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  • 1
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    Two-photon vibrational excitation of air by long-wave infrared laser pulses (2016)
    American Physical Society (APS)
    Details
    Publication Date: 2016-08-06
    Description: Author(s): J. P. Palastro, J. Peñano, L. A. Johnson, B. Hafizi, J. K. Wahlstrand, and H. M. Milchberg Ultrashort long-wave infrared (LWIR) laser pulses can resonantly excite vibrations in N 2 and O 2 through a two-photon transition. The absorptive vibrational component of the ultrafast optical nonlinearity grows in time, starting smaller than but quickly surpassing the electronic, rotational, and vibr… [Phys. Rev. A 94, 023816] Published Fri Aug 05, 2016
    Keywords: Quantum optics, physics of lasers, nonlinear optics, classical optics
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
    Published by American Physical Society (APS)
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  • 2
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    Magellan LDSS3 emission confirmation of galaxies hosting metal-rich Lyman {alpha} absorption systems (2016)
    Oxford University Press
    Details
    Publication Date: 2016-04-07
    Description: Using the Low Dispersion Survey Spectrograph 3 at the Magellan II Clay Telescope, we target candidate absorption host galaxies detected in deep optical imaging (reaching limiting apparent magnitudes of 23.0–26.5 in g , r , i , and z filters) in the fields of three QSOs, each of which shows the presence of high metallicity, high $N_{\rm H\,\small {i}}$ absorption systems in their spectra (Q0826-2230: z abs = 0.9110, Q1323-0021: z abs = 0.7160, Q1436-0051: z abs = 0.7377, 0.9281). We confirm three host galaxies at redshifts 0.7387, 0.7401, and 0.9286 for two of the Lyman α absorption systems (one with two galaxies interacting). For these systems, we are able to determine the star formation rates (SFRs); impact parameters (from previous imaging detections); the velocity shift between the absorption and emission redshifts; and, for one system, also the emission metallicity. Based on previous photometry, we find these galaxies have L 〉 L *. The [O ii ] SFRs for these galaxies are in the range 11–25 M  yr –1 (uncorrected for dust), while the impact parameters lie in the range 35–54 kpc. Despite the fact that we have confirmed galaxies at 50 kpc from the QSO, no gradient in metallicity is indicated between the absorption metallicity along the QSO line of sight and the emission line metallicity in the galaxies. We confirm the anticorrelation between impact parameter and $N_{\rm H\,\small {i}}$ from the literature. We also report the emission redshift of five other galaxies: three at z em 〉 z QSO , and two ( L 〈 L *) at z em 〈 z QSO not corresponding to any known absorption systems.
    Print ISSN: 0035-8711
    Electronic ISSN: 1365-2966
    Topics: Physics
    Published by Oxford University Press
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  • 3
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    Plasma lenses for ultrashort multi-petawatt laser pulses (2015)
    American Institute of Physics (AIP)
    Details
    Publication Date: 2015-12-02
    Description: An ideal plasma lens can provide the focusing power of a small f-number, solid-state focusing optic at a fraction of the diameter. An ideal plasma lens, however, relies on a steady-state, linear laser pulse-plasma interaction. Ultrashort multi-petawatt (MPW) pulses possess broad bandwidths and extreme intensities, and, as a result, their interaction with the plasma lens is neither steady state nor linear. Here, we examine nonlinear and time-dependent modifications to plasma lens focusing, and show that these result in chromatic and phase aberrations and amplitude distortion. We find that a plasma lens can provide enhanced focusing for 30 fs pulses with peak power up to ∼1 PW. The performance degrades through the MPW regime, until finally a focusing penalty is incurred at ∼10 PW.
    Print ISSN: 1070-664X
    Electronic ISSN: 1089-7674
    Topics: Physics
    Published by American Institute of Physics (AIP)
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  • 4
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    THz generation by optical Cherenkov emission from ionizing two-color laser pulses (2013)
    American Physical Society (APS)
    Details
    Publication Date: 2013-12-03
    Description: Author(s): L. A. Johnson, J. P. Palastro, T. M. Antonsen, and K. Y. Kim Two-color photoionization produces a cycle-averaged current driving broadband, conically emitted THz radiation. We investigate, through simulation, the processes determining the angle of conical emission. We find that the emission angle is determined by an optical Cherenkov effect, where the front v... [Phys. Rev. A 88, 063804] Published Mon Dec 02, 2013
    Keywords: Quantum optics, physics of lasers, nonlinear optics, classical optics
    Print ISSN: 1050-2947
    Electronic ISSN: 1094-1622
    Topics: Physics
    Published by American Physical Society (APS)
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  • 5
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    Regulation of phenotypic heterogeneity permits Salmonella evasion of the host caspase-1 inflammatory response [Microbiology] (2011)
    National Academy of Sciences
    Details
    Publication Date: 2011-12-21
    Description: Sensing and adapting to the environment is one strategy by which bacteria attempt to maximize fitness in an unpredictable world; another is the stochastic generation of phenotypically distinct subgroups within a genetically clonal population. In culture, Salmonella Typhimurium populations are bistable for the expression of flagellin. We report that YdiV controls this expression pattern by preventing transcription of the sigma factor that recruits RNA polymerase to the flagellin promoter. Bistability ensues when the sigma factor is repressed in a subpopulation of cells, resulting in two phenotypes: flagellin expressors and flagellin nonexpressors. Although the ability to swim is presumably a critical survival trait, flagellin activates eukaryotic defense pathways, and Salmonella restrict the production of flagellin during systemic infection. Salmonella mutants lacking YdiV are unable to fully repress flagellin at systemic sites, rendering them vulnerable to caspase-1 mediated colonization restriction. Thus, a regulatory mechanism producing bistability also impacts Salmonella virulence.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 6
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    Rare and common variants in extracellular matrix gene Fibrillin 2 (FBN2) are associated with macular degeneration (2014)
    Ratnapriya, R., Zhan, X., Fariss, R. N., Branham, K. E., Zipprer, D., Chakarova, C. F., Sergeev, Y. V., Campos, M. M., Othman, M., Friedman, J. S., Maminishkis, A., Waseem, N. H., Brooks, M., Rajasimha, H. K., Edwards, A. O., Lotery, A., Klein, B. E., Truitt, B. J., Li, B., Schaumberg, D. A., Morgan, D. J., Morrison, M. A., Souied, E., Tsironi, E. E., Grassmann, F., Fishman, G. A., Silvestri, G., Scholl, H. P. N., Kim, I. K., Ramke, J., Tuo, J., Merriam, J. E., Merriam, J. C., Park, K. H., Olson, L. M., Farrer, L. A., Johnson, M. P., Peachey, N. S., Lathrop, M., Baron, R. V., Igo, R. P., Klein, R., Hagstrom, S. A., Kamatani, Y., Martin, T. M., Jiang, Y., Conley, Y., Sahel, J.-A., Zack, D. J., Chan, C.-C., Pericak-Vance, M. A., Jacobson, S. G., Gorin, M. B., Klein, M. L., Allikmets, R., Iyengar, S. K., Weber, B. H., Haines, J. L., Leveillard, T., Deangelis, M. M., Stambolian, D., Weeks, D. E., Bhattacharya, S. S., Chew, E. Y., Heckenlively, J. R., Abecasis, G. R., Swaroop, A.
    Oxford University Press
    Details
    Publication Date: 2014-10-09
    Description: Neurodegenerative diseases affecting the macula constitute a major cause of incurable vision loss and exhibit considerable clinical and genetic heterogeneity, from early-onset monogenic disease to multifactorial late-onset age-related macular degeneration (AMD). As part of our continued efforts to define genetic causes of macular degeneration, we performed whole exome sequencing in four individuals of a two-generation family with autosomal dominant maculopathy and identified a rare variant p.Glu1144Lys in Fibrillin 2 (FBN2), a glycoprotein of the elastin-rich extracellular matrix (ECM). Sanger sequencing validated the segregation of this variant in the complete pedigree, including two additional affected and one unaffected individual. Sequencing of 192 maculopathy patients revealed additional rare variants, predicted to disrupt FBN2 function. We then undertook additional studies to explore the relationship of FBN2 to macular disease. We show that FBN2 localizes to Bruch's membrane and its expression appears to be reduced in aging and AMD eyes, prompting us to examine its relationship with AMD. We detect suggestive association of a common FBN2 non-synonymous variant, rs154001 (p.Val965Ile) with AMD in 10 337 cases and 11 174 controls (OR = 1.10; P -value = 3.79 x 10 –5 ). Thus, it appears that rare and common variants in a single gene— FBN2 —can contribute to Mendelian and complex forms of macular degeneration. Our studies provide genetic evidence for a key role of elastin microfibers and Bruch's membrane in maintaining blood–retina homeostasis and establish the importance of studying orphan diseases for understanding more common clinical phenotypes.
    Print ISSN: 0964-6906
    Electronic ISSN: 1460-2083
    Topics: Biology , Medicine
    Published by Oxford University Press
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  • 7
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    COT drives resistance to RAF inhibition through MAP kinase pathway reactivation (2010)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2010-11-26
    Description: Oncogenic mutations in the serine/threonine kinase B-RAF (also known as BRAF) are found in 50-70% of malignant melanomas. Pre-clinical studies have demonstrated that the B-RAF(V600E) mutation predicts a dependency on the mitogen-activated protein kinase (MAPK) signalling cascade in melanoma-an observation that has been validated by the success of RAF and MEK inhibitors in clinical trials. However, clinical responses to targeted anticancer therapeutics are frequently confounded by de novo or acquired resistance. Identification of resistance mechanisms in a manner that elucidates alternative 'druggable' targets may inform effective long-term treatment strategies. Here we expressed approximately 600 kinase and kinase-related open reading frames (ORFs) in parallel to interrogate resistance to a selective RAF kinase inhibitor. We identified MAP3K8 (the gene encoding COT/Tpl2) as a MAPK pathway agonist that drives resistance to RAF inhibition in B-RAF(V600E) cell lines. COT activates ERK primarily through MEK-dependent mechanisms that do not require RAF signalling. Moreover, COT expression is associated with de novo resistance in B-RAF(V600E) cultured cell lines and acquired resistance in melanoma cells and tissue obtained from relapsing patients following treatment with MEK or RAF inhibitors. We further identify combinatorial MAPK pathway inhibition or targeting of COT kinase activity as possible therapeutic strategies for reducing MAPK pathway activation in this setting. Together, these results provide new insights into resistance mechanisms involving the MAPK pathway and articulate an integrative approach through which high-throughput functional screens may inform the development of novel therapeutic strategies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058384/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3058384/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johannessen, Cory M -- Boehm, Jesse S -- Kim, So Young -- Thomas, Sapana R -- Wardwell, Leslie -- Johnson, Laura A -- Emery, Caroline M -- Stransky, Nicolas -- Cogdill, Alexandria P -- Barretina, Jordi -- Caponigro, Giordano -- Hieronymus, Haley -- Murray, Ryan R -- Salehi-Ashtiani, Kourosh -- Hill, David E -- Vidal, Marc -- Zhao, Jean J -- Yang, Xiaoping -- Alkan, Ozan -- Kim, Sungjoon -- Harris, Jennifer L -- Wilson, Christopher J -- Myer, Vic E -- Finan, Peter M -- Root, David E -- Roberts, Thomas M -- Golub, Todd -- Flaherty, Keith T -- Dummer, Reinhard -- Weber, Barbara L -- Sellers, William R -- Schlegel, Robert -- Wargo, Jennifer A -- Hahn, William C -- Garraway, Levi A -- CA134502/CA/NCI NIH HHS/ -- DP2 OD002750/OD/NIH HHS/ -- DP2 OD002750-01/OD/NIH HHS/ -- K08 CA115927/CA/NCI NIH HHS/ -- K08 CA115927-05/CA/NCI NIH HHS/ -- P50 CA093683/CA/NCI NIH HHS/ -- R01 CA134502/CA/NCI NIH HHS/ -- R33 CA128625/CA/NCI NIH HHS/ -- RC2 CA148268/CA/NCI NIH HHS/ -- England -- Nature. 2010 Dec 16;468(7326):968-72. doi: 10.1038/nature09627. Epub 2010 Nov 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Broad Institute of Harvard and Massachusetts Institute of Technology, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21107320" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Cell Line, Tumor ; Clinical Trials as Topic ; *Drug Resistance, Neoplasm/drug effects/genetics ; Enzyme Activation/drug effects ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic ; Gene Library ; Humans ; Indoles/pharmacology/therapeutic use ; MAP Kinase Kinase Kinases/genetics/*metabolism ; *MAP Kinase Signaling System ; Melanoma/drug therapy/enzymology/genetics/metabolism ; Mitogen-Activated Protein Kinase Kinases/antagonists & inhibitors/metabolism ; Mitogen-Activated Protein Kinases/*metabolism ; Open Reading Frames/genetics ; Protein Kinase Inhibitors/pharmacology/therapeutic use ; Proto-Oncogene Proteins/genetics/*metabolism ; Proto-Oncogene Proteins B-raf/*antagonists & ; inhibitors/chemistry/genetics/metabolism ; Proto-Oncogene Proteins c-raf/genetics/metabolism ; Sulfonamides/pharmacology/therapeutic use
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 8
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    The histone methyltransferase SETDB1 is recurrently amplified in melanoma and accelerates its onset (2011)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2011-03-25
    Description: The most common mutation in human melanoma, BRAF(V600E), activates the serine/threonine kinase BRAF and causes excessive activity in the mitogen-activated protein kinase pathway. BRAF(V600E) mutations are also present in benign melanocytic naevi, highlighting the importance of additional genetic alterations in the genesis of malignant tumours. Such changes include recurrent copy number variations that result in the amplification of oncogenes. For certain amplifications, the large number of genes in the interval has precluded an understanding of the cooperating oncogenic events. Here we have used a zebrafish melanoma model to test genes in a recurrently amplified region of chromosome 1 for the ability to cooperate with BRAF(V600E) and accelerate melanoma. SETDB1, an enzyme that methylates histone H3 on lysine 9 (H3K9), was found to accelerate melanoma formation significantly in zebrafish. Chromatin immunoprecipitation coupled with massively parallel DNA sequencing and gene expression analyses uncovered genes, including HOX genes, that are transcriptionally dysregulated in response to increased levels of SETDB1. Our studies establish SETDB1 as an oncogene in melanoma and underscore the role of chromatin factors in regulating tumorigenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3348545/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3348545/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ceol, Craig J -- Houvras, Yariv -- Jane-Valbuena, Judit -- Bilodeau, Steve -- Orlando, David A -- Battisti, Valentine -- Fritsch, Lauriane -- Lin, William M -- Hollmann, Travis J -- Ferre, Fabrizio -- Bourque, Caitlin -- Burke, Christopher J -- Turner, Laura -- Uong, Audrey -- Johnson, Laura A -- Beroukhim, Rameen -- Mermel, Craig H -- Loda, Massimo -- Ait-Si-Ali, Slimane -- Garraway, Levi A -- Young, Richard A -- Zon, Leonard I -- CA103846/CA/NCI NIH HHS/ -- CA146455/CA/NCI NIH HHS/ -- DK055381/DK/NIDDK NIH HHS/ -- HG002668/HG/NHGRI NIH HHS/ -- K08 DK075432/DK/NIDDK NIH HHS/ -- K08 DK075432-04/DK/NIDDK NIH HHS/ -- K08DK075432-04/DK/NIDDK NIH HHS/ -- K99AR056899-02/AR/NIAMS NIH HHS/ -- R00 AR056899/AR/NIAMS NIH HHS/ -- R00 AR056899-02/AR/NIAMS NIH HHS/ -- R01 CA103846/CA/NCI NIH HHS/ -- R01 CA103846-09/CA/NCI NIH HHS/ -- R01 CA146445/CA/NCI NIH HHS/ -- R01 CA146445-03/CA/NCI NIH HHS/ -- R01 HG002668/HG/NHGRI NIH HHS/ -- R01 HG002668-08/HG/NHGRI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- Canadian Institutes of Health Research/Canada -- Howard Hughes Medical Institute/ -- England -- Nature. 2011 Mar 24;471(7339):513-7. doi: 10.1038/nature09806.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Stem Cell Program and Hematology/Oncology, Children's Hospital Boston, Howard Hughes Medical Institute, Harvard Medical School, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21430779" target="_blank"〉PubMed〈/a〉
    Keywords: Age of Onset ; Amino Acid Substitution ; Animals ; Animals, Genetically Modified ; Cell Transformation, Neoplastic/genetics ; Chromatin Immunoprecipitation ; Chromosomes, Human, Pair 1/genetics ; DNA Copy Number Variations/*genetics ; Disease Models, Animal ; Gene Amplification/*genetics ; Gene Expression Profiling ; Gene Expression Regulation, Neoplastic/genetics ; Genes, Homeobox/genetics ; Histone-Lysine N-Methyltransferase/*genetics/metabolism ; Humans ; Melanocytes/cytology/enzymology/metabolism/pathology ; Melanoma/enzymology/*genetics/*pathology ; Nevus/enzymology ; Oncogenes/genetics ; Protein Methyltransferases/*genetics/*metabolism ; Proto-Oncogene Proteins B-raf/chemistry/genetics/metabolism ; Zebrafish/genetics
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 9
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    A melanocyte lineage program confers resistance to MAP kinase pathway inhibition (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-11-05
    Description: Malignant melanomas harbouring point mutations (Val600Glu) in the serine/threonine-protein kinase BRAF (BRAF(V600E)) depend on RAF-MEK-ERK signalling for tumour cell growth. RAF and MEK inhibitors show remarkable clinical efficacy in BRAF(V600E) melanoma; however, resistance to these agents remains a formidable challenge. Global characterization of resistance mechanisms may inform the development of more effective therapeutic combinations. Here we carried out systematic gain-of-function resistance studies by expressing more than 15,500 genes individually in a BRAF(V600E) melanoma cell line treated with RAF, MEK, ERK or combined RAF-MEK inhibitors. These studies revealed a cyclic-AMP-dependent melanocytic signalling network not previously associated with drug resistance, including G-protein-coupled receptors, adenyl cyclase, protein kinase A and cAMP response element binding protein (CREB). Preliminary analysis of biopsies from BRAF(V600E) melanoma patients revealed that phosphorylated (active) CREB was suppressed by RAF-MEK inhibition but restored in relapsing tumours. Expression of transcription factors activated downstream of MAP kinase and cAMP pathways also conferred resistance, including c-FOS, NR4A1, NR4A2 and MITF. Combined treatment with MAPK-pathway and histone-deacetylase inhibitors suppressed MITF expression and cAMP-mediated resistance. Collectively, these data suggest that oncogenic dysregulation of a melanocyte lineage dependency can cause resistance to RAF-MEK-ERK inhibition, which may be overcome by combining signalling- and chromatin-directed therapeutics.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4098832/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4098832/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Johannessen, Cory M -- Johnson, Laura A -- Piccioni, Federica -- Townes, Aisha -- Frederick, Dennie T -- Donahue, Melanie K -- Narayan, Rajiv -- Flaherty, Keith T -- Wargo, Jennifer A -- Root, David E -- Garraway, Levi A -- DP2 OD002750/OD/NIH HHS/ -- DP2OD002750/OD/NIH HHS/ -- P01 CA163222/CA/NCI NIH HHS/ -- P50CA93683/CA/NCI NIH HHS/ -- R33 CA155554/CA/NCI NIH HHS/ -- U01 HG006492/HG/NHGRI NIH HHS/ -- U54 CA112962/CA/NCI NIH HHS/ -- U54 HG006093/HG/NHGRI NIH HHS/ -- England -- Nature. 2013 Dec 5;504(7478):138-42. doi: 10.1038/nature12688. Epub 2013 Nov 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] The Broad Institute of Harvard University and Massachusetts Institute of Technology, 7 Cambridge Center, Cambridge, Massachusetts 02142, USA [2] Department of Medical Oncology, Dana-Farber Cancer Institute, 44 Binney Street, Boston, Massachusetts 02115, USA [3] Harvard Medical School, 25 Shattuck Street, Boston, Massachusetts 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24185007" target="_blank"〉PubMed〈/a〉
    Keywords: Antineoplastic Agents/*pharmacology ; CREB-Binding Protein/metabolism ; Cell Line, Tumor ; Cell Lineage ; Cyclic AMP/metabolism ; Drug Resistance, Neoplasm/*genetics ; Gene Expression Regulation, Neoplastic ; HEK293 Cells ; Humans ; Melanocytes/cytology/*drug effects/enzymology ; Melanoma/enzymology/physiopathology ; Mitogen-Activated Protein Kinases/*metabolism ; Protein Kinase Inhibitors/*pharmacology ; Signal Transduction ; Transcription Factors/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 10
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    Tumor cell growth arrest caused by subchromosomal transferable DNA fragments from chromosome 11 (1993)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1993-04-16
    Description: A fundamental problem in the identification and isolation of tumor suppressor and other growth-inhibiting genes is the loss of power of genetic complementation at the subchromosomal level. A direct genetic strategy was developed to isolate subchromosomal transferable fragments (STFs) from any chromosome, each containing a selectable marker within the human DNA, that could be transferred to any mammalian cell. As a test of the method, several overlapping STFs from 11p15 were shown to cause in vitro growth arrest of rhabdomyosarcoma cells. This activity mapped between the beta-globin and insulin genes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koi, M -- Johnson, L A -- Kalikin, L M -- Little, P F -- Nakamura, Y -- Feinberg, A P -- CA54358/CA/NCI NIH HHS/ -- T32GM07314/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1993 Apr 16;260(5106):361-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Internal Medicine, University of Michigan Medical School, Ann Arbor 48109.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8469989" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; CHO Cells ; Cell Division ; Cell Line ; *Chromosomes, Human, Pair 11 ; Cricetinae ; DNA/*genetics ; *Genes, Tumor Suppressor ; Genetic Markers ; *Genetic Techniques ; Globins/genetics ; Humans ; Insulin/genetics ; Mice ; Molecular Sequence Data ; Rhabdomyosarcoma/*pathology ; Tumor Cells, Cultured
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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