DOCSLIB.ORG

Supplemental Table 1. Genes with at Least 2-Fold Change After 24 H and 72 H Incubation with PD- 0332991 Gene Symbol Description

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Supplemental Table 1. Genes with at Least 2-Fold Change After 24 H and 72 H Incubation with PD- 0332991 Gene Symbol Description Supplemental Table 1. Genes with At Least 2-Fold Change After 24 h and 72 h Incubation with PD- 0332991 AsPC-1 COLO-357 Gene Symbol Description Fold Change Fold Change 24 h 72 h 24 h 72 h CDT1 Homo sapiens chromatin licensing 0.38 0.95 0.39 0.86 and DNA replication factor 1 HMGB2 Homo sapiens high-mobility group 0.36 0.69 0.16 0.37 box 2 FANCI Homo sapiens Fanconi anemia, 0.48 0.98 0.45 0.8 complementation group I STMN1 Homo sapiens stathmin 1 (STMN1) 0.42 0.82 0.23 0.53 FAM116B Homo sapiens family with sequence 2.08 0.73 2 1.58 similarity 116, member B RFC5 Homo sapiens replication factor C 0.5 0.76 0.46 0.58 (activator 1) MCM7 Homo sapiens minichromosome 0.47 0.85 0.48 0.53 maintenance complex component 7 CDC20 Homo sapiens cell division cycle 20 0.5 0.84 0.37 0.56 homolog (S. cerevisiae) (CDC20) NDC80 Homo sapiens NDC80 homolog, 0.45 0.8 0.4 0.69 kinetochore complex component CENPF Homo sapiens centromere protein 0.41 0.81 0.3 0.82 F, 350/400ka (mitosin) TUBB Homo sapiens tubulin, beta 0.5 0.89 0.5 0.72 CDKN3 Homo sapiens cyclin-dependent 0.31 0.66 0.32 0.42 kinase inhibitor 3 CDC45L Homo sapiens CDC45 cell division 0.36 0.96 0.38 0.49 cycle 45-like (S. cerevisiae) RAD51AP1 Homo sapiens RAD51 associated 0.4 0.97 0.34 0.58 protein 1 PSRC1 Homo sapiens proline/serine-rich 0.3 0.7 0.18 0.53 coiled-coil 1 PBK Homo sapiens PDZ binding kinase 0.35 0.95 0.44 0.75 EXO1 Homo sapiens exonuclease 1 0.35 0.99 0.36 0.57 (EXO1) MGC40489 PREDICTED: Homo sapiens 0.37 0.92 0.41 0.69 hypothetical protein MGC40489 RRM2 Homo sapiens ribonucleotide 0.29 1.13 0.29 0.83 reductase M2 polypeptide CDCA5 Homo sapiens cell division cycle 0.44 0.97 0.49 0.73 associated 5 AURKB Homo sapiens aurora kinase B 0.26 0.75 0.2 0.52 KIF2C Homo sapiens kinesin family 0.35 0.76 0.26 0.55 member 2C TOP2A Homo sapiens topoisomerase 0.24 0.82 0.24 0.68 (DNA) II alpha 170kDa PCNA Homo sapiens proliferating cell 0.42 0.92 0.45 0.69 nuclear antigen ASF1B Homo sapiens ASF1 anti-silencing 0.36 0.86 0.38 0.82 function 1 homolog B KIF20A Homo sapiens kinesin family 0.18 0.52 0.11 0.43 member 20A (KIF20A) POLA2 Homo sapiens polymerase (DNA 0.48 0.91 0.49 0.7 directed), alpha 2 (70kD subunit) TTC14 Homo sapiens tetratricopeptide 2.27 2.04 2.27 1.67 repeat domain 14 TROAP Homo sapiens trophinin associated 0.37 0.65 0.23 0.5 protein (tastin) C9orf140 Homo sapiens chromosome 9 open 0.44 0.57 0.42 0.54 reading frame 140 HJURP Homo sapiens Holliday junction 0.25 0.73 0.24 0.7 recognition protein CDCA8 Homo sapiens cell division cycle 0.38 0.84 0.45 0.82 associated 8 FBXO5 Homo sapiens F-box protein 5 0.39 0.87 0.35 0.59 CDC25A Homo sapiens cell division cycle 25 0.41 1.11 0.4 0.79 homolog A (S. pombe) UBE2T Homo sapiens ubiquitin-conjugating 0.39 0.86 0.38 0.58 enzyme E2T (putative) CCNB1 Homo sapiens cyclin B1 0.32 0.81 0.27 0.57 UBE2C Homo sapiens ubiquitin-conjugating 0.35 0.85 0.2 0.55 enzyme E2C (UBE2C) CENPE Homo sapiens centromere protein 0.41 0.84 0.29 0.64 E, 312kDa GMNN Homo sapiens geminin, DNA 0.47 0.9 0.47 0.59 replication inhibitor KPNA2 Homo sapiens karyopherin alpha 2 0.34 0.89 0.37 0.66 (RAG cohort 1, importin alpha 1) CDC25C Homo sapiens cell division cycle 25 0.4 0.77 0.43 0.58 homolog C (S. pombe) NUSAP1 Homo sapiens nucleolar and 0.28 0.68 0.22 0.5 spindle associated protein 1 PRC1 Homo sapiens protein regulator of 0.36 0.96 0.38 0.62 cytokinesis 1 FAM64A Homo sapiens family with sequence 0.42 0.59 0.26 0.61 similarity 64, member A LOC651816 PREDICTED: Homo sapiens similar 0.33 0.89 0.31 0.63 to Ubiquitin-conjugating enzyme E2S PLK1 Homo sapiens polo-like kinase 1 0.39 0.71 0.31 0.57 (Drosophila) CDCA3 Homo sapiens cell division cycle 0.28 0.75 0.15 0.49 associated 3 ANLN Homo sapiens anillin, actin binding 0.5 1.03 0.32 0.62 protein PHF19 Homo sapiens PHD finger protein 0.48 0.88 0.29 0.58 19 (PHF19) CEP55 Homo sapiens centrosomal protein 0.39 0.97 0.4 0.63 55kDa CDC2 Homo sapiens cell division cycle 2, 0.31 0.77 0.34 0.65 G1 to S and G2 to M DLGAP5 Homo sapiens discs, large 0.26 0.65 0.2 0.44 (Drosophila) homolog-associated protein 5 NCAPG Homo sapiens non-SMC condensin 0.29 0.76 0.26 0.51 I complex, subunit G CKAP2L Homo sapiens cytoskeleton 0.37 0.83 0.24 0.74 associated protein 2-like KIF15 Homo sapiens kinesin family 0.48 0.79 0.48 0.54 member 15 FEN1 Homo sapiens flap structure- 0.44 1.11 0.46 0.73 specific endonuclease 1 MXD4 Homo sapiens MAX dimerization 2.33 1.43 4 3.36 protein 4 DONSON Homo sapiens downstream 0.43 0.95 0.41 0.56 neighbor of SON C13orf34 Homo sapiens chromosome 13 0.45 0.63 0.4 0.5 open reading frame 34 LOC399942 PREDICTED: Homo sapiens similar 0.47 0.7 0.33 0.52 to Tubulin alpha-2 chain ABCA1 Homo sapiens ATP-binding 2.27 2.61 2.44 2.28 cassette, sub-family A (ABC1), member 1 TMPO Homo sapiens thymopoietin 0.41 0.78 0.36 0.6 (TMPO), transcript variant 1 RRM1 Homo sapiens ribonucleotide 0.45 0.95 0.44 0.7 reductase M1 polypeptide CCNF Homo sapiens cyclin F (CCNF) 0.28 0.66 0.22 0.47 RDH5 Homo sapiens retinol 2.17 1.1 2.38 1.96 dehydrogenase 5 (11-cis/9-cis) POLE2 Homo sapiens polymerase (DNA 0.43 0.77 0.39 0.49 directed), epsilon 2 (p59 subunit) NCAPD2 Homo sapiens non-SMC condensin 0.3 0.76 0.29 0.62 I complex, subunit D2 E2F2 Homo sapiens E2F transcription 0.35 0.84 0.43 0.72 factor 2 FAM111A Homo sapiens family with sequence 0.47 0.93 0.49 1.05 similarity 111, member A TUBB2C Homo sapiens tubulin, beta 2C 0.38 0.78 0.48 0.83 (TUBB2C) HMMR Homo sapiens hyaluronan- 0.29 0.69 0.22 0.49 mediated motility receptor FAM83D Homo sapiens family with sequence 0.31 0.73 0.25 0.53 similarity 83, member D PRR11 Homo sapiens proline rich 11 0.42 0.85 0.34 0.68 (PRR11) LOC731314 PREDICTED: Homo sapiens similar 0.38 0.77 0.29 0.64 to H2A histone family, member X UHRF1 Homo sapiens ubiquitin-like with 0.47 0.95 0.43 0.64 PHD and ring finger domains 1 CCNA2 Homo sapiens cyclin A2 (CCNA2) 0.22 0.63 0.23 0.46 TTK Homo sapiens TTK protein kinase 0.41 0.8 0.42 0.59 (TTK) KIF11 Homo sapiens kinesin family 0.47 0.68 0.34 0.58 member 11 TPX2 Homo sapiens TPX2, microtubule- 0.33 0.8 0.28 0.68 associated, homolog (Xenopus laevis) KIF4A Homo sapiens kinesin family 0.37 0.79 0.29 0.67 member 4A CENPA Homo sapiens centromere protein 0.25 0.65 0.17 0.5 A (CENPA), transcript variant 2 CCNB2 Homo sapiens cyclin B2 0.35 0.7 0.33 0.47 SLC16A4 Homo sapiens solute carrier family 2.7 1.54 2.44 2.14 16, member 4 TK1 Homo sapiens thymidine kinase 1, 0.36 0.97 0.37 0.56 soluble TYMS Homo sapiens thymidylate 0.29 0.74 0.27 0.69 synthetase KIF14 Homo sapiens kinesin family 0.4 0.73 0.31 0.56 member 14 LOC731049 PREDICTED: Homo sapiens similar 0.4 0.93 0.32 0.61 to Ubiquitin-conjugating enzyme E2S GINS2 Homo sapiens GINS complex 0.29 0.74 0.28 0.6 subunit 2 (Psf2 homolog) KIF23 Homo sapiens kinesin family 0.36 0.86 0.31 0.73 member 23, transcript variant 2 SPC25 Homo sapiens SPC25, NDC80 0.43 0.84 0.24 0.43 kinetochore complex component PTTG1 Homo sapiens pituitary tumor- 0.26 0.73 0.26 0.6 transforming 1 PTTG3P Homo sapiens pituitary tumor- 0.3 0.68 0.25 0.5 transforming 3 (pseudogene) (PTTG3P) NEK2 Homo sapiens NIMA (never in 0.33 0.68 0.29 0.53 mitosis gene a)-related kinase 2 NCAPG2 Homo sapiens non-SMC condensin 0.5 0.95 0.4 0.64 II complex, subunit G2 BARD1 Homo sapiens BRCA1 associated 0.45 0.79 0.44 0.66 RING domain 1 HIST1H4C Homo sapiens histone cluster 1, 0.44 0.8 0.39 0.68 H4c RACGAP1 Homo sapiens Rac GTPase 0.4 0.86 0.36 0.63 activating protein 1 DEPDC1B Homo sapiens DEP domain 0.45 0.65 0.45 0.66 containing 1B LMNB1 Homo sapiens lamin B1 0.27 0.62 0.24 0.47 GPSM2 Homo sapiens G-protein signalling 0.44 0.63 0.33 0.48 modulator 2 (AGS3-like, C.elegans) C15orf23 Homo sapiens chromosome 15 0.47 0.91 0.39 0.54 open reading frame 23 (C15orf23) SPC24 Homo sapiens SPC24, NDC80 0.48 0.67 0.3 0.45 kinetochore complex component OIP5 Homo sapiens Opa interacting 0.49 0.72 0.45 0.51 protein 5 BUB1 Homo sapiens BUB1 budding 0.38 0.67 0.36 0.52 uninhibited by benzimidazoles 1 homolog (yeast) PRIM1 Homo sapiens primase, DNA, 0.4 0.82 0.32 0.49 polypeptide 1 (49kDa) MELK Homo sapiens maternal embryonic 0.43 0.76 0.44 0.52 leucine zipper kinase KIFC1 Homo sapiens kinesin family 0.24 0.7 0.25 0.63 member C1 SMC4 Homo sapiens structural 0.49 0.66 0.36 0.63 maintenance of chromosomes, transcript variant KIAA0101 Homo sapiens KIAA0101, transcript 0.25 0.67 0.26 0.59 variant 1 RPS29 Homo sapiens ribosomal protein 2.13 1.41 2.27 1.53 S29, transcript variant 2, mRNA.
Load more

Recommended publications
  • Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model
    Downloaded from http://www.jimmunol.org/ by guest on September 25, 2021 T + is online at: average * The Journal of Immunology , 34 of which you can access for free at: 2016; 197:1477-1488; Prepublished online 1 July from submission to initial decision 4 weeks from acceptance to publication 2016; doi: 10.4049/jimmunol.1600589 http://www.jimmunol.org/content/197/4/1477 Molecular Profile of Tumor-Specific CD8 Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A. Waugh, Sonia M. Leach, Brandon L. Moore, Tullia C. Bruno, Jonathan D. Buhrman and Jill E. Slansky J Immunol cites 95 articles Submit online. Every submission reviewed by practicing scientists ? is published twice each month by Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts http://jimmunol.org/subscription Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html http://www.jimmunol.org/content/suppl/2016/07/01/jimmunol.160058 9.DCSupplemental This article http://www.jimmunol.org/content/197/4/1477.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 25, 2021. The Journal of Immunology Molecular Profile of Tumor-Specific CD8+ T Cell Hypofunction in a Transplantable Murine Cancer Model Katherine A.
    [Show full text]
  • 1 Metabolic Dysfunction Is Restricted to the Sciatic Nerve in Experimental
    Page 1 of 255 Diabetes Metabolic dysfunction is restricted to the sciatic nerve in experimental diabetic neuropathy Oliver J. Freeman1,2, Richard D. Unwin2,3, Andrew W. Dowsey2,3, Paul Begley2,3, Sumia Ali1, Katherine A. Hollywood2,3, Nitin Rustogi2,3, Rasmus S. Petersen1, Warwick B. Dunn2,3†, Garth J.S. Cooper2,3,4,5* & Natalie J. Gardiner1* 1 Faculty of Life Sciences, University of Manchester, UK 2 Centre for Advanced Discovery and Experimental Therapeutics (CADET), Central Manchester University Hospitals NHS Foundation Trust, Manchester Academic Health Sciences Centre, Manchester, UK 3 Centre for Endocrinology and Diabetes, Institute of Human Development, Faculty of Medical and Human Sciences, University of Manchester, UK 4 School of Biological Sciences, University of Auckland, New Zealand 5 Department of Pharmacology, Medical Sciences Division, University of Oxford, UK † Present address: School of Biosciences, University of Birmingham, UK *Joint corresponding authors: Natalie J. Gardiner and Garth J.S. Cooper Email: [email protected]; [email protected] Address: University of Manchester, AV Hill Building, Oxford Road, Manchester, M13 9PT, United Kingdom Telephone: +44 161 275 5768; +44 161 701 0240 Word count: 4,490 Number of tables: 1, Number of figures: 6 Running title: Metabolic dysfunction in diabetic neuropathy 1 Diabetes Publish Ahead of Print, published online October 15, 2015 Diabetes Page 2 of 255 Abstract High glucose levels in the peripheral nervous system (PNS) have been implicated in the pathogenesis of diabetic neuropathy (DN). However our understanding of the molecular mechanisms which cause the marked distal pathology is incomplete. Here we performed a comprehensive, system-wide analysis of the PNS of a rodent model of DN.
    [Show full text]
  • IL21R Expressing CD14+CD16+ Monocytes Expand in Multiple
    Plasma Cell Disorders SUPPLEMENTARY APPENDIX IL21R expressing CD14 +CD16 + monocytes expand in multiple myeloma patients leading to increased osteoclasts Marina Bolzoni, 1 Domenica Ronchetti, 2,3 Paola Storti, 1,4 Gaetano Donofrio, 5 Valentina Marchica, 1,4 Federica Costa, 1 Luca Agnelli, 2,3 Denise Toscani, 1 Rosanna Vescovini, 1 Katia Todoerti, 6 Sabrina Bonomini, 7 Gabriella Sammarelli, 1,7 Andrea Vecchi, 8 Daniela Guasco, 1 Fabrizio Accardi, 1,7 Benedetta Dalla Palma, 1,7 Barbara Gamberi, 9 Carlo Ferrari, 8 Antonino Neri, 2,3 Franco Aversa 1,4,7 and Nicola Giuliani 1,4,7 1Myeloma Unit, Dept. of Medicine and Surgery, University of Parma; 2Dept. of Oncology and Hemato-Oncology, University of Milan; 3Hematology Unit, “Fondazione IRCCS Ca’ Granda”, Ospedale Maggiore Policlinico, Milan; 4CoreLab, University Hospital of Parma; 5Dept. of Medical-Veterinary Science, University of Parma; 6Laboratory of Pre-clinical and Translational Research, IRCCS-CROB, Referral Cancer Center of Basilicata, Rionero in Vulture; 7Hematology and BMT Center, University Hospital of Parma; 8Infectious Disease Unit, University Hospital of Parma and 9“Dip. Oncologico e Tecnologie Avanzate”, IRCCS Arcispedale Santa Maria Nuova, Reggio Emilia, Italy ©2017 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol. 2016.153841 Received: August 5, 2016. Accepted: December 23, 2016. Pre-published: January 5, 2017. Correspondence: [email protected] SUPPLEMENTAL METHODS Immunophenotype of BM CD14+ in patients with monoclonal gammopathies. Briefly, 100 μl of total BM aspirate was incubated in the dark with anti-human HLA-DR-PE (clone L243; BD), anti-human CD14-PerCP-Cy 5.5, anti-human CD16-PE-Cy7 (clone B73.1; BD) and anti-human CD45-APC-H 7 (clone 2D1; BD) for 20 min.
    [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]
  • Exacerbated Staphylococcus Aureus Foot
    Exacerbated Staphylococcus aureus Foot Infections in Obese/Diabetic Mice Are Associated with Impaired Germinal Center Reactions, Ig Class Switching, and Humoral This information is current as Immunity of October 1, 2021. Christopher W. Farnsworth, Eric M. Schott, Abigail Benvie, Stephen L. Kates, Edward M. Schwarz, Steven R. Gill, Michael J. Zuscik and Robert A. Mooney J Immunol 2018; 201:560-572; Prepublished online 1 June Downloaded from 2018; doi: 10.4049/jimmunol.1800253 http://www.jimmunol.org/content/201/2/560 http://www.jimmunol.org/ Supplementary http://www.jimmunol.org/content/suppl/2018/05/31/jimmunol.180025 Material 3.DCSupplemental References This article cites 46 articles, 20 of which you can access for free at: http://www.jimmunol.org/content/201/2/560.full#ref-list-1 Why The JI? Submit online. by guest on October 1, 2021 • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2018 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Exacerbated Staphylococcus aureus Foot Infections in Obese/Diabetic Mice Are Associated with Impaired Germinal Center Reactions, Ig Class Switching, and Humoral Immunity Christopher W.
    [Show full text]
  • KIF15 Is Involved in Development and Progression of Burkitt Lymphoma Zhao Wang1, Meiting Chen1, Xiaojie Fang1, Huangming Hong2, Yuyi Yao1 and He Huang1*
    Wang et al. Cancer Cell Int (2021) 21:261 https://doi.org/10.1186/s12935-021-01967-z Cancer Cell International PRIMARY RESEARCH Open Access KIF15 is involved in development and progression of Burkitt lymphoma Zhao Wang1, Meiting Chen1, Xiaojie Fang1, Huangming Hong2, Yuyi Yao1 and He Huang1* Abstract Background: Burkitt lymphoma (BL) is a highly aggressive, fast-growing B-cell non-Hodgkin’s lymphoma, manifested in several subtypes, including sporadic, endemic, and immunodefciency-related forms, the mechanism of which is still not clear. Abundant evidence reported that KIF15 was involved in the progression of human cancer. The emphasis of this study is to explore the functions of KIF15 in the development of BL. Methods: Firstly, tumor and normal tissues were collected for detecting expression of KIF15 in BL. Lentivirus-medi- ated shRNA knockdown of KIF15 was used to construct BL cell model, which was verifed by qRT-PCR and Western Blot. The cell proliferation was detected by CCK8 assay, cell apoptosis and cell cycle were measured through fow cytometry. Transwell assay was conducted to detect the migration. Results: We frst found that KIF15 is highly expressed in BL. Knockdown of KIF15 can inhibit proliferation and migra- tion, promote apoptosis and arrest the cell cycle. Moreover, KIF15 is involved in BL cell activity through regulating expression of apoptosis-related proteins (Caspase3, Caspase8, HTRA, IGFBP-6, p53, SMAC, sTNF-R1, TNF-β and Bcl-2) and downstream pathways, such as p-Akt, CCND1, CDK6 and PIK3CA. Conclusions: These fndings justify the search for small molecule inhibitors targeting KIF15 as a novel therapeutic strategy in BL.
    [Show full text]
  • Molecular Signatures of Membrane Protein Complexes Underlying Muscular Dystrophy*□S
    crossmark Research Author’s Choice © 2016 by The American Society for Biochemistry and Molecular Biology, Inc. This paper is available on line at http://www.mcponline.org Molecular Signatures of Membrane Protein Complexes Underlying Muscular Dystrophy*□S Rolf Turk‡§¶ʈ**, Jordy J. Hsiao¶, Melinda M. Smits¶, Brandon H. Ng¶, Tyler C. Pospisil‡§¶ʈ**, Kayla S. Jones‡§¶ʈ**, Kevin P. Campbell‡§¶ʈ**, and Michael E. Wright¶‡‡ Mutations in genes encoding components of the sar- The muscular dystrophies are hereditary diseases charac- colemmal dystrophin-glycoprotein complex (DGC) are re- terized primarily by the progressive degeneration and weak- sponsible for a large number of muscular dystrophies. As ness of skeletal muscle. Most are caused by deficiencies in such, molecular dissection of the DGC is expected to both proteins associated with the cell membrane (i.e. the sarco- reveal pathological mechanisms, and provides a biologi- lemma in skeletal muscle), and typical features include insta- cal framework for validating new DGC components. Es- bility of the sarcolemma and consequent death of the myofi- tablishment of the molecular composition of plasma- ber (1). membrane protein complexes has been hampered by a One class of muscular dystrophies is caused by mutations lack of suitable biochemical approaches. Here we present in genes that encode components of the sarcolemmal dys- an analytical workflow based upon the principles of pro- tein correlation profiling that has enabled us to model the trophin-glycoprotein complex (DGC). In differentiated skeletal molecular composition of the DGC in mouse skeletal mus- muscle, this structure links the extracellular matrix to the cle. We also report our analysis of protein complexes in intracellular cytoskeleton.
    [Show full text]
  • The Kinesin Spindle Protein Inhibitor Filanesib Enhances the Activity of Pomalidomide and Dexamethasone in Multiple Myeloma
    Plasma Cell Disorders SUPPLEMENTARY APPENDIX The kinesin spindle protein inhibitor filanesib enhances the activity of pomalidomide and dexamethasone in multiple myeloma Susana Hernández-García, 1 Laura San-Segundo, 1 Lorena González-Méndez, 1 Luis A. Corchete, 1 Irena Misiewicz- Krzeminska, 1,2 Montserrat Martín-Sánchez, 1 Ana-Alicia López-Iglesias, 1 Esperanza Macarena Algarín, 1 Pedro Mogollón, 1 Andrea Díaz-Tejedor, 1 Teresa Paíno, 1 Brian Tunquist, 3 María-Victoria Mateos, 1 Norma C Gutiérrez, 1 Elena Díaz- Rodriguez, 1 Mercedes Garayoa 1* and Enrique M Ocio 1* 1Centro Investigación del Cáncer-IBMCC (CSIC-USAL) and Hospital Universitario-IBSAL, Salamanca, Spain; 2National Medicines Insti - tute, Warsaw, Poland and 3Array BioPharma, Boulder, Colorado, USA *MG and EMO contributed equally to this work ©2017 Ferrata Storti Foundation. This is an open-access paper. doi:10.3324/haematol. 2017.168666 Received: March 13, 2017. Accepted: August 29, 2017. Pre-published: August 31, 2017. Correspondence: [email protected] MATERIAL AND METHODS Reagents and drugs. Filanesib (F) was provided by Array BioPharma Inc. (Boulder, CO, USA). Thalidomide (T), lenalidomide (L) and pomalidomide (P) were purchased from Selleckchem (Houston, TX, USA), dexamethasone (D) from Sigma-Aldrich (St Louis, MO, USA) and bortezomib from LC Laboratories (Woburn, MA, USA). Generic chemicals were acquired from Sigma Chemical Co., Roche Biochemicals (Mannheim, Germany), Merck & Co., Inc. (Darmstadt, Germany). MM cell lines, patient samples and cultures. Origin, authentication and in vitro growth conditions of human MM cell lines have already been characterized (17, 18). The study of drug activity in the presence of IL-6, IGF-1 or in co-culture with primary bone marrow mesenchymal stromal cells (BMSCs) or the human mesenchymal stromal cell line (hMSC–TERT) was performed as described previously (19, 20).
    [Show full text]
  • Transdifferentiation of Human Mesenchymal Stem Cells
    Transdifferentiation of Human Mesenchymal Stem Cells Dissertation zur Erlangung des naturwissenschaftlichen Doktorgrades der Julius-Maximilians-Universität Würzburg vorgelegt von Tatjana Schilling aus San Miguel de Tucuman, Argentinien Würzburg, 2007 Eingereicht am: Mitglieder der Promotionskommission: Vorsitzender: Prof. Dr. Martin J. Müller Gutachter: PD Dr. Norbert Schütze Gutachter: Prof. Dr. Georg Krohne Tag des Promotionskolloquiums: Doktorurkunde ausgehändigt am: Hiermit erkläre ich ehrenwörtlich, dass ich die vorliegende Dissertation selbstständig angefertigt und keine anderen als die von mir angegebenen Hilfsmittel und Quellen verwendet habe. Des Weiteren erkläre ich, dass diese Arbeit weder in gleicher noch in ähnlicher Form in einem Prüfungsverfahren vorgelegen hat und ich noch keinen Promotionsversuch unternommen habe. Gerbrunn, 4. Mai 2007 Tatjana Schilling Table of contents i Table of contents 1 Summary ........................................................................................................................ 1 1.1 Summary.................................................................................................................... 1 1.2 Zusammenfassung..................................................................................................... 2 2 Introduction.................................................................................................................... 4 2.1 Osteoporosis and the fatty degeneration of the bone marrow..................................... 4 2.2 Adipose and bone
    [Show full text]
  • K-Fiber Bundles in the Mitotic Spindle Are Mechanically Reinforced by Kif15
    bioRxiv preprint doi: https://doi.org/10.1101/2020.05.19.104661; this version posted May 20, 2020. The copyright holder for this preprint (which was not certified by peer review) is the author/funder. All rights reserved. No reuse allowed without permission. K-fiber bundles in the mitotic spindle are mechanically reinforced by Kif15 1 2 1 Marcus A Begley ,​ April L Solon ,​ Elizabeth Mae Davis ,​ Michael Grant ​ ​ ​ 1 2 1,3* Sherrill ,​ Ryoma Ohi ,​ Mary Williard Elting ​ ​ ​ 1 Department​ of Physics, North Carolina State University, Raleigh, NC 2 Department​ of Cell & Developmental Biology, University of Michigan, Ann Arbor, MI 3 Quantitative​ and Computational Developmental Biology Cluster, North Carolina State University, Raleigh, NC *Correspondence: [email protected] Abstract The mitotic spindle, a self-constructed microtubule-based machine, segregates chromosomes into two eventual daughter nuclei. In mammalian cells, microtubule bundles called kinetochore-fibers (k-fibers) anchor chromosomes to the spindle poles, vitally supporting spindle function. Yet, how they achieve mechanical integrity is not well-understood. We sever k-fibers using laser ablation, testing the contribution that forces at minus-ends make to k-fiber cohesion. We measure the physical response of the remaining kinetochore-bound segments. We observe that microtubules within ablated k-fibers often, but not always, splay apart from their minus-ends. Furthermore, we find that minus-end clustering forces induced in response to ablation seem at least partially responsible for k-fiber splaying. We also investigate the role of the putative k-fiber binding molecule kinesin-12 Kif15. We find that pharmacological inhibition of Kif15 microtubule binding reduces k-fiber mechanical integrity.
    [Show full text]
  • Downloaded from Bioscientifica.Com at 09/28/2021 01:26:33PM Via Free Access
    249 S Agarwal and D Varma A glimpse into a new era of 24:9 T65–T82 Thematic Review anti-mitotic cancer therapeutics Targeting mitotic pathways for endocrine-related cancer therapeutics Correspondence Shivangi Agarwal and Dileep Varma should be addressed to D Varma Department of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, Email Chicago, Illinois, USA dileep.varma@northwestern. edu Abstract A colossal amount of basic research over the past few decades has provided Key Words unprecedented insights into the highly complex process of cell division. There is an f microtubules ever-expanding catalog of proteins that orchestrate, participate and coordinate in the f mitosis exquisite processes of spindle formation, chromosome dynamics and the formation f spindle and regulation of kinetochore microtubule attachments. Use of classical microtubule f endocrine poisons has still been widely and often successfully used to combat a variety of cancers, f cancer but their non-selective interference in other crucial physiologic processes necessitate the f therapeutics identification of novel druggable components specific to the cell cycle/division pathway. f kinetochores Considering cell cycle deregulation, unscheduled proliferation, genomic instability and chromosomal instability as a hallmark of tumor cells, there lies an enormous untapped terrain that needs to be unearthed before a drug can pave its way from bench to bedside. This review attempts to systematically summarize the advances made in this Endocrine-Related Cancer Endocrine-Related context so far with an emphasis on endocrine-related cancers and the avenues for future Endocrine-Related Cancer progress to target mitotic mechanisms in an effort to combat these dreadful cancers.
    [Show full text]
  • Tubular P53 Regulates Multiple Genes to Mediate AKI
    BASIC RESEARCH www.jasn.org Tubular p53 Regulates Multiple Genes to Mediate AKI † † † † † Dongshan Zhang,* Yu Liu,* Qingqing Wei, Yuqing Huo, Kebin Liu, Fuyou Liu,* and † Zheng Dong* *Departments of Emergency Medicine and Nephrology, Second Xiangya Hospital, Central South University, Changsha, Hunan, China; and †Department of Cellular Biology and Anatomy, Vascular Biology Center and Department of Biochemistry and Molecular Biology, Georgia Regents University and Charlie Norwood Veterans Affairs Medical Center, Augusta, Georgia ABSTRACT A pathogenic role of p53 in AKI was suggested a decade ago but remains controversial. Indeed, recent work indicates that inhibition of p53 protects against ischemic AKI in rats but exacerbates AKI in mice. One intriguing possibility is that p53 has cell type-specific roles in AKI. To determine the role of tubular p53, we generated two conditional gene knockout mouse models, in which p53 is specifically ablated from proximal tubules or other tubular segments, including distal tubules, loops of Henle, and medullary collecting ducts. Proximal tubule p53 knockout (PT-p53-KO) mice were resistant to ischemic and cisplatin nephrotoxic AKI, which was indicated by the analysis of renal function, histology, apoptosis, and inflammation. However, other tubular p53 knockout (OT-p53-KO) mice were sensitive to AKI. Mechanis- tically, AKI associated with the upregulation of several known p53 target genes, including Bax, p53- upregulated modulator of apoptosis-a, p21, and Siva, and this association was attenuated in PT-p53-KO mice. In global expression analysis, ischemic AKI induced 371 genes in wild-type kidney cortical tissues, but the induction of 31 of these genes was abrogated in PT-p53-KO tissues.
    [Show full text]