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  1. Book: Anticancer genes

    Grimm, Stefan

    (Advances in experimental medicine and biology ; 818)

    2014  

    Author's details Stefan Grimm (ed.)
    Series title Advances in experimental medicine and biology ; 818
    Collection
    Language English
    Size XII, 283 S. : Ill., graph. Darst.
    Publisher Springer
    Publishing place London u.a.
    Publishing country Great Britain
    Document type Book
    HBZ-ID HT018362584
    ISBN 978-1-4471-6457-9 ; 1-4471-6457-1 ; 9781447164586 ; 144716458X
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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    Zs A 3192 -818- not available for loan Zeitschriften-Lesesaal

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  2. Book ; Thesis: NMDA-Rezeptorexpression in Spinalganglien und Rückenmark

    Grimm, Stefan

    Morphometrie an Bennettratten und methodische Weiterentwicklung für Humangewebe

    2008  

    Author's details eingereicht von Stefan Grimm
    Language German
    Size 63 Bl., Ill., graph. Darst., 30 cm
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Leipzig, Univ., Diss., 2008
    HBZ-ID HT015906431
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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    2009 E 662 order for loan Magazin

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  3. Book: Anticancer genes

    Grimm, Stefan

    (Advances in experimental medicine and biology, ; v. 818)

    2014  

    Abstract: This book discusses the emergence of a new class of genes with a specific anticancer activity. These genes, recently defined as 'Anticancer Genes', are reviewed in individual chapters on their mode of action, the specific cell death signals they induce, ... ...

    Author's details Stefan Grimm, editor
    Series title Advances in experimental medicine and biology, ; v. 818
    Abstract This book discusses the emergence of a new class of genes with a specific anticancer activity. These genes, recently defined as 'Anticancer Genes', are reviewed in individual chapters on their mode of action, the specific cell death signals they induce, and the status of attempts to translate them into clinical application. Anticancer Genes provides an overview of this nascent field, its genesis, current state, and prospect. It discusses how Anticancer Genes might lead to the identification of a repertoire of signaling pathways directed against cellular alterations that are specific for tumor cells. With contributions from experts worldwide, Anticancer Genes is an essential guide to this dynamic topic for researchers and students in cancer research, molecular medicine, pharmacology and toxicology and genetics as well as clinicians and clinical researchers interested in the therapeutic potential of this exciting new field.
    MeSH term(s) Neoplasms/genetics ; Apoptosis Regulatory Proteins/therapeutic use ; Genetic Therapy/methods
    Language English
    Dates of publication 2014-2014
    Size xii, 283 pages :, illustrations (some color) ;, 25 cm.
    Document type Book
    ISBN 9781447164579 ; 1447164571 ; 9781447164586 ; 144716458X
    Database Catalogue of the US National Library of Medicine (NLM)

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  4. Article: Introduction.

    Grimm, Stefan

    Advances in experimental medicine and biology

    2014  Volume 818, Page(s) 1–8

    MeSH term(s) Animals ; Antineoplastic Agents/therapeutic use ; Drug Screening Assays, Antitumor/methods ; Genes, Tumor Suppressor ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics
    Chemical Substances Antineoplastic Agents
    Language English
    Publishing date 2014
    Publishing country United States
    Document type Introductory Journal Article
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/978-1-4471-6458-6_1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Dissecting mitochondrial apoptosis pathways by gain-of-function cell culture screens.

    Grimm, Stefan

    Mitochondrion

    2013  Volume 13, Issue 3, Page(s) 189–194

    Abstract: While more primitive organism such as Caenorhabditis elegans and Drosophila melanogaster feature a limited, and by now probably mostly known, array of basic cell death factors, the mammalian cell is replete with additional regulators of the cell's demise. ...

    Abstract While more primitive organism such as Caenorhabditis elegans and Drosophila melanogaster feature a limited, and by now probably mostly known, array of basic cell death factors, the mammalian cell is replete with additional regulators of the cell's demise. This abundance of apoptosis mediators has made it imperative to set up a systematic inventory of mammalian cell death genes. Genetic screens in this biological system have recently uncovered the rich diversity of cell death signalling and have in particular highlighted mitochondria as an organelle loaded with apoptosis regulators. Many of the screens that have addressed this utilised the novel technique of RNA interference but some also looked at gain-of-functions with transfected cDNAs. Here we give an overview of the rationale for the latter approach, present the genes discovered by this strategy and in particular describe the involvement of mitochondria and their signalling pathways defined by those genes.
    MeSH term(s) Animals ; Apoptosis/physiology ; Caenorhabditis elegans ; Cell Culture Techniques ; Drosophila melanogaster ; Humans ; Mitochondria/genetics ; Mitochondria/metabolism ; Signal Transduction/physiology
    Language English
    Publishing date 2013-05
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2056923-3
    ISSN 1872-8278 ; 1567-7249
    ISSN (online) 1872-8278
    ISSN 1567-7249
    DOI 10.1016/j.mito.2012.06.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: The ER-mitochondria interface: the social network of cell death.

    Grimm, Stefan

    Biochimica et biophysica acta

    2012  Volume 1823, Issue 2, Page(s) 327–334

    Abstract: When cellular organelles communicate bad things can happen. Recent findings uncovered that the junction between the endoplasmic reticulum (ER) and the mitochondria holds a crucial role for cell death regulation. Not only does this locale connect the two ... ...

    Abstract When cellular organelles communicate bad things can happen. Recent findings uncovered that the junction between the endoplasmic reticulum (ER) and the mitochondria holds a crucial role for cell death regulation. Not only does this locale connect the two best-known organelles in apoptosis, numerous regulators of cell death are concentrated at this spot, providing a terrain for intense signal transfers. Ca2+ is the most prominent signalling factor that is released from the ER and, at high concentration, mediates the transfer of an apoptosis signal to mitochondria as the executioner organelle for cell death. An elaborate array of checks and balances is fine-tuning this process including Bcl-2 family members. Moreover, MAMs, "mitochondria-associated membranes", are distinct membrane sections at the ER that are in close contact with mitochondria and have been found to exchange lipids and lipid-derived molecules such as ceramide for apoptosis induction. Recent work has also described a reverse transfer of apoptosis signals, from mitochondria to the ER, via cytochrome c release and prolonged IP3R opening or through the mitochondrial fission factor Fis1 and Bap31 at the ER, which form the ARCosome, a novel caspase-activation complex.
    MeSH term(s) Animals ; Calcium/metabolism ; Cell Death/physiology ; Cytoskeleton/metabolism ; Cytoskeleton/ultrastructure ; Endoplasmic Reticulum/metabolism ; Endoplasmic Reticulum/ultrastructure ; Mitochondria/metabolism ; Mitochondria/ultrastructure ; Signal Transduction/physiology
    Chemical Substances Calcium (SY7Q814VUP)
    Language English
    Publishing date 2012-02
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbamcr.2011.11.018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  7. Article: Respiratory chain complex II as general sensor for apoptosis.

    Grimm, Stefan

    Biochimica et biophysica acta

    2012  Volume 1827, Issue 5, Page(s) 565–572

    Abstract: I review here the evidence that complex II of the respiratory chain (RC) constitutes a general sensor for apoptosis induction. This concept emerged from work on neurodegenerative diseases and from recent data on metabolic alterations in cancer cells ... ...

    Abstract I review here the evidence that complex II of the respiratory chain (RC) constitutes a general sensor for apoptosis induction. This concept emerged from work on neurodegenerative diseases and from recent data on metabolic alterations in cancer cells affecting the RC and in particular on mutations of complex II subunits. It is also supported by experiments with many anticancer compounds that compared the apoptosis sensitivities of complex II-deficient versus WT cells. These results are explained by the mechanistic understanding of how complex II mediates the diverse range of apoptosis signals. This protein aggregate is specifically activated for apoptosis by pH change as a common and early feature of dying cells. This leads to the dissociation of its SDHA and SDHB subunits from the remaining membrane-anchored subunits and the consequent block of it enzymatic SQR activity, while its SDH activity, which is contained in the SDHA/SDHB subcomplex, remains intact. The uncontrolled SDH activity then generates excessive amounts of reactive oxygen species for the demise of the cell. Future studies on these mitochondrial processes will help refine this model, unravel the contribution of mutations in complex II subunits as the cause of degenerative neurological diseases and tumorigenesis, and aid in discovering novel interference options. This article is part of a Special Issue entitled: Respiratory complex II: Role in cellular physiology and disease.
    MeSH term(s) Apoptosis ; Electron Transport/genetics ; Electron Transport Complex II/genetics ; Electron Transport Complex II/metabolism ; Humans ; Hydrogen-Ion Concentration ; Models, Biological ; Mutation ; Reactive Oxygen Species/metabolism ; Succinate Dehydrogenase/genetics ; Succinate Dehydrogenase/metabolism
    Chemical Substances Reactive Oxygen Species ; respiratory complex II ; Electron Transport Complex II (EC 1.3.5.1) ; SDHA protein, human (EC 1.3.5.1) ; SDHB protein, human (EC 1.3.5.1) ; Succinate Dehydrogenase (EC 1.3.99.1)
    Language English
    Publishing date 2012-09-18
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 60-7
    ISSN 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650 ; 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    ISSN (online) 1879-2596 ; 1879-260X ; 1872-8006 ; 1879-2642 ; 1879-2618 ; 1879-2650
    ISSN 0006-3002 ; 0005-2728 ; 0005-2736 ; 0304-4165 ; 0167-4838 ; 1388-1981 ; 0167-4889 ; 0167-4781 ; 0304-419X ; 1570-9639 ; 0925-4439 ; 1874-9399
    DOI 10.1016/j.bbabio.2012.09.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  8. Book ; Online: Blaming the refugees?

    Grimm, Stefan / Klimm, Felix

    experimental evidence on responsibility attribution

    (Munich discussion paper ; no. 2018, 2)

    2018  

    Abstract: Do people blame refugees for negative events? We propose a novel experimental paradigm to measure discrimination in responsibility attribution towards Arabic refugees. Participants in the laboratory experience a positive or negative income shock, which ... ...

    Author's details Stefan Grimm und Felix Klimm
    Series title Munich discussion paper ; no. 2018, 2
    Abstract Do people blame refugees for negative events? We propose a novel experimental paradigm to measure discrimination in responsibility attribution towards Arabic refugees. Participants in the laboratory experience a positive or negative income shock, which is with equal probability caused by a random draw or another participant’s performance in a real effort task. Responsibility attribution is measured by beliefs about whether the shock is due to the other participant's performance or the random draw. We find evidence for reverse discrimination: Natives attribute responsibility more favorably to refugees than to other natives. In particular, refugees are less often held responsible for negative income shocks. Moreover, natives with negative implicit a sociations towards Arabic names attribute responsibility less favorably to refugees than natives with positive associations. Since neither actual performance differences nor beliefs about natives' and refugees' performance can explain our finding of reverse discrimination, we rule out statistical discrimination as the driving force. We discuss explanations based on theories of self-image and identity concerns.
    Keywords Refugees ; discrimination ; responsibility attribution
    Language English
    Size 1 Online-Ressource (circa 52 Seiten), Illustrationen
    Document type Book ; Online
    Database ECONomics Information System

    Full text online

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  9. Book ; Online: Anticancer Genes

    Grimm, Stefan

    (Advances in Experimental Medicine and Biology ; 818)

    2014  

    Abstract: This book discusses the emergence of a new class of genes with a specific anticancer activity. These genes, recently defined as “Anticancer Genes”, are reviewed in individual chapters on their mode of action, the specific cell death signals they induce, ... ...

    Author's details edited by Stefan Grimm
    Series title Advances in Experimental Medicine and Biology ; 818
    Abstract This book discusses the emergence of a new class of genes with a specific anticancer activity. These genes, recently defined as “Anticancer Genes”, are reviewed in individual chapters on their mode of action, the specific cell death signals they induce, and the status of attempts to translate them into clinical application. Anticancer Genes provides an overview of this nascent field, its genesis, current state, and prospect. It discusses how Anticancer Genes might lead to the identification of a repertoire of signaling pathways directed against cellular alterations that are specific for tumor cells. With contributions from experts worldwide, Anticancer Genes is an essential guide to this dynamic topic for researchers and students in cancer research, molecular medicine, pharmacology and toxicology and genetics as well as clinicians and clinical researchers interested in the therapeutic potential of this exciting new field
    Keywords Gene therapy ; Human genetics ; Medicine ; Oncology ; Toxicology ; Medizin / Gesundheit # Biochemie / Labormedizin ; Medizin / Gesundheit # Genetik ; Medizin / Gesundheit # Onkologie ; Medizin / Gesundheit # Sonstiges
    Language English
    Size Online-Ressource (XII, 283 p. 40 illus., 31 illus. in color), online resource
    Publisher Springer London
    Publishing place London ;s.l
    Document type Book ; Online
    Note Description based upon print version of record
    ISBN 9781447164579 ; 9781447164586 ; 1447164571 ; 144716458X
    DOI 10.1007/978-1-4471-6458-6
    Database Former special subject collection: coastal and deep sea fishing

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  10. Article ; Online: Genetic screening for anticancer genes highlights FBLN5 as a synthetic lethal partner of MYC.

    Masood, Motasim / Ding, Qize / Cawte, Adam D / Rueda, David S / Grimm, Stefan W / Yagüe, Ernesto / El-Bahrawy, Mona

    Cell communication and signaling : CCS

    2023  Volume 21, Issue 1, Page(s) 295

    Abstract: Background: When ectopically overexpressed, anticancer genes, such as TRAIL, PAR4 and ORCTL3, specifically destroy tumour cells without harming untransformed cells. Anticancer genes can not only serve as powerful tumour specific therapy tools but ... ...

    Abstract Background: When ectopically overexpressed, anticancer genes, such as TRAIL, PAR4 and ORCTL3, specifically destroy tumour cells without harming untransformed cells. Anticancer genes can not only serve as powerful tumour specific therapy tools but studying their mode of action can reveal mechanisms underlying the neoplastic transformation, sustenance and spread.
    Methods: Anticancer gene discovery is normally accidental. Here we describe a systematic, gain of function, forward genetic screen in mammalian cells to isolate novel anticancer genes of human origin. Continuing with over 30,000 transcripts from our previous study, 377 cell death inducing genes were subjected to screening. FBLN5 was chosen, as a proof of principle, for mechanistic gene expression profiling, comparison pathways analyses and functional studies.
    Results: Sixteen novel anticancer genes were isolated; these included non-coding RNAs, protein-coding genes and novel transcripts, such as ZNF436-AS1, SMLR1, TMEFF2, LINC01529, HYAL2, NEIL2, FBLN5, YPEL4 and PHKA2-processed transcript. FBLN5 selectively caused inhibition of MYC in COS-7 (transformed) cells but not in CV-1 (normal) cells. MYC was identified as synthetic lethality partner of FBLN5 where MYC transformed CV-1 cells experienced cell death upon FBLN5 transfection, whereas FBLN5 lost cell death induction in MCF-7 cells upon MYC knockdown.
    Conclusions: Sixteen novel anticancer genes are present in human genome including FBLN5. MYC is a synthetic lethality partner of FBLN5. Video Abstract.
    MeSH term(s) Animals ; Humans ; Cell Transformation, Neoplastic ; Extracellular Matrix Proteins/metabolism ; Gene Expression Profiling ; Genetic Testing ; Mammals/metabolism ; MCF-7 Cells ; Membrane Proteins/genetics ; Neoplasm Proteins/genetics ; Phosphorylase Kinase ; Transcription Factors/genetics
    Chemical Substances Extracellular Matrix Proteins ; FBLN5 protein, human ; Membrane Proteins ; Neoplasm Proteins ; PHKA2 protein, human (EC 2.7.1.19) ; Phosphorylase Kinase (EC 2.7.1.19) ; TMEFF2 protein, human ; Transcription Factors ; ZNF436 protein, human ; MYC protein, human
    Language English
    Publishing date 2023-10-20
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Video-Audio Media
    ZDB-ID 2126315-2
    ISSN 1478-811X ; 1478-811X
    ISSN (online) 1478-811X
    ISSN 1478-811X
    DOI 10.1186/s12964-023-01300-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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