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Oncogene (2002) 20, 8378 ± 8392 ã 2002 Nature Publishing Group All rights reserved 0950 ± 9232/02 $25.00 www.nature.com/onc Volume 20 keyword index 11q23 ± q24 7753 Acute lymphoblastic AFP-GC (AFP Animal models 5726, 14-3-3 1839, 3949, 4393, leukemia 3969 producing gastric 7216 5087, 6331 Acute lymphocytic cancer) 869 Anisomycin 2243 14-3-3 s 3348 leukemias 874 AG490 7925 Anoikis 4710, 6960, 7413 14-3-3 proteins 346 Acute myelogeneous Aggressive ®bromatosis Anthracyclin 859 14q32.1 5638 leukemia 88 451 Anti-angiogenic signal- 1a,25 Di-hydroxyvitamin Acute myeloid leukemia Aging 2551 ling 3443 D3 1860 5680 AKAP 6225 Anti-apoptosis 198 1p36 5075, 7307, 8042 Acute myeloid leukemias Akt 1981, 2197, 2514, Anti-cancer drugs 6263 1q21 7686 3110 3746, 3845, 4419, 4542, Antibody-mediated 4101 20q deletion 4150 Acute promyelocytic 5638, 5991, 6018, 6073, Anticancer drug 1193, 3' UTR 7472, 4537 leukemia (APL) 7779 6048 3p 1509 7146 Akt kinase 5420 Antimicrotubule agents 3p tumour suppressor Ad E4 gene function ALCL 4466, 5623 6123 gene 7573 7847 ALK 5623, 7386 Antioxidant 3906 3p21 3563 ADAMs 1594 Alkylating agent 6627 Antisense 6643, 8019 3p21.3 2713 Adapter 6382, 6448 Alkylation 3580 Antisense MEL-CAM 5' upstream region 5215 Adapter molecule 6291 ALL-1/MLL/HRX gene 4676 5' UTR 893, 7472 Adapter protein and 2900 Antitumor drug 1110 53BP2 2720 signal transduction Allelic imbalance 4424, AP-1 669, 2205, 2334, 5qNCA 6946 6270 6095, 7809 2336, 2347, 2390, 2401, 6-thioguanine 6181 Adapters 6270, 6273, Allelic losses 4586 2771, 3266, 3332, 5132, 6q 8042 6403 Alternative lengthening 7597, 7761, 8009 [131I]MIBG 7804 Adaptor protein 5373, of telomeres 3835 AP-1 proteins 634 6435 Alternative splicing 1015, AP-2 2570 Adaptor protein Grap2 2976, 5562 AP1 1135 a-lipoic acid 289 1703 Alternative transcripts Apaf-1 3449 aIIbb3 6291 Adaptor proteins 951, 4665 Apaf-1/Nod1/CED4 Aa subunit 10 6372 Alu-PCR 6233 family 6473 Ab subunit 1892 Adenocarcinoma 5093, Amifostine 3533 APC 3528, 6871 AATYK 1015 7710 AML 8236 APL 3116, 5726, 7161, Abasic sites 7945 Adenomatous polyposis AML1 (RUNX-1) 6225 7204, 7216, 7274, 7287 Abelson 7744 coli (APC) 451, AML1 5660 APL blasts 7154 Abelson murine leukemia 6250 AML1/MDS1/EVI1 8236 Apo2L 1010 virus 4926 Adenomatous polyposis Amphiphysin IIb-1 6689 Apoptosis 16, 167, 147, Aberrant transcription coli 4884 Amphiregulin 4019 260, 303, 358, 430, 461, factors 5747 Adenomatous polyposis Ampli®cation 2023, 514, 571, 659, 677, 704, AC133 8249 coli tumour-suppressor 4853 812, 879, 910, 1010, Acetyltransferase 2988 protein 5920 Anagen 7536 1022, 1063, 1193, 1212, Acidosis 3751 Adenovirus 2281, 4466, Anaplastic carcinoma 1246, 1254, 1343, 1465, Actin 5359, 5366, 6435, 4793, 5279, 7824, 7836, 3235 1476, 1497, 1860, 1913, 6973 7855, 8270 Anaplastic large cell 1939, 1981, 2144, 2178, Actin cytoskeleton 3457, Adenovirus E1A 6828 lymphoma (ALCL) 2190, 2243, 2254, 2314, 3995, 6418 Adenylate kinase 6891 590, 7386 2378, 2390, 2537, 2713, Actin ®lament Adhesion 759, 997, 1739, Anchorage-independent 2720, 2737, 2749, 2805, reorganization 8175 4554, 7318 growth 2254, 5087 2814, 2826, 2836, 2877, Actin ®laments 6607 Adhesion molecule 4519 Androgen 2791, 7597 2908, 2927, 2937, 2982, Actinomycin D 2243, Adrenomedullin 2937 Androgen signaling 3880 3193, 3266, 3354, 3420, 3306 Adriamycin 113, 1076 Androgen-independent 3449, 3506, 3580, 3597, Activation domain 4161 Adult T-cell leukemia/ 6718 3620, 3597, 3620, 3629, Activation function-2 lymphoma 3301 Androgens 1455, 7965 3703, 3726, 3746, 3757, (AF-2) 77 AF4 gene 2900 Angiogenesis 270, 1403, 3888, 3929, 4050, 4070, Activation loop 8075 AF10 3281 1556, 2655, 2791, 3363, 4085, 4101, 4128, 4198, Activin 704, 5409 AFAP-110 6435, 6607 3751, 3959, 4188, 4685, 4235, 4258, 4305, 4317, Acute leukemia 3281, AFP (Alpha-fetoprotein) 7293, 8288, 8326, 8334 4365, 4476, 4507, 4542, 5718 869 Angiotensin II 1556 4591, 4601, 4710, 4757, Volume 20 keyword index 8379 4768, 4777, 4807, 4817, b-catenin 252, 395, 450, BMP 4383 c-erbB2 (neu) 2101 4891, 4925, 4995, 5043, 3247, 4249, 5093, 5972, BMP-6 7761 c-FLIP-s 4601 5087, 5124, 5225, 5341, 6250, 6871, 7812 BNP1350 5249 c-Fos 942, 1357, 7563 5595, 5718, 5779, 5789, b-galactosidase 7096 Bodily ¯uids 5195 c-H-ras 3683 5799, 5826, 5836, 5846, b2-microglobulin 7006 Bone biology 2401 c-Jun 1816, 2490 5865, 5982, 5991, 6026, B cell dierentiation 3226 Bone resorption inhibitor c-Jun transcription 6073, 6084, 6111, 6172, B-cell ontogeny 3969 2068 factor ± phosphoryl- 6473, 6493, 6503, 6731, B-Myb 1425, 3376 BPOZ 4457 ation sites 7425 6752, 6764, 6805, 6910, Ba/F3 849 Brain 1015, 1022, 4128 c-Kit 5054, 6752 6973, 6983, 6994, 7006, BAD 4507 Brain lesions 692 c-Kit mutation 4528 7029, 7128, 7136, 7146, BAG-1 4095 Brain tumors 5378 c-Myb 759, 1688, 1784, 7250, 7257, 7334, 7352, Bak 7668 Branching 3258, 3746, 4554, 5595, 7334, 7352, 7386, 7478, Barrett's esophagus 7987 morphogenesis 3845 6084, 6205, 6983, 7514 7579, 7668, 7761, 7779, Basal cell carcinoma 198 Brca2 3937 c-myc 1176, 2814, 4542, 7836, 7855, 7836, 7855, Basic helix ± loop ± helix BRCA1 440, 5331, 6597 6544 7925, 7965, 7992, 8009, (bHLH) 1771, 8290, Brca11700T 2544 c-neu transgenic mice 8136, 8175, 8203, 8215, 8342 BRCA1 77, 4433, 4596, 6009 8258 Basic helix ± loop ± helix 4640, 4827, 6123, 7110, c-Rel 7098 Apoptosis susceptibility factors 4750 7514, 8215 c-Src 1816 3609 Bax 1852, 1939, 2805, BRCA1/BRCA1a/1b C-terminal domain 5493 ARE 4344 4476, 5249, 7464 1357 C-terminal SH3 domain ARF 1033, 4951, 7447 Bax conformational BRCA2 336 951 Arp2/3 complex 6418 change 7779 BrdU 2010, 3486 C/EBP 1730 Arsenic 7136 Bax expression and Breakpoint cloning 4249 C/EBPb 2301 2+ Arsenic trioxide (AS2O3) translocation 4817 Breast 6881 Ca 6372 7146 Bcl-2 240, 1176, 7342 Breast cancer 77, 440, Cadherin 3323, 4942 Arsenite 3585 Bc1-2 4807, 5789, 6026 514, 1246, 1287, 1300, CAG/CTG repeat Asbestos 7301 Bc1-2 family 5846 1357, 1465, 1509, 1688, expansion 5548 Astrocytes 7976 BCC 7770 1715, 2101, 2325, 2499, Calcium-binding protein Astrocytoma 7976, 8281 BCCIP 336 2771, 2791, 3247, 3301, 336 ASY 3929 Bcl-2 1476, 1939, 2122, 3348, 3428, 3497, 3506, Calpain 1287 Ataxia-telangiectasia 289, 2190, 2291, 2836, 2937, 3814, 4019, 4209, 4409, cAMP 8019 4409 3240, 3757, 3806, 4305, 4433, 4586, 4961, 4995, cAMP-dependent kinase Ataxia-telangiectasia 6172, 6983, 7098, 7128, 5093, 5420, 5511, 5810, 1186 ATM 4281 7579, 7597, 7836, 8258 6570, 6960, 7064, 7115, cAMP/PKA 4696 ATBF1 (AT motif Bcl-2 cleavage 4591 7408, 7551, 7753, 7925, Cancer 686, 748, 1128, binding factor 1) 869 Bcl-2 thapsigargin 933 8066, 8109, 8215 1497, 2611, 2805, 3116, ATF 2453, 7998 Bcl-XL 167, 2122, 4507, Breast cancer speci®c 3139, 3156, 3786, 3929, ATF2 1816, 8116 6983, 7668, 7925, 8281 gene 1 5173 5366, 5726, 5763, 6066, ATF3 1135 Bcl10 4317 Breast neoplasms 7318 6233, 6309, 6851, 7342, ATM 113, 278, 289, Bcr 1873 BRG1 3039 7820 3341, 4029, 5100, BCR/ABL 2636, 5826 Brn-3 4961 Cancer cells 1563 6095 Bcr ± Abl 1873, 5644, Brn-3a transcription Cancer frequency 4621 ATM/ATR 921 6188, 8236 factor 4899 Cancer gene expression ATP 7579 BER 581 Bromodomain 3076 8085 ATP-dependent bFGF 1913 Bronchial epithelial cells Cancer Genome chromatin remodeling BGP 219 634 Anatomy Project 4877 3047 BH3 proteins 5087 BS69 125 Cancer predisposition ATPase 2988 bHLH 8308 BTG1 2691 4621 ATPase/GTPases 6473 Bioinformatic 4581 Budding yeast 1128 Cancer risk 2264 ATRA 7161 Birt-Hogg-Dube Burkitt lymphoma 748, Cancer testis antigen Autocrine 1563, 8125 syndrome 5239 2171, 6084 7699 Autocrine growth factor Bladder 686 Butyrate 375, 3387 Capacitative Ca2+ entry 4019 Bladder cancer 531, 5005 Bystander 7085 933 Avian 4433 Bladder neoplasms 1042 Carbonic anhydrase II Avian retrovirus 1118 Bleomycin 5100 775, 3100 AXIN1 5062 BLM protein 8276 c-Abl 3845, 4298 Carcinogenesis 997, 1678, Axon guidance 3995 Bloom helicase 1143 c-Abl isoform 2618 2771, 3620, 5059, 5302, Bloom syndrome 1143, C-CAM 219 5341, 7761 8276 c-Cbl 1739, 7326 Carcinoma in situ 5155, b-arrestin 1532 Bmi-1 2171 c-Crk 6348 5897, 6538 Oncogene Volume 20 keyword index 8380 Cardiac 1626 CDK2 3173, 6851 Cell proliferation 3857, Chromosomal instability Cardiomyocyte 1626 Cdk6 2000 4696, 6315 1143, 3301, 3835, 4871 Cas 6057, 6448 cdk8 551 Cell proliferation, Chromosomal local- Casein kinase 2 1784, CDKN2D 7787 dierentiation and ization 5067, 5920 2010 Cdks 4354 apoptosis 4877 Chromosomal trans- Casein kinase II 3247, CDKs 8317 Cell signaling 1318, 4209, location 48, 4412, 5951 CDNA array 2537, 2826, 5511 5580, 5718, 5755, 5763 Caspase 10 4424 6700 Cell spreading 5908 Chromosomal trans- Caspase 167, 358, 571, cDNA chip technology Cell stress 7992 location t(4;11) 2900 1193, 1203, 1476, 1852, 4402 Cell survival 5680 Chromosome 3979 2122, 2877, 2918, 3354, cDNA microarray 3674 Cell transfection 2655 Chromosome 1 7307 3726, 4070, 6111 cDNA microarrays 1300 Cell transformation 1135, Chromosome 10 5378 Caspase 3 4629 Cds1 7453 1229, 5493, 6559, 7486, Chromosome 10p 828 Caspase 8 3629, 4424, Cdx1 4180 7908 Chromosome 10p15 314 6910 CDX2 4884 Cell ± cell adhesion 4676 Chromosome 11p15.5 Caspase-2 isoforms 260 CEA 219 Cellular growth 7992 8154 Caspase-3 1254, 2749, CEACAM1 219 Cellular localization 2587 Chromosome 12 5562 5982 CEF 5118 Cellular senescence 2264 Chromosome 16 5005, Caspase-7 8258 CEF-4/9E3 chemokine Cellular transformation 5232 Caspase-8 2190, 5865, 2301 3651, 5350 Chromosome 18q 2273 6764 Cell adhesion 490, 899, Centrosome duplication Chromosome 19 2186 Caspase-9 5991 1425 3173, 6851 Chromosome 2q 4424 Caspases 1063, 4085, Cell adhesion molecule
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  • The EWS/ATF1 Fusion Protein Contains a Dispersed Activation Domain That Functions Directly

    The EWS/ATF1 Fusion Protein Contains a Dispersed Activation Domain That Functions Directly

    Oncogene (1998) 16, 1625 ± 1631 1998 Stockton Press All rights reserved 0950 ± 9232/98 $12.00 The EWS/ATF1 fusion protein contains a dispersed activation domain that functions directly Shu Pan, Koh Yee Ming, Theresa A Dunn, Kim KC Li and Kevin AW Lee Department of Biology, Hong Kong University of Science & Technology, Clear Water Bay, Kowloon, Hong Kong, P.R.C. Naturally occurring chromosomal fusion of the Ewings 1994). For all of the above malignancies, the EWS Sarcoma Oncogene (EWS) to distinct cellular transcrip- fusion proteins function as potent transcriptional tion factors, produces aberrant transcriptional activators activators (May et al., 1993b; Ohno et al., 1993; that function as dominant oncogenes. In Malignant Bailly et al., 1994; Brown et al., 1995; Lessnick et al., Melanoma of Soft Parts the N-terminal region of 1995; Fujimura et al., 1996) in a manner that is EWS is fused to C-terminal region of the cAMP- dependent on the EWS N-terminal region, hereafter inducible transcription factor ATF1. The EWS/ATF1 referred to as the EWS Activation Domain (EAD). It is fusion protein binds to ATF sites present in cAMP- envisioned that distinct tumors arise via de-regulation responsive promoters via the ATF1 bZIP domain and of dierent genes, depending on the fusion partner for activates transcription constitutively in a manner that is EWS. In cases where it has been examined, agents that dependent on an activation domain (EAD) present in antagonise EWS-fusion proteins also inhibit cellular EWS. To further de®ne the requirements for trans- proliferation (Ouchida et al., 1995; Kovar et al., 1996; activation we have performed mutational analysis of Yi et al., 1997; Tanaka et al., 1997), indicating that EWS/ATF1 in mammalian cells and report several new EWS fusions can play a role in both tumor formation ®ndings.
  • Erk Direction of CD4 T Cell Subsets Chiung-Fang Chang, Warren N

    Erk Direction of CD4 T Cell Subsets Chiung-Fang Chang, Warren N

    Polar Opposites: Erk Direction of CD4 T Cell Subsets Chiung-Fang Chang, Warren N. D'Souza, Irene L. Ch'en, Gilles Pages, Jacques Pouyssegur and Stephen M. Hedrick This information is current as of September 25, 2021. J Immunol 2012; 189:721-731; Prepublished online 6 June 2012; doi: 10.4049/jimmunol.1103015 http://www.jimmunol.org/content/189/2/721 Downloaded from Supplementary http://www.jimmunol.org/content/suppl/2012/06/06/jimmunol.110301 Material 5.DC1 References This article cites 67 articles, 28 of which you can access for free at: http://www.jimmunol.org/ http://www.jimmunol.org/content/189/2/721.full#ref-list-1 Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists by guest on September 25, 2021 • 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 © 2012 by The American Association of Immunologists, Inc. All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Polar Opposites: Erk Direction of CD4 T Cell Subsets Chiung-Fang Chang,* Warren N. D’Souza,† Irene L.
  • Confirmation of Pathogenic Mechanisms by SARS-Cov-2–Host

    Confirmation of Pathogenic Mechanisms by SARS-Cov-2–Host

    Messina et al. Cell Death and Disease (2021) 12:788 https://doi.org/10.1038/s41419-021-03881-8 Cell Death & Disease ARTICLE Open Access Looking for pathways related to COVID-19: confirmation of pathogenic mechanisms by SARS-CoV-2–host interactome Francesco Messina 1, Emanuela Giombini1, Chiara Montaldo1, Ashish Arunkumar Sharma2, Antonio Zoccoli3, Rafick-Pierre Sekaly2, Franco Locatelli4, Alimuddin Zumla5, Markus Maeurer6,7, Maria R. Capobianchi1, Francesco Nicola Lauria1 and Giuseppe Ippolito 1 Abstract In the last months, many studies have clearly described several mechanisms of SARS-CoV-2 infection at cell and tissue level, but the mechanisms of interaction between host and SARS-CoV-2, determining the grade of COVID-19 severity, are still unknown. We provide a network analysis on protein–protein interactions (PPI) between viral and host proteins to better identify host biological responses, induced by both whole proteome of SARS-CoV-2 and specific viral proteins. A host-virus interactome was inferred, applying an explorative algorithm (Random Walk with Restart, RWR) triggered by 28 proteins of SARS-CoV-2. The analysis of PPI allowed to estimate the distribution of SARS-CoV-2 proteins in the host cell. Interactome built around one single viral protein allowed to define a different response, underlining as ORF8 and ORF3a modulated cardiovascular diseases and pro-inflammatory pathways, respectively. Finally, the network-based approach highlighted a possible direct action of ORF3a and NS7b to enhancing Bradykinin Storm. This network-based representation of SARS-CoV-2 infection could be a framework for pathogenic evaluation of specific 1234567890():,; 1234567890():,; 1234567890():,; 1234567890():,; clinical outcomes.
  • Atbf1 Is Required for the Pit1 Gene Early Activation

    Atbf1 Is Required for the Pit1 Gene Early Activation

    Atbf1 is required for the Pit1 gene early activation Yingchuan Qi*, Jeffrey A. Ranish†, Xiaoyan Zhu*, Anna Krones*, Jie Zhang*, Ruedi Aebersold†‡, David W. Rose§, Michael G. Rosenfeld*¶, and Catherine Carrie` re¶ʈ *Howard Hughes Medical Institute and Department of Medicine, School of Medicine, University of California at San Diego, La Jolla, CA 92093; †Institute for Systems Biology, 1441 North 34th Street, Seattle, WA 98103; ‡Institute of Molecular Systems Biology, Swiss Federal Institute of Technology (ETH) Ho¨nggerberg and Faculty of Sciences, University of Zu¨rich, CH-8093 Zu¨rich, Switzerland; §Department of Medicine, Division of Endocrinology and Metabolism, School of Medicine, University of California at San Diego, La Jolla, CA 92093; and ʈDepartment of Medicine, Dartmouth Medical School, Norris Cotton Cancer Center, 1 Medical Center Drive, Lebanon, NH 03756 Contributed by Michael G. Rosenfeld, December 24, 2007 (sent for review November 28, 2007) Enhancers have been functionally described for >35 years, but the Pit1-defective Snell (dw/dw) mutant mice, demonstrating that the molecular principles underlying the integration of regulatory in- elements required for Pit1 early activation were present in the same puts to alternate gene enhancers used during mammalian orga- genomic region (10). Further mapping showed that the regions nogenesis remain incompletely understood. Using a combination required for the Pit1 early activation were located between Ϫ10 kb of in vivo enhancer mapping and proteomics approaches, we have and Ϫ3.5 kb (10). Thus, Pit1 expression appears to be under the established that two distant and distinct early enhancers, each control of multiple enhancers, at least one for its activation and one requiring different transcription complexes, are required for full for its maintained expression.