistry of the Ufa Federal Research Centre of the Russian Academy of Sciences, 71, pr. Oktyabrya, 450054 Ufa, Russian Federation 2Scientific Center for Innovative Drugs, Volgograd State Medical University, Novorossiyskaya st. 39, Volgograd 400087, Russian Federation Correspondence Prof. Dr. Oxana B. Kazakova Ufa Institute of Chemistry of the Ufa Federal Research Centre of the Russian Academy of Sciences 71 Prospeсt Oktyabrya Ufa, 450054 Russian Federation E-mail: [email protected] Prof. Dr. Alexander A. Spasov Scientific Center for Innovative Drugs of the Volgograd State Medical University 39 Novorossiyskaya st. Volgograd, 400087 Russian Federation E-mail: [email protected] Figure S1. 1H and 13C of compound 2. H NH N H O H O H 2 2 Figure S2. 1H and 13C of compound 4. NH2 O H O H CH3 O O H H3C O H 4 3 Figure S3. Anticancer screening data of compound 2 at single dose assay 4 Figure S4. Anticancer screening data of compound 7 at single dose assay 5 Figure S5. Anticancer screening data of compound 8 at single dose assay 6 Figure S6. Anticancer screening data of compound 9 at single dose assay 7 Figure S7. Anticancer screening data of compound 12 at single dose assay 8 Figure S8. Anticancer screening data of compound 13 at single dose assay 9 Figure S9. Anticancer screening data of compound 14 at single dose assay 10 Figure S10.
    [Show full text]
  • Genomic Alterations of Ground-Glass Nodular Lung Adenocarcinoma
    www.nature.com/scientificreports OPEN Genomic alterations of ground- glass nodular lung adenocarcinoma Hyun Lee1, Je-Gun Joung2, Hyun-Tae Shin2, Duk-Hwan Kim3, Yujin Kim3, Hojoong Kim1, O. Jung Kwon1, Young Mog Shim4, Ho Yun Lee5, Kyung Soo Lee5, Yoon-La Choi6, 2 7 1 Received: 1 February 2018 Woong-Yang Park , D. Neil Hayes & Sang-Won Um Accepted: 30 April 2018 In-depth molecular pathogenesis of ground-glass nodular lung adenocarcinoma has not been well Published: xx xx xxxx understood. The objectives of this study were to identify genomic alterations in ground-glass nodular lung adenocarcinomas and to investigate whether viral transcripts were detected in these tumors. Nine patients with pure (n = 4) and part-solid (n = 5) ground-glass nodular adenocarcinomas were included. Six were females with a median age of 58 years. We performed targeted exon sequencing and RNA sequencing. EGFR (n = 10), IDH2 (n = 2), TP53 (n = 1), PTEN (n = 1), EPHB4 (n = 1), and BRAF (n = 1) were identifed as driver mutations by targeted exon sequencing. Vasculogenesis-associated genes including NOTCH4 and TGFBR3 expression were signifcantly downregulated in adenocarcinoma tissue versus normal tissue (adjusted P values < 0.001 for both NOTCH4 and TGFBR3). In addition, fve novel fusion gene loci were identifed in four lung adenocarcinomas. However, no signifcant virus-associated transcripts were detected in tumors. In conclusions, EGFR, IDH2, TP53, PTEN, EPHB4, and BRAF were identifed as putative driver mutations of ground-glass nodular adenocarcinomas. Five novel fusion genes were also identifed in four tumors. Viruses do not appear to be involved in the tumorigenesis of ground-glass nodular lung adenocarcinoma.
    [Show full text]
  • The Oviductal Extracellular Vesicles' RNA Cargo Regulates the Bovine
    International Journal of Molecular Sciences Article The Oviductal Extracellular Vesicles’ RNA Cargo Regulates the Bovine Embryonic Transcriptome Stefan Bauersachs 1 , Pascal Mermillod 2 and Carmen Almiñana 1,2,* 1 Genetics and Functional Genomics, VetSuisse Faculty Zurich, University of Zurich, 8315 Lindau (ZH), Switzerland; [email protected] 2 UMR85 PRC, INRA, CNRS 7247, Université de Tours, IFCE, 37380 Nouzilly, France; [email protected] * Correspondence: [email protected] Received: 21 January 2020; Accepted: 12 February 2020; Published: 14 February 2020 Abstract: Oviductal extracellular vesicles (oEVs) are emerging as key players in the gamete/embryo–oviduct interactions that contribute to successful pregnancy. Various positive effects of oEVs on gametes and early embryos have been found in vitro. To determine whether these effects are associated with changes of embryonic gene expression, the transcriptomes of embryos supplemented with bovine fresh (FeEVs) or frozen (FoEVs) oEVs during in vitro culture compared to controls without oEVs were analyzed by low-input RNA sequencing. Analysis of RNA-seq data revealed 221 differentially expressed genes (DEGs) between FoEV treatment and control, 67 DEGs for FeEV and FoEV treatments, and minor differences between FeEV treatment and control (28 DEGs). An integrative analysis of mRNAs and miRNAs contained in oEVs obtained in a previous study with embryonic mRNA alterations pointed to direct effects of oEV cargo on embryos (1) by increasing the concentration of delivered transcripts; (2) by translating delivered mRNAs to proteins that regulate embryonic gene expression; and (3) by oEV-derived miRNAs which downregulate embryonic mRNAs or modify gene expression in other ways. Our study provided the first high-throughput analysis of the embryonic transcriptome regulated by oEVs, increasing our knowledge on the impact of oEVs on the embryo and revealing the oEV RNA components that potentially regulate embryonic development.
    [Show full text]
  • (12) United States Patent (10) Patent No.: US 9.284.609 B2 Tomlins Et Al
    USOO9284609B2 (12) United States Patent (10) Patent No.: US 9.284.609 B2 Tomlins et al. (45) Date of Patent: Mar. 15, 2016 (54) RECURRENT GENE FUSIONS IN PROSTATE 4,683, 195 A 7, 1987 Mullis et al. CANCER 4,683.202 A 7, 1987 Mullis et al. 4,800,159 A 1/1989 Mullis et al. 4,873,191 A 10/1989 Wagner et al. (75) Inventors: Scott Tomlins, Ann Arbor, MI (US); 4,965,188 A 10/1990 Mullis et al. Daniel Rhodes, Ann Arbor, MI (US); 4,968,103 A 1 1/1990 McNab et al. Arul Chinnaiyan, Ann Arbor, MI (US); 5,130,238 A 7, 1992 Malek et al. Rohit Mehra, Ann Arbor, MI (US); 5,225,326 A 7/1993 Bresser 5,270,184 A 12/1993 Walker et al. Mark Rubin New York, NY (US); 5,283,174. A 2/1994 Arnold, Jr. et al. Xiao-Wei Sun, New York, NY (US); 5,283,317. A 2/1994 Saifer et al. Sven Perner, Ellwaugen (DE); Charles 5,399,491 A 3, 1995 Kacian et al. Lee, Marlborough, MA (US); Francesca 5,455,166 A 10/1995 Walker Demichelis, New York, NY (US) 5,480,784. A 1/1996 Kacian et al. s s 5,545,524 A 8, 1996 Trent 5,614,396 A 3/1997 Bradley et al. (73) Assignees: THE BRIGHAMAND WOMENS 5,631, 169 A 5/1997 Lakowicz et al. HOSPITAL, INC., Boston, MA (US); 5,710,029 A 1/1998 Ryder et al. THE REGENTS OF THE 5,776,782 A 7/1998 Tsuji UNIVERSITY OF MICHIGAN, Ann 5,814,447 A 9/1998 Ishiguro et al.
    [Show full text]
  • Mouse Lsm10 Knockout Project (CRISPR/Cas9)
    https://www.alphaknockout.com Mouse Lsm10 Knockout Project (CRISPR/Cas9) Objective: To create a Lsm10 knockout Mouse model (C57BL/6J) by CRISPR/Cas-mediated genome engineering. Strategy summary: The Lsm10 gene (NCBI Reference Sequence: NM_138721 ; Ensembl: ENSMUSG00000050188 ) is located on Mouse chromosome 4. 2 exons are identified, with the ATG start codon in exon 2 and the TGA stop codon in exon 2 (Transcript: ENSMUST00000055575). Exon 2 will be selected as target site. Cas9 and gRNA will be co-injected into fertilized eggs for KO Mouse production. The pups will be genotyped by PCR followed by sequencing analysis. Note: Exon 2 starts from about 0.27% of the coding region. Exon 2 covers 100.0% of the coding region. The size of effective KO region: ~366 bp. The KO region does not have any other known gene. Page 1 of 8 https://www.alphaknockout.com Overview of the Targeting Strategy Wildtype allele 5' gRNA region gRNA region 3' 1 2 Legends Exon of mouse Lsm10 Knockout region Page 2 of 8 https://www.alphaknockout.com Overview of the Dot Plot (up) Window size: 15 bp Forward Reverse Complement Sequence 12 Note: The 2000 bp section upstream of start codon is aligned with itself to determine if there are tandem repeats. Tandem repeats are found in the dot plot matrix. The gRNA site is selected outside of these tandem repeats. Overview of the Dot Plot (down) Window size: 15 bp Forward Reverse Complement Sequence 12 Note: The 2000 bp section downstream of stop codon is aligned with itself to determine if there are tandem repeats.
    [Show full text]
  • The Capacity of Long-Term in Vitro Proliferation of Acute Myeloid
    The Capacity of Long-Term in Vitro Proliferation of Acute Myeloid Leukemia Cells Supported Only by Exogenous Cytokines Is Associated with a Patient Subset with Adverse Outcome Annette K. Brenner, Elise Aasebø, Maria Hernandez-Valladares, Frode Selheim, Frode Berven, Ida-Sofie Grønningsæter, Sushma Bartaula-Brevik and Øystein Bruserud Supplementary Material S2 of S31 Table S1. Detailed information about the 68 AML patients included in the study. # of blasts Viability Proliferation Cytokine Viable cells Change in ID Gender Age Etiology FAB Cytogenetics Mutations CD34 Colonies (109/L) (%) 48 h (cpm) secretion (106) 5 weeks phenotype 1 M 42 de novo 241 M2 normal Flt3 pos 31.0 3848 low 0.24 7 yes 2 M 82 MF 12.4 M2 t(9;22) wt pos 81.6 74,686 low 1.43 969 yes 3 F 49 CML/relapse 149 M2 complex n.d. pos 26.2 3472 low 0.08 n.d. no 4 M 33 de novo 62.0 M2 normal wt pos 67.5 6206 low 0.08 6.5 no 5 M 71 relapse 91.0 M4 normal NPM1 pos 63.5 21,331 low 0.17 n.d. yes 6 M 83 de novo 109 M1 n.d. wt pos 19.1 8764 low 1.65 693 no 7 F 77 MDS 26.4 M1 normal wt pos 89.4 53,799 high 3.43 2746 no 8 M 46 de novo 26.9 M1 normal NPM1 n.d. n.d. 3472 low 1.56 n.d. no 9 M 68 MF 50.8 M4 normal D835 pos 69.4 1640 low 0.08 n.d.
    [Show full text]
  • Análise Integrativa De Perfis Transcricionais De Pacientes Com
    UNIVERSIDADE DE SÃO PAULO FACULDADE DE MEDICINA DE RIBEIRÃO PRETO PROGRAMA DE PÓS-GRADUAÇÃO EM GENÉTICA ADRIANE FEIJÓ EVANGELISTA Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas Ribeirão Preto – 2012 ADRIANE FEIJÓ EVANGELISTA Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas Tese apresentada à Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo para obtenção do título de Doutor em Ciências. Área de Concentração: Genética Orientador: Prof. Dr. Eduardo Antonio Donadi Co-orientador: Prof. Dr. Geraldo A. S. Passos Ribeirão Preto – 2012 AUTORIZO A REPRODUÇÃO E DIVULGAÇÃO TOTAL OU PARCIAL DESTE TRABALHO, POR QUALQUER MEIO CONVENCIONAL OU ELETRÔNICO, PARA FINS DE ESTUDO E PESQUISA, DESDE QUE CITADA A FONTE. FICHA CATALOGRÁFICA Evangelista, Adriane Feijó Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas. Ribeirão Preto, 2012 192p. Tese de Doutorado apresentada à Faculdade de Medicina de Ribeirão Preto da Universidade de São Paulo. Área de Concentração: Genética. Orientador: Donadi, Eduardo Antonio Co-orientador: Passos, Geraldo A. 1. Expressão gênica – microarrays 2. Análise bioinformática por module maps 3. Diabetes mellitus tipo 1 4. Diabetes mellitus tipo 2 5. Diabetes mellitus gestacional FOLHA DE APROVAÇÃO ADRIANE FEIJÓ EVANGELISTA Análise integrativa de perfis transcricionais de pacientes com diabetes mellitus tipo 1, tipo 2 e gestacional, comparando-os com manifestações demográficas, clínicas, laboratoriais, fisiopatológicas e terapêuticas.
    [Show full text]
  • (A) Co-IP of HA Tagged ARMC9 with Flag Tagged Interactors
    Supplemental Figures Supplemental Figure 1 Validation of ARMC9 interactome. (A) Co-IP of HA tagged ARMC9 with Flag tagged interactors. HA tagged ARMC9 was transfected alone or in conjunction with Flag tagged interactor constructs, HA beads were used to pull down the bait construct and blots were probed for the presence of the Flag tagged interactors. Experiment was performed in biological triplicates. Full blots are viewable in Plemental Figure 10. (B) Single transfection of PalmMyr-CFP-ARMC9 (green) and (C) single transfection of mRFP-TOGARAM1 (red) shows the localization in the absence of the respective interactor. (D) Co-expression of mRFP-TOGARAM1 and PalmMyr-CFP-ARMC9 shows microtubule colocalization. Scale bar indicates 20 μm. 1 Supplemental Figure 2 In silico modeling of the TOG2 variants. (A) Ribbon model of the wild type TOG2 domain structure of TOGARAM1 generated using HOPE. The protein is colored by the following elements: alpha-helices are show in blue, beta-strand is shown in red, turns are green, 3/10 helix is yellow, and random coil is cyan. (B) p. Arg368Trp missense variant in the TOG2 domain in ribbon-presentation generated using HOPE. TOG2 is shown in grey, the side chain of the mutated residue is shown in magenta. (C) A close up of the side chain of both wild type and mutated residue is shown in green and red respectively. (D) Inverted view of wild type TOG2 domain structure of TOGARAM1 as compared to (a). (E) p.Leu375Pro missense variant modeled in the TOG2 domain of TOGARAM1 in ribbon-presentation. TOG2 is shown in grey, the side chain of the mutated residue is shown in magenta.
    [Show full text]
  • Noelia Díaz Blanco
    Effects of environmental factors on the gonadal transcriptome of European sea bass (Dicentrarchus labrax), juvenile growth and sex ratios Noelia Díaz Blanco Ph.D. thesis 2014 Submitted in partial fulfillment of the requirements for the Ph.D. degree from the Universitat Pompeu Fabra (UPF). This work has been carried out at the Group of Biology of Reproduction (GBR), at the Department of Renewable Marine Resources of the Institute of Marine Sciences (ICM-CSIC). Thesis supervisor: Dr. Francesc Piferrer Professor d’Investigació Institut de Ciències del Mar (ICM-CSIC) i ii A mis padres A Xavi iii iv Acknowledgements This thesis has been made possible by the support of many people who in one way or another, many times unknowingly, gave me the strength to overcome this "long and winding road". First of all, I would like to thank my supervisor, Dr. Francesc Piferrer, for his patience, guidance and wise advice throughout all this Ph.D. experience. But above all, for the trust he placed on me almost seven years ago when he offered me the opportunity to be part of his team. Thanks also for teaching me how to question always everything, for sharing with me your enthusiasm for science and for giving me the opportunity of learning from you by participating in many projects, collaborations and scientific meetings. I am also thankful to my colleagues (former and present Group of Biology of Reproduction members) for your support and encouragement throughout this journey. To the “exGBRs”, thanks for helping me with my first steps into this world. Working as an undergrad with you Dr.
    [Show full text]
  • An Integrated Genomic Analysis of Gene-Function Correlation on Schizophrenia Susceptibility Genes
    Journal of Human Genetics (2010) 55, 285–292 & 2010 The Japan Society of Human Genetics All rights reserved 1434-5161/10 $32.00 www.nature.com/jhg ORIGINAL ARTICLE An integrated genomic analysis of gene-function correlation on schizophrenia susceptibility genes Tearina T Chu and Ying Liu Schizophrenia is a highly complex inheritable disease characterized by numerous genetic susceptibility elements, each contributing a modest increase in risk for the disease. Although numerous linkage or association studies have identified a large set of schizophrenia-associated loci, many are controversial. In addition, only a small portion of these loci overlaps with the large cumulative pool of genes that have shown changes of expression in schizophrenia. Here, we applied a genomic gene-function approach to identify susceptibility loci that show direct effect on gene expression, leading to functional abnormalities in schizophrenia. We carried out an integrated analysis by cross-examination of the literature-based susceptibility loci with the schizophrenia-associated expression gene list obtained from our previous microarray study (Journal of Human Genetics (2009) 54: 665–75) using bioinformatic tools, followed by confirmation of gene expression changes using qPCR. We found nine genes (CHGB, SLC18A2, SLC25A27, ESD, C4A/C4B, TCP1, CHL1 and CTNNA2) demonstrate gene-function correlation involving: synapse and neurotransmission; energy metabolism and defense mechanisms; and molecular chaperone and cytoskeleton. Our findings further support the roles of these genes in genetic influence and functional consequences on the development of schizophrenia. It is interesting to note that four of the nine genes are located on chromosome 6, suggesting a special chromosomal vulnerability in schizophrenia.
    [Show full text]
  • Quantigene Flowrna Probe Sets Currently Available
    QuantiGene FlowRNA Probe Sets Currently Available Accession No. Species Symbol Gene Name Catalog No. NM_003452 Human ZNF189 zinc finger protein 189 VA1-10009 NM_000057 Human BLM Bloom syndrome VA1-10010 NM_005269 Human GLI glioma-associated oncogene homolog (zinc finger protein) VA1-10011 NM_002614 Human PDZK1 PDZ domain containing 1 VA1-10015 NM_003225 Human TFF1 Trefoil factor 1 (breast cancer, estrogen-inducible sequence expressed in) VA1-10016 NM_002276 Human KRT19 keratin 19 VA1-10022 NM_002659 Human PLAUR plasminogen activator, urokinase receptor VA1-10025 NM_017669 Human ERCC6L excision repair cross-complementing rodent repair deficiency, complementation group 6-like VA1-10029 NM_017699 Human SIDT1 SID1 transmembrane family, member 1 VA1-10032 NM_000077 Human CDKN2A cyclin-dependent kinase inhibitor 2A (melanoma, p16, inhibits CDK4) VA1-10040 NM_003150 Human STAT3 signal transducer and activator of transcripton 3 (acute-phase response factor) VA1-10046 NM_004707 Human ATG12 ATG12 autophagy related 12 homolog (S. cerevisiae) VA1-10047 NM_000737 Human CGB chorionic gonadotropin, beta polypeptide VA1-10048 NM_001017420 Human ESCO2 establishment of cohesion 1 homolog 2 (S. cerevisiae) VA1-10050 NM_197978 Human HEMGN hemogen VA1-10051 NM_001738 Human CA1 Carbonic anhydrase I VA1-10052 NM_000184 Human HBG2 Hemoglobin, gamma G VA1-10053 NM_005330 Human HBE1 Hemoglobin, epsilon 1 VA1-10054 NR_003367 Human PVT1 Pvt1 oncogene homolog (mouse) VA1-10061 NM_000454 Human SOD1 Superoxide dismutase 1, soluble (amyotrophic lateral sclerosis 1 (adult))
    [Show full text]
  • Genomic Signatures of Recent Adaptive Divergence in the Swamp Sparrow (Melospiza Georgiana)
    GENOMIC SIGNATURES OF RECENT ADAPTIVE DIVERGENCE IN THE SWAMP SPARROW (MELOSPIZA GEORGIANA) A Dissertation Presented to the Faculty of the Graduate School of Cornell University In Partial Fulfillment of the Requirements for the Degree of Doctor of Philosophy by Petra Elizabeth Deane December 2017 © 2017 Petra Elizabeth Deane GENOMIC SIGNATURES OF RECENT ADAPTIVE DIVERGENCE IN THE SWAMP SPARROW (MELOSPIZA GEORGIANA) Petra Elizabeth Deane, Ph. D. Cornell University 2017 Populations that have recently diverged across sharp environmental gradients provide an opportunity to study the mechanisms by which natural selection drives adaptive divergence. Inland and coastal populations of the North American swamp sparrow (Melospiza georgiana) have become an emerging model system for studies of natural selection because they are morphologically and behaviorally distinct despite a very recent divergence time (<15,000 years), yet common garden experiments have demonstrated a genetic basis for their differences. I characterized genomic patterns of variation within and between inland and coastal swamp sparrows via reduced representation sequencing and demonstrated that background genomic differentiation (FST=0.02) and divergence (ΦST=0.05) between these populations is very low, rendering signatures of natural selection highly detectable (max FST=0.8). I then sequenced and assembled a de novo reference genome for the species and conducted a scan for genes involved in coastal adaptation, particularly the evolution of a deeper bill, darker plumage, and tolerance for salinity. I recovered a multigenic snapshot of adaptation via robust signatures of selection at 31 genes. As in Darwin’s finches, bone morphogenetic protein (BMP) signaling appears responsible for changes in bill depth, a putative magic trait for ecological speciation.
    [Show full text]