EPLIN (LIMA1) (NM 016357) Human Tagged ORF Clone – RG211066

Total Page:16

File Type:pdf, Size:1020Kb

EPLIN (LIMA1) (NM 016357) Human Tagged ORF Clone – RG211066 OriGene Technologies, Inc. 9620 Medical Center Drive, Ste 200 Rockville, MD 20850, US Phone: +1-888-267-4436 [email protected] EU: [email protected] CN: [email protected] Product datasheet for RG211066 EPLIN (LIMA1) (NM_016357) Human Tagged ORF Clone Product data: Product Type: Expression Plasmids Product Name: EPLIN (LIMA1) (NM_016357) Human Tagged ORF Clone Tag: TurboGFP Symbol: LIMA1 Synonyms: EPLIN; LDLCQ8; SREBP3 Vector: pCMV6-AC-GFP (PS100010) E. coli Selection: Ampicillin (100 ug/mL) Cell Selection: Neomycin This product is to be used for laboratory only. Not for diagnostic or therapeutic use. View online » ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 1 / 4 EPLIN (LIMA1) (NM_016357) Human Tagged ORF Clone – RG211066 ORF Nucleotide >RG211066 representing NM_016357 Sequence: Red=Cloning site Blue=ORF Green=Tags(s) TTTTGTAATACGACTCACTATAGGGCGGCCGGGAATTCGTCGACTGGATCCGGTACCGAGGAGATCTGCC GCCGCGATCGCC ATGGAATCATCTCCATTTAATAGACGGCAATGGACCTCACTATCATTGAGGGTAACAGCCAAAGAACTTT CTCTTGTCAACAAGAACAAGTCATCGGCTATTGTGGAAATATTCTCCAAGTACCAGAAAGCAGCTGAAGA AACAAACATGGAGAAGAAGAGAAGTAACACCGAAAATCTCTCCCAGCACTTTAGAAAGGGGACCCTGACT GTGTTAAAGAAGAAGTGGGAGAACCCAGGGCTGGGAGCAGAGTCTCACACAGACTCTCTACGGAACAGCA GCACTGAGATTAGGCACAGAGCAGACCATCCTCCTGCTGAAGTGACAAGCCACGCTGCTTCTGGAGCCAA AGCTGACCAAGAAGAACAAATCCACCCCAGATCTAGACTCAGGTCACCTCCTGAAGCCCTCGTTCAGGGT CGATATCCCCACATCAAGGACGGTGAGGATCTTAAAGACCACTCAACAGAAAGTAAAAAAATGGAAAATT GTCTAGGAGAATCCAGGCATGAAGTAGAAAAATCAGAAATCAGTGAAAACACAGATGCTTCGGGCAAAAT AGAGAAATATAATGTTCCGCTGAACAGGCTTAAGATGATGTTTGAGAAAGGTGAACCAACTCAAACTAAG ATTCTCCGGGCCCAAAGCCGAAGTGCAAGTGGAAGGAAGATCTCTGAAAACAGCTATTCTCTAGATGACC TGGAAATAGGCCCAGGTCAGTTGTCATCTTCTACATTTGACTCGGAGAAAAATGAGAGTAGACGAAATCT GGAACTTCCACGCCTCTCAGAAACCTCTATAAAGGATCGAATGGCCAAGTACCAGGCAGCTGTGTCCAAA CAAAGCAGCTCAACCAACTATACAAATGAGCTGAAAGCCAGTGGTGGCGAAATCAAAATTCATAAAATGG AGCAAAAGGAGAATGTGCCCCCAGGTCCTGAGGTCTGCATCACCCATCAGGAAGGGGAAAAGATTTCTGC AAATGAGAATAGCCTGGCAGTCCGTTCCACCCCTGCCGAAGATGACTCCCGTGACTCCCAGGTTAAGAGT GAGGTTCAACAGCCTGTCCATCCCAAGCCACTAAGTCCAGATTCCAGAGCCTCCAGTCTTTCTGAAAGTT CTCCTCCCAAAGCAATGAAGAAGTTTCAGGCACCTGCAAGAGAGACCTGCGTGGAATGTCAGAAGACAGT CTATCCAATGGAGCGTCTCTTGGCCAACCAGCAGGTGTTTCACATCAGCTGCTTCCGTTGCTCCTATTGC AACAACAAACTCAGTCTAGGAACATATGCATCTTTACATGGAAGAATCTATTGTAAGCCTCACTTCAATC AACTCTTTAAATCTAAGGGCAACTATGATGAAGGCTTTGGGCACAGACCACACAAGGATCTATGGGCAAG CAAAAATGAAAACGAAGAGATTTTGGAGAGACCAGCCCAGCTTGCAAATGCAAGGGAGACCCCTCACAGC CCAGGGGTAGAAGATGCCCCTATTGCTAAGGTGGGTGTCCTGGCTGCAAGTATGGAAGCCAAGGCCTCCT CTCAGCAGGAGAAGGAAGACAAGCCAGCTGAAACCAAGAAGCTGAGGATCGCCTGGCCACCCCCCACTGA ACTTGGAAGTTCAGGAAGTGCCTTGGAGGAAGGGATCAAAATGTCAAAGCCCAAATGGCCTCCTGAAGAC GAAATCAGCAAGCCCGAAGTTCCTGAGGATGTCGATCTAGATCTGAAGAAGCTAAGACGATCTTCTTCAC TGAAGGAAAGAAGCCGCCCATTCACTGTAGCAGCTTCATTTCAAAGCACCTCTGTCAAGAGCCCAAAAAC TGTGTCCCCACCTATCAGGAAAGGCTGGAGCATGTCAGAGCAGAGTGAAGAGTCTGTGGGTGGAAGAGTT GCAGAAAGGAAACAAGTGGAAAATGCCAAGGCTTCTAAGAAGAATGGGAATGTGGGAAAAACAACCTGGC AAAACAAAGAATCTAAAGGAGAGACAGGGAAGAGAAGTAAGGAAGGTCATAGTTTGGAGATGGAGAATGA GAATCTTGTAGAAAATGGTGCAGACTCCGATGAAGATGATAACAGCTTCCTCAAACAACAATCTCCACAA GAACCCAAGTCTCTGAATTGGTCGAGTTTTGTAGACAACACCTTTGCTGAAGAATTCACTACTCAGAATC AGAAATCCCAGGATGTGGAACTCTGGGAGGGAGAAGTGGTCAAAGAGCTCTCTGTGGAAGAACAGATAAA GAGAAATCGGTATTATGATGAGGATGAGGATGAAGAG ACGCGTACGCGGCCGCTCGAG - GFP Tag - GTTTAA This product is to be used for laboratory only. Not for diagnostic or therapeutic use. ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 2 / 4 EPLIN (LIMA1) (NM_016357) Human Tagged ORF Clone – RG211066 Protein Sequence: >RG211066 representing NM_016357 Red=Cloning site Green=Tags(s) MESSPFNRRQWTSLSLRVTAKELSLVNKNKSSAIVEIFSKYQKAAEETNMEKKRSNTENLSQHFRKGTLT VLKKKWENPGLGAESHTDSLRNSSTEIRHRADHPPAEVTSHAASGAKADQEEQIHPRSRLRSPPEALVQG RYPHIKDGEDLKDHSTESKKMENCLGESRHEVEKSEISENTDASGKIEKYNVPLNRLKMMFEKGEPTQTK ILRAQSRSASGRKISENSYSLDDLEIGPGQLSSSTFDSEKNESRRNLELPRLSETSIKDRMAKYQAAVSK QSSSTNYTNELKASGGEIKIHKMEQKENVPPGPEVCITHQEGEKISANENSLAVRSTPAEDDSRDSQVKS EVQQPVHPKPLSPDSRASSLSESSPPKAMKKFQAPARETCVECQKTVYPMERLLANQQVFHISCFRCSYC NNKLSLGTYASLHGRIYCKPHFNQLFKSKGNYDEGFGHRPHKDLWASKNENEEILERPAQLANARETPHS PGVEDAPIAKVGVLAASMEAKASSQQEKEDKPAETKKLRIAWPPPTELGSSGSALEEGIKMSKPKWPPED EISKPEVPEDVDLDLKKLRRSSSLKERSRPFTVAASFQSTSVKSPKTVSPPIRKGWSMSEQSEESVGGRV AERKQVENAKASKKNGNVGKTTWQNKESKGETGKRSKEGHSLEMENENLVENGADSDEDDNSFLKQQSPQ EPKSLNWSSFVDNTFAEEFTTQNQKSQDVELWEGEVVKELSVEEQIKRNRYYDEDEDEE TRTRPLE - GFP Tag - V Restriction Sites: SgfI-MluI Cloning Scheme: This product is to be used for laboratory only. Not for diagnostic or therapeutic use. ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 3 / 4 EPLIN (LIMA1) (NM_016357) Human Tagged ORF Clone – RG211066 Plasmid Map: ACCN: NM_016357 ORF Size: 2277 bp OTI Disclaimer: The molecular sequence of this clone aligns with the gene accession number as a point of reference only. However, individual transcript sequences of the same gene can differ through naturally occurring variations (e.g. polymorphisms), each with its own valid existence. This clone is substantially in agreement with the reference, but a complete review of all prevailing variants is recommended prior to use. More info OTI Annotation: This clone was engineered to express the complete ORF with an expression tag. Expression varies depending on the nature of the gene. RefSeq: NM_016357.5 RefSeq Size: 3664 bp RefSeq ORF: 2280 bp Locus ID: 51474 UniProt ID: Q9UHB6 Domains: LIM Gene Summary: This gene encodes a cytoskeleton-associated protein that inhibits actin filament depolymerization and cross-links filaments in bundles. It is downregulated in some cancer cell lines. Alternatively spliced transcript variants encoding different isoforms have been described for this gene, and expression of some of the variants maybe independently regulated. [provided by RefSeq, Aug 2011] This product is to be used for laboratory only. Not for diagnostic or therapeutic use. ©2021 OriGene Technologies, Inc., 9620 Medical Center Drive, Ste 200, Rockville, MD 20850, US 4 / 4.
Recommended publications
  • Epithelial Protein Lost in Neoplasm a (Eplin-A) Is Transcriptionally Regulated by G-Actin and MAL/MRTF Coactivators
    Leitner et al. Molecular Cancer 2010, 9:60 http://www.molecular-cancer.com/content/9/1/60 SHORT COMMUNICATION Open Access Epithelial Protein Lost in Neoplasm a (Eplin-a)is transcriptionally regulated by G-actin and MAL/MRTF coactivators Laura Leitner1, Dmitry Shaposhnikov1, Arnaud Descot1, Reinhard Hoffmann2, Guido Posern1* Abstract Epithelial Protein Lost in Neoplasm a is a novel cytoskeleton-associated tumor suppressor whose expression inver- sely correlates with cell growth, motility, invasion and cancer mortality. Here we show that Eplin-a transcription is regulated by actin-MAL-SRF signalling. Upon signal induction, the coactivator MAL/MRTF is released from a repres- sive complex with monomeric actin, binds the transcription factor SRF and activates target gene expression. In a transcriptome analysis with a combination of actin binding drugs which specifically and differentially interfere with the actin-MAL complex (Descot et al., 2009), we identified Eplin to be primarily controlled by monomeric actin. Further analysis revealed that induction of the Eplin-a mRNA and its promoter was sensitive to drugs and mutant actins which stabilise the repressive actin-MAL complex. In contrast, the Eplin-b isoform remained unaffected. Knockdown of MRTFs or dominant negative MAL which inhibits SRF-mediated transcription impaired Eplin-a expression. Conversely, constitutively active mutant actins and MAL induced Eplin-a. MAL and SRF were bound to a consensus SRF binding site of the Eplin-a promoter; the recruitment of MAL to this region was enhanced sever- alfold upon induction. The tumor suppressor Eplin-a is thus a novel cytoskeletal target gene transcriptionally regu- lated by the actin-MAL-SRF pathway, which supports a role in cancer biology.
    [Show full text]
  • LIMA1 Antibody (N-Term) Blocking Peptide Synthetic Peptide Catalog # Bp16362a
    10320 Camino Santa Fe, Suite G San Diego, CA 92121 Tel: 858.875.1900 Fax: 858.622.0609 LIMA1 Antibody (N-term) Blocking Peptide Synthetic peptide Catalog # BP16362a Specification LIMA1 Antibody (N-term) Blocking Peptide LIMA1 Antibody (N-term) Blocking Peptide - - Background Product Information EPLIN is a cytoskeleton-associated protein that Primary Accession Q9UHB6 inhibitsactin filament depolymerization and cross-links filaments inbundles (Maul et al., 2003 [PubMed 12566430]). LIMA1 Antibody (N-term) Blocking Peptide - Additional Information LIMA1 Antibody (N-term) Blocking Peptide - References Gene ID 51474 Chircop, M., et al. Cell Cycle Other Names 8(5):757-764(2009)Abe, K., et al. Proc. Natl. LIM domain and actin-binding protein 1, Acad. Sci. U.S.A. 105(1):13-19(2008)Jiang, Epithelial protein lost in neoplasm, LIMA1, W.G., et al. Mol. Cancer 7, 71 (2008) EPLIN, SREBP3 :Sugiyama, N., et al. Mol. Cell Proteomics 6(6):1103-1109(2007)Olsen, J.V., et al. Cell Format Peptides are lyophilized in a solid powder 127(3):635-648(2006) format. Peptides can be reconstituted in solution using the appropriate buffer as needed. Storage Maintain refrigerated at 2-8°C for up to 6 months. For long term storage store at -20°C. Precautions This product is for research use only. Not for use in diagnostic or therapeutic procedures. LIMA1 Antibody (N-term) Blocking Peptide - Protein Information Name LIMA1 (HGNC:24636) Function Actin-binding protein involved in actin cytoskeleton regulation and dynamics. Increases the number and size of actin stress fibers and inhibits membrane ruffling. Inhibits actin filament depolymerization.
    [Show full text]
  • “Subfossil” Koala Lemur Megaladapis Edwardsi
    Evolutionary and phylogenetic insights from a nuclear genome sequence of the extinct, giant, “subfossil” koala lemur Megaladapis edwardsi Stephanie Marciniaka, Mehreen R. Mughalb, Laurie R. Godfreyc, Richard J. Bankoffa, Heritiana Randrianatoandroa,d, Brooke E. Crowleye,f, Christina M. Bergeya,g,h, Kathleen M. Muldooni, Jeannot Randrianasyd, Brigitte M. Raharivololonad, Stephan C. Schusterj, Ripan S. Malhik,l, Anne D. Yoderm,n, Edward E. Louis Jro,1, Logan Kistlerp,1, and George H. Perrya,b,g,q,1 aDepartment of Anthropology, Pennsylvania State University, University Park, PA 16802; bBioinformatics and Genomics Intercollege Graduate Program, Pennsylvania State University, University Park, PA 16082; cDepartment of Anthropology, University of Massachusetts, Amherst, MA 01003; dMention Anthropobiologie et Développement Durable, Faculté des Sciences, Université d’Antananarivo, Antananarivo 101, Madagascar; eDepartment of Geology, University of Cincinnati, Cincinnati, OH 45220; fDepartment of Anthropology, University of Cincinnati, Cincinnati, OH 45220; gDepartment of Biology, Pennsylvania State University, University Park, PA 16802; hDepartment of Genetics, Rutgers University, New Brunswick, NJ 08854; iDepartment of Anatomy, Midwestern University, Glendale, AZ 85308; jSingapore Centre for Environmental Life Sciences Engineering, Nanyang Technological University, Singapore 639798; kDepartment of Anthropology, University of Illinois Urbana–Champaign, Urbana, IL 61801; lDepartment of Ecology, Evolution and Behavior, Carl R. Woese Institute for
    [Show full text]
  • 1 Supporting Information for a Microrna Network Regulates
    Supporting Information for A microRNA Network Regulates Expression and Biosynthesis of CFTR and CFTR-ΔF508 Shyam Ramachandrana,b, Philip H. Karpc, Peng Jiangc, Lynda S. Ostedgaardc, Amy E. Walza, John T. Fishere, Shaf Keshavjeeh, Kim A. Lennoxi, Ashley M. Jacobii, Scott D. Rosei, Mark A. Behlkei, Michael J. Welshb,c,d,g, Yi Xingb,c,f, Paul B. McCray Jr.a,b,c Author Affiliations: Department of Pediatricsa, Interdisciplinary Program in Geneticsb, Departments of Internal Medicinec, Molecular Physiology and Biophysicsd, Anatomy and Cell Biologye, Biomedical Engineeringf, Howard Hughes Medical Instituteg, Carver College of Medicine, University of Iowa, Iowa City, IA-52242 Division of Thoracic Surgeryh, Toronto General Hospital, University Health Network, University of Toronto, Toronto, Canada-M5G 2C4 Integrated DNA Technologiesi, Coralville, IA-52241 To whom correspondence should be addressed: Email: [email protected] (M.J.W.); yi- [email protected] (Y.X.); Email: [email protected] (P.B.M.) This PDF file includes: Materials and Methods References Fig. S1. miR-138 regulates SIN3A in a dose-dependent and site-specific manner. Fig. S2. miR-138 regulates endogenous SIN3A protein expression. Fig. S3. miR-138 regulates endogenous CFTR protein expression in Calu-3 cells. Fig. S4. miR-138 regulates endogenous CFTR protein expression in primary human airway epithelia. Fig. S5. miR-138 regulates CFTR expression in HeLa cells. Fig. S6. miR-138 regulates CFTR expression in HEK293T cells. Fig. S7. HeLa cells exhibit CFTR channel activity. Fig. S8. miR-138 improves CFTR processing. Fig. S9. miR-138 improves CFTR-ΔF508 processing. Fig. S10. SIN3A inhibition yields partial rescue of Cl- transport in CF epithelia.
    [Show full text]
  • Generation of a Conditional Lima1a Allele in Zebrafish Using the Flex Switch Technology
    Generation of a conditional lima1a allele in zebrafish using the FLEx switch technology Peggy Jungke§, Stefan Hans§*, Mansi Gupta, Anja Machate, Daniela Zöller, Michael Brand* Biotechnology Center and Center for Regenerative Therapies Dresden, Dresden University of Technology, Tatzberg 47-49, 01307 Dresden, Germany § Contributed equally. * Corresponding authors: [email protected] [email protected] Running Title: FLEx technology in zebrafish Key words: conditional alleles; FLEx switch; Lima1a; zebrafish 1 Abstract Gene trapping has emerged as a valuable tool to create conditional alleles in various model organisms. Here we report the FLEx-based gene trap vector SAGFLEx that allows the generation of conditional mutations in zebrafish by gene-trap mutagenesis. The SAGFLEx gene trap cassette comprises the rabbit β-globin splice acceptor and the coding sequence of GFP, flanked by pairs of inversely oriented heterotypic target sites for the site-specific recombinases Cre and Flp. Insertion of the gene-trap cassette into endogenous genes can result in conditional mutations that are stably inverted by Cre and Flp, respectively. To test the functionality of this system we performed a pilot screen and analyzed the insertion of the gene-trap cassette into the lima1a gene locus. In this lima1a allele, GFP expression faithfully recapitulated the endogenous lima1a expression and resulted in a complete knockout of the gene in homozygosity. Application of either Cre or Flp was able to mediate the stable inversion of the gene trap cassette and showed the ability to conditionally rescue or reintroduce the gene inactivation. Combined with pharmacologically inducible site specific recombinases the SAGFLEx vector insertions will enable precise conditional knockout studies in a spatial- and temporal-controlled manner.
    [Show full text]
  • S41467-020-18249-3.Pdf
    ARTICLE https://doi.org/10.1038/s41467-020-18249-3 OPEN Pharmacologically reversible zonation-dependent endothelial cell transcriptomic changes with neurodegenerative disease associations in the aged brain Lei Zhao1,2,17, Zhongqi Li 1,2,17, Joaquim S. L. Vong2,3,17, Xinyi Chen1,2, Hei-Ming Lai1,2,4,5,6, Leo Y. C. Yan1,2, Junzhe Huang1,2, Samuel K. H. Sy1,2,7, Xiaoyu Tian 8, Yu Huang 8, Ho Yin Edwin Chan5,9, Hon-Cheong So6,8, ✉ ✉ Wai-Lung Ng 10, Yamei Tang11, Wei-Jye Lin12,13, Vincent C. T. Mok1,5,6,14,15 &HoKo 1,2,4,5,6,8,14,16 1234567890():,; The molecular signatures of cells in the brain have been revealed in unprecedented detail, yet the ageing-associated genome-wide expression changes that may contribute to neurovas- cular dysfunction in neurodegenerative diseases remain elusive. Here, we report zonation- dependent transcriptomic changes in aged mouse brain endothelial cells (ECs), which pro- minently implicate altered immune/cytokine signaling in ECs of all vascular segments, and functional changes impacting the blood–brain barrier (BBB) and glucose/energy metabolism especially in capillary ECs (capECs). An overrepresentation of Alzheimer disease (AD) GWAS genes is evident among the human orthologs of the differentially expressed genes of aged capECs, while comparative analysis revealed a subset of concordantly downregulated, functionally important genes in human AD brains. Treatment with exenatide, a glucagon-like peptide-1 receptor agonist, strongly reverses aged mouse brain EC transcriptomic changes and BBB leakage, with associated attenuation of microglial priming. We thus revealed tran- scriptomic alterations underlying brain EC ageing that are complex yet pharmacologically reversible.
    [Show full text]
  • (BPA) Exposure Biomarkers in Ovarian Cancer
    Journal of Clinical Medicine Article Identification of Potential Bisphenol A (BPA) Exposure Biomarkers in Ovarian Cancer Aeman Zahra 1, Qiduo Dong 1, Marcia Hall 1,2 , Jeyarooban Jeyaneethi 1, Elisabete Silva 1, Emmanouil Karteris 1,* and Cristina Sisu 1,* 1 Biosciences, College of Health, Medicine and Life Sciences, Brunel University London, Uxbridge UB8 3PH, UK; [email protected] (A.Z.); [email protected] (Q.D.); [email protected] (M.H.); [email protected] (J.J.); [email protected] (E.S.) 2 Mount Vernon Cancer Centre, Northwood HA6 2RN, UK * Correspondence: [email protected] (E.K.); [email protected] (C.S.) Abstract: Endocrine-disrupting chemicals (EDCs) can exert multiple deleterious effects and have been implicated in carcinogenesis. The xenoestrogen Bisphenol A (BPA) that is found in various consumer products has been involved in the dysregulation of numerous signalling pathways. In this paper, we present the analysis of a set of 94 genes that have been shown to be dysregulated in presence of BPA in ovarian cancer cell lines since we hypothesised that these genes might be of biomarker potential. This study sought to identify biomarkers of disease and biomarkers of disease- associated exposure. In silico analyses took place using gene expression data extracted from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) databases. Differential expression was further validated at protein level using immunohistochemistry on an ovarian cancer tissue microarray. We found that 14 out of 94 genes are solely dysregulated in the presence of BPA, while the remaining 80 genes are already dysregulated (p-value < 0.05) in their expression pattern Citation: Zahra, A.; Dong, Q.; Hall, as a consequence of the disease.
    [Show full text]
  • Supplementary Materials
    Supplementary materials Supplementary Table S1: MGNC compound library Ingredien Molecule Caco- Mol ID MW AlogP OB (%) BBB DL FASA- HL t Name Name 2 shengdi MOL012254 campesterol 400.8 7.63 37.58 1.34 0.98 0.7 0.21 20.2 shengdi MOL000519 coniferin 314.4 3.16 31.11 0.42 -0.2 0.3 0.27 74.6 beta- shengdi MOL000359 414.8 8.08 36.91 1.32 0.99 0.8 0.23 20.2 sitosterol pachymic shengdi MOL000289 528.9 6.54 33.63 0.1 -0.6 0.8 0 9.27 acid Poricoic acid shengdi MOL000291 484.7 5.64 30.52 -0.08 -0.9 0.8 0 8.67 B Chrysanthem shengdi MOL004492 585 8.24 38.72 0.51 -1 0.6 0.3 17.5 axanthin 20- shengdi MOL011455 Hexadecano 418.6 1.91 32.7 -0.24 -0.4 0.7 0.29 104 ylingenol huanglian MOL001454 berberine 336.4 3.45 36.86 1.24 0.57 0.8 0.19 6.57 huanglian MOL013352 Obacunone 454.6 2.68 43.29 0.01 -0.4 0.8 0.31 -13 huanglian MOL002894 berberrubine 322.4 3.2 35.74 1.07 0.17 0.7 0.24 6.46 huanglian MOL002897 epiberberine 336.4 3.45 43.09 1.17 0.4 0.8 0.19 6.1 huanglian MOL002903 (R)-Canadine 339.4 3.4 55.37 1.04 0.57 0.8 0.2 6.41 huanglian MOL002904 Berlambine 351.4 2.49 36.68 0.97 0.17 0.8 0.28 7.33 Corchorosid huanglian MOL002907 404.6 1.34 105 -0.91 -1.3 0.8 0.29 6.68 e A_qt Magnogrand huanglian MOL000622 266.4 1.18 63.71 0.02 -0.2 0.2 0.3 3.17 iolide huanglian MOL000762 Palmidin A 510.5 4.52 35.36 -0.38 -1.5 0.7 0.39 33.2 huanglian MOL000785 palmatine 352.4 3.65 64.6 1.33 0.37 0.7 0.13 2.25 huanglian MOL000098 quercetin 302.3 1.5 46.43 0.05 -0.8 0.3 0.38 14.4 huanglian MOL001458 coptisine 320.3 3.25 30.67 1.21 0.32 0.9 0.26 9.33 huanglian MOL002668 Worenine
    [Show full text]
  • Redalyc.Detection of Genes Providing Salinity-Tolerance in Rice
    Acta Scientiarum. Biological Sciences ISSN: 1679-9283 [email protected] Universidade Estadual de Maringá Brasil da Graça de Souza Lima, Maria; Fernandes Lopes, Nei; Dejalma Zimmer, Paulo; Meneghello, Geri Eduardo; Ferrari, Cibele; Rodrigues Mendes, Cristina Detection of genes providing salinity-tolerance in rice Acta Scientiarum. Biological Sciences, vol. 36, núm. 1, enero-marzo, 2014, pp. 79-85 Universidade Estadual de Maringá .png, Brasil Available in: http://www.redalyc.org/articulo.oa?id=187129844010 How to cite Complete issue Scientific Information System More information about this article Network of Scientific Journals from Latin America, the Caribbean, Spain and Portugal Journal's homepage in redalyc.org Non-profit academic project, developed under the open access initiative Acta Scientiarum http://www.uem.br/acta ISSN printed: 1679-9283 ISSN on-line: 1807-863X Doi: 10.4025/actascibiolsci.v36i1.15437 Detection of genes providing salinity-tolerance in rice Maria da Graça de Souza Lima1*, Nei Fernandes Lopes1, Paulo Dejalma Zimmer2, Geri Eduardo Meneghello2, Cibele Ferrari2 and Cristina Rodrigues Mendes1 1Departamento de Botânica, Instituto de Biologia, Universidade Federal de Pelotas, Campus Universitário Capão do Leão, s/n, 96010-900, Cx. Postal 354, Pelotas, Rio Grande do Sul, Brazil. 2Departamento de Fitotecnia, Faculdade de Agronomia Eliseu Maciel, Universidade Federal de Pelotas, Campus Universitário Capão do Leão, Pelotas, Rio Grande do Sul, Brazil. *Author for correspondence. E-mail: [email protected] ABSTRACT. The present study aimed to identify salinity-tolerant genes in three cultivars (BRS-7 Taim, BRS Querência and BRS Atalanta) of Oryza sativa L. ssp. indica S. Kato and in three cultivars (BRS Bojurú, IAS 12-9 Formosa and Goyakuman) of Oryza sativa L.
    [Show full text]
  • Post-Translational Modifications of the CARMA1-BCL10-MALT1 Complex
    Post-translational Modifications of the CARMA1-BCL10-MALT1 Complex in Lymphocytes and Activated B-cell Like Subtype of Diffuse Large B-cell Lymphoma An Thys, Tiphaine Douanne, Nicolas Bidère To cite this version: An Thys, Tiphaine Douanne, Nicolas Bidère. Post-translational Modifications of the CARMA1- BCL10-MALT1 Complex in Lymphocytes and Activated B-cell Like Subtype of Diffuse Large B-cell Lymphoma. Frontiers in Oncology, Frontiers, In press, Epub ahead of print. 10.3389/fonc.2018.00498. inserm-01908802 HAL Id: inserm-01908802 https://www.hal.inserm.fr/inserm-01908802 Submitted on 30 Oct 2018 HAL is a multi-disciplinary open access L’archive ouverte pluridisciplinaire HAL, est archive for the deposit and dissemination of sci- destinée au dépôt et à la diffusion de documents entific research documents, whether they are pub- scientifiques de niveau recherche, publiés ou non, lished or not. The documents may come from émanant des établissements d’enseignement et de teaching and research institutions in France or recherche français ou étrangers, des laboratoires abroad, or from public or private research centers. publics ou privés. Post-translational Modifications of the CARMA1-BCL10-MALT1 Complex in Lymphocytes and Activated B-cell Like Subtype of Diffuse Large B-cell Lymphoma An Thys1, Tiphaine Douanne1, Nicolas Bidere1* 1 Institut National de la Santé et de la Recherche Médicale (INSERM), France Submitted to Journal: Frontiers in Oncology Specialty Section: Hematologic Malignancies Article type: Review Article Manuscript ID: 423762 Received on: In07 Sepreview 2018 Revised on: 11 Oct 2018 Accepted on: 15 Oct 2018 Frontiers website link: www.frontiersin.org Conflict of interest statement The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest Author contribution statement AT, TD, and NB designed and wrote the review.
    [Show full text]
  • Supplementary Tables S1-S3
    Supplementary Table S1: Real time RT-PCR primers COX-2 Forward 5’- CCACTTCAAGGGAGTCTGGA -3’ Reverse 5’- AAGGGCCCTGGTGTAGTAGG -3’ Wnt5a Forward 5’- TGAATAACCCTGTTCAGATGTCA -3’ Reverse 5’- TGTACTGCATGTGGTCCTGA -3’ Spp1 Forward 5'- GACCCATCTCAGAAGCAGAA -3' Reverse 5'- TTCGTCAGATTCATCCGAGT -3' CUGBP2 Forward 5’- ATGCAACAGCTCAACACTGC -3’ Reverse 5’- CAGCGTTGCCAGATTCTGTA -3’ Supplementary Table S2: Genes synergistically regulated by oncogenic Ras and TGF-β AU-rich probe_id Gene Name Gene Symbol element Fold change RasV12 + TGF-β RasV12 TGF-β 1368519_at serine (or cysteine) peptidase inhibitor, clade E, member 1 Serpine1 ARE 42.22 5.53 75.28 1373000_at sushi-repeat-containing protein, X-linked 2 (predicted) Srpx2 19.24 25.59 73.63 1383486_at Transcribed locus --- ARE 5.93 27.94 52.85 1367581_a_at secreted phosphoprotein 1 Spp1 2.46 19.28 49.76 1368359_a_at VGF nerve growth factor inducible Vgf 3.11 4.61 48.10 1392618_at Transcribed locus --- ARE 3.48 24.30 45.76 1398302_at prolactin-like protein F Prlpf ARE 1.39 3.29 45.23 1392264_s_at serine (or cysteine) peptidase inhibitor, clade E, member 1 Serpine1 ARE 24.92 3.67 40.09 1391022_at laminin, beta 3 Lamb3 2.13 3.31 38.15 1384605_at Transcribed locus --- 2.94 14.57 37.91 1367973_at chemokine (C-C motif) ligand 2 Ccl2 ARE 5.47 17.28 37.90 1369249_at progressive ankylosis homolog (mouse) Ank ARE 3.12 8.33 33.58 1398479_at ryanodine receptor 3 Ryr3 ARE 1.42 9.28 29.65 1371194_at tumor necrosis factor alpha induced protein 6 Tnfaip6 ARE 2.95 7.90 29.24 1386344_at Progressive ankylosis homolog (mouse)
    [Show full text]
  • The Paracaspase MALT1 Cleaves HOIL1 Reducing Linear Ubiquitination by LUBAC to Dampen Lymphocyte NF-Kb Signalling
    ARTICLE Received 27 Jul 2015 | Accepted 2 Oct 2015 | Published 3 Nov 2015 DOI: 10.1038/ncomms9777 OPEN The paracaspase MALT1 cleaves HOIL1 reducing linear ubiquitination by LUBAC to dampen lymphocyte NF-kB signalling Theo Klein1,2,3,*, Shan-Yu Fung4,5,*, Florian Renner6,*,w, Michael A. Blank7, Antoine Dufour1,2, Sohyeong Kang5,8, Madison Bolger-Munro9, Joshua M. Scurll10, John J. Priatel5,8, Patrick Schweigler6, Samu Melkko6, Michael R. Gold9, Rosa I. Viner7, Catherine H. Re´gnier6,**, Stuart E. Turvey4,5,** & Christopher M. Overall1,2,3,** Antigen receptor signalling activates the canonical NF-kB pathway via the CARD11/BCL10/ MALT1 (CBM) signalosome involving key, yet ill-defined roles for linear ubiquitination. The paracaspase MALT1 cleaves and removes negative checkpoint proteins, amplifying lymphocyte responses in NF-kB activation and in B-cell lymphoma subtypes. To identify new human MALT1 substrates, we compare B cells from the only known living MALT1mut/mut patient with healthy MALT1 þ /mut family members using 10-plex Tandem Mass Tag TAILS N-terminal peptide proteomics. We identify HOIL1 of the linear ubiquitin chain assembly complex as a novel MALT1 substrate. We show linear ubiquitination at B-cell receptor microclusters and signalosomes. Late in the NF-kB activation cycle HOIL1 cleavage transiently reduces linear ubiquitination, including of NEMO and RIP1, dampening NF-kB activation and preventing reactivation. By regulating linear ubiquitination, MALT1 is both a positive and negative pleiotropic regulator of the human canonical NF-kB pathway—first promoting activation via the CBM—then triggering HOIL1-dependent negative-feedback termination, preventing reactivation. 1 Department of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, British Columbia, Canada V6T 1Z3.
    [Show full text]