LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 93

Search options

  1. Article ; Online: Erwin Knecht-the intelligent and mad, funny and grumpy man of autophagy.

    Knecht, Erwin / Klionsky, Daniel J

    Autophagy

    2021  Volume 18, Issue 4, Page(s) 711–725

    Abstract: Getting to know Erwin Knecht is not so simple. This view was summarized in a comment from Dr. Marta ... Martinez Vicente, who obtained her PhD degree working in a lab that shared space with Erwin's group: "Erwin ... Knecht is a complex character, who awakens contradictory feelings. To define him I would say that he is ...

    Abstract Getting to know Erwin Knecht is not so simple. This view was summarized in a comment from Dr. Marta Martinez Vicente, who obtained her PhD degree working in a lab that shared space with Erwin's group: "Erwin Knecht is a complex character, who awakens contradictory feelings. To define him I would say that he is a mixture of intelligence and madness, he's witty, very funny but also grumpy and cranky, all mixed and all simultaneously. Without a doubt he is a person who will not leave anyone indifferent, his original personality marked all who crossed his path, doctoral students, collaborators, people who attended his talks, etc … I remember the weekly lab meetings with him; we, the students, had a lot of respect for him (not to mention fear), but his comments were always smart, helpful and constructive, he has always been prone to helping everyone. In the lab, he was extremely demanding, but got people under his supervision to do their best. And despite his usual moodiness, he managed to make everyone love him and have a special affection for him. Above all, I remember his screams throughout the laboratory that could be heard from all over the building, calling out to his laboratory technician: 'Asunción!' They were like an old couple, arguing all day but they couldn't be without each other, it was like watching a sitcom every day." If you are intrigued, please read on.
    MeSH term(s) Autophagy ; Humans ; Intelligence ; Male
    Language English
    Publishing date 2021-09-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2021.1962206
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 6741: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Book: Current trends in the study of intracellular protein degradation / 1

    Knecht, Erwin

    (Revisiones sobre biologia celular ; 20)

    1989  

    Author's details ed. by Erwin Knecht
    Series title Revisiones sobre biologia celular ; 20
    Current trends in the study of intracellular protein degradation
    Collection Current trends in the study of intracellular protein degradation
    Size VIII, 282 S. : Ill., graph. Darst.
    Publisher Servicio Ed. Universidad del País Vasco u.a.
    Publishing place Leioa
    Publishing country Spain
    Document type Book
    HBZ-ID HT003520106
    Database Catalogue ZB MED Medicine, Health

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    1990 A 3143 -1- order for loan Magazin

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  3. Book: Current trends in the study of intracellular protein degradation / 2

    Knecht, Erwin

    (Revisiones sobre biologia celular ; 21)

    1989  

    Author's details ed. by Erwin Knecht
    Series title Revisiones sobre biologia celular ; 21
    Current trends in the study of intracellular protein degradation
    Collection Current trends in the study of intracellular protein degradation
    Size VIII S., S. 283 - 546 : Ill., graph. Darst.
    Publisher Servicio Ed. Universidad del País Vasco u.a.
    Publishing place Leioa
    Publishing country Spain
    Document type Book
    HBZ-ID HT003520110
    Database Catalogue ZB MED Medicine, Health

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    1990 A 3143 -2- order for loan Magazin

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  4. Article: Lafora Disease: A Ubiquitination-Related Pathology.

    García-Gimeno, Maria Adelaida / Knecht, Erwin / Sanz, Pascual

    Cells

    2018  Volume 7, Issue 8

    Abstract: Lafora disease (LD, OMIM254780) is a rare and fatal form of progressive myoclonus epilepsy (PME). Among PMEs, LD is unique because of the rapid neurological deterioration of the patients and the appearance in brain and peripheral tissues of insoluble ... ...

    Abstract Lafora disease (LD, OMIM254780) is a rare and fatal form of progressive myoclonus epilepsy (PME). Among PMEs, LD is unique because of the rapid neurological deterioration of the patients and the appearance in brain and peripheral tissues of insoluble glycogen-like (polyglucosan) inclusions, named Lafora bodies (LBs). LD is caused by mutations in the
    Language English
    Publishing date 2018-07-26
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2661518-6
    ISSN 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells7080087
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  5. Article ; Online: Withdrawal: Tissue-specific autophagy alterations and increased tumorigenesis in mice deficient in Atg4C/autophagin-3.

    Mariño, Guillermo / Salvador-Montoliu, Natalia / Fueyo, Antonio / Knecht, Erwin / Mizushima, Noboru / López-Otín, Carlos

    The Journal of biological chemistry

    2019  Volume 294, Issue 4, Page(s) 1435

    Language English
    Publishing date 2019-02-25
    Publishing country United States
    Document type Journal Article ; Retraction of Publication
    ZDB-ID 2997-x
    ISSN 1083-351X ; 0021-9258
    ISSN (online) 1083-351X
    ISSN 0021-9258
    DOI 10.1074/jbc.W118.007329
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.108: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  6. Article ; Online: Lafora Disease

    Maria Adelaida García-Gimeno / Erwin Knecht / Pascual Sanz

    Cells, Vol 7, Iss 8, p

    A Ubiquitination-Related Pathology

    2018  Volume 87

    Abstract: Lafora disease (LD, OMIM254780) is a rare and fatal form of progressive myoclonus epilepsy (PME). Among PMEs, LD is unique because of the rapid neurological deterioration of the patients and the appearance in brain and peripheral tissues of insoluble ... ...

    Abstract Lafora disease (LD, OMIM254780) is a rare and fatal form of progressive myoclonus epilepsy (PME). Among PMEs, LD is unique because of the rapid neurological deterioration of the patients and the appearance in brain and peripheral tissues of insoluble glycogen-like (polyglucosan) inclusions, named Lafora bodies (LBs). LD is caused by mutations in the EPM2A gene, encoding the dual phosphatase laforin, or the EPM2B gene, encoding the E3-ubiquitin ligase malin. Laforin and malin form a functional complex that is involved in the regulation of glycogen synthesis. Thus, in the absence of a functional complex glycogen accumulates in LBs. In addition, it has been suggested that the laforin-malin complex participates in alternative physiological pathways, such as intracellular protein degradation, oxidative stress, and the endoplasmic reticulum unfolded protein response. In this work we review the possible cellular functions of laforin and malin with a special focus on their role in the ubiquitination of specific substrates. We also discuss here the pathological consequences of defects in laforin or malin functions, as well as the therapeutic strategies that are being explored for LD.
    Keywords Lafora disease ; ubiquitination ; malin ; E3-ligase ; proteostasis ; glycogen accumulation ; Biology (General) ; QH301-705.5
    Language English
    Publishing date 2018-07-01T00:00:00Z
    Publisher MDPI AG
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

    More links

    Kategorien

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  7. Article: Chaperonopathies: Spotlight on Hereditary Motor Neuropathies.

    Lupo, Vincenzo / Aguado, Carmen / Knecht, Erwin / Espinós, Carmen

    Frontiers in molecular biosciences

    2016  Volume 3, Page(s) 81

    Abstract: Distal hereditary motor neuropathies (dHMN) are a group of rare hereditary neuromuscular disorders characterized by an atrophy that affects peroneal muscles in the absence of sensory symptoms. To date, 23 genes are thought to be responsible for dHMN, ... ...

    Abstract Distal hereditary motor neuropathies (dHMN) are a group of rare hereditary neuromuscular disorders characterized by an atrophy that affects peroneal muscles in the absence of sensory symptoms. To date, 23 genes are thought to be responsible for dHMN, four of which encode chaperones:
    Language English
    Publishing date 2016-12-14
    Publishing country Switzerland
    Document type Review ; Journal Article
    ZDB-ID 2814330-9
    ISSN 2296-889X
    ISSN 2296-889X
    DOI 10.3389/fmolb.2016.00081
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  8. Thesis ; Online: Identification of phage receptors and enzymes essential for phage infection in Erwinia amylovora

    Knecht, Leandra

    2019  

    Keywords info:eu-repo/classification/ddc/570 ; info:eu-repo/classification/ddc/630 ; Life sciences ; Agriculture
    Language English
    Publishing date 2019-05-10
    Publisher ETH Zurich
    Publishing country ch
    Document type Thesis ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

    More links

    Kategorien

    Inter-library loan at ZB MED

    Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

  9. Article ; Online: Ca²⁺-sensor proteins in the autophagic and endocytic traffic.

    Ghislat, Ghita / Knecht, Erwin

    Current protein & peptide science

    2013  Volume 14, Issue 2, Page(s) 97–110

    Abstract: Autophagy and endocytosis are two evolutionarily conserved catabolic processes that comprise vesicle trafficking events for the clearance of the sequestered intracellular and extracellular cargo. Both start differently but end in the same compartment, ... ...

    Abstract Autophagy and endocytosis are two evolutionarily conserved catabolic processes that comprise vesicle trafficking events for the clearance of the sequestered intracellular and extracellular cargo. Both start differently but end in the same compartment, the lysosome. Mounting evidences from the last years have established the involvement of proteins sensitive to intracellular Ca(2+) in the control of the early autophagic steps and in the traffic of autophagic, endocytic and lysosomal vesicles. However, this knowledge is based on dispersed outcomes that do not set up a consensus model of the Ca(2+)-dependent control of autophagy and endocytosis. Here, we will provide a critical synopsis of insights from the last decade on the involvement of Ca(2+)-sensor proteins in the activation of autophagy and in fusion events of endocytic vesicles, autophagosomes and lysosomes.
    MeSH term(s) Animals ; Autophagy/physiology ; Calcium/metabolism ; Endocytosis/physiology ; Humans ; Intracellular Calcium-Sensing Proteins/metabolism ; Lysosomes/metabolism ; Phagosomes/metabolism ; Protein Transport
    Chemical Substances Intracellular Calcium-Sensing Proteins ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2013-03-01
    Publishing country United Arab Emirates
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2045662-1
    ISSN 1875-5550 ; 1389-2037
    ISSN (online) 1875-5550
    ISSN 1389-2037
    DOI 10.2174/13892037112139990033
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 5884: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  10. Article ; Online: Regulation of the autophagic PI3KC3 complex by laforin/malin E3-ubiquitin ligase, two proteins involved in Lafora disease.

    Sanchez-Martin, Pablo / Lahuerta, Marcos / Viana, Rosa / Knecht, Erwin / Sanz, Pascual

    Biochimica et biophysica acta. Molecular cell research

    2019  Volume 1867, Issue 2, Page(s) 118613

    Abstract: Lafora progressive myoclonus epilepsy is a fatal rare neurodegenerative disorder characterized by the accumulation of insoluble abnormal glycogen deposits in the brain and peripheral tissues. Mutations in at least two genes are responsible for the ... ...

    Abstract Lafora progressive myoclonus epilepsy is a fatal rare neurodegenerative disorder characterized by the accumulation of insoluble abnormal glycogen deposits in the brain and peripheral tissues. Mutations in at least two genes are responsible for the disease: EPM2A, encoding the glucan phosphatase laforin, and EPM2B, encoding the RING-type E3-ubiquitin ligase malin. Both laforin and malin form a functional complex in which laforin recruits the substrates to be ubiquitinated by malin. We and others have described that, in cellular and animal models of this disease, there is an autophagy impairment which leads to the accumulation of dysfunctional mitochondria. In addition, we established that the autophagic defect occurred at the initial steps of autophagosome formation. In this work, we present evidence that in cellular models of the disease there is a decrease in the amount of phosphatidylinositol-3P. This is probably due to defective regulation of the autophagic PI3KC3 complex, in the absence of a functional laforin/malin complex. In fact, we demonstrate that the laforin/malin complex interacts physically and co-localizes intracellularly with core components of the PI3KC3 complex (Beclin1, Vps34 and Vps15), and that this interaction is specific and results in the polyubiquitination of these proteins. In addition, the laforin/malin complex is also able to polyubiquitinate ATG14L and UVRAG. Finally, we show that overexpression of the laforin/malin complex increases PI3KC3 activity. All these results suggest a new role of the laforin/malin complex in the activation of autophagy via regulation of the PI3KC3 complex and explain the defect in autophagy described in Lafora disease.
    MeSH term(s) Adaptor Proteins, Vesicular Transport/metabolism ; Autophagy ; Autophagy-Related Proteins/metabolism ; Beclin-1/chemistry ; Beclin-1/metabolism ; Cells, Cultured ; Humans ; Lafora Disease/metabolism ; Lafora Disease/pathology ; Microscopy, Fluorescence ; Protein Binding ; Protein Tyrosine Phosphatases, Non-Receptor/chemistry ; Protein Tyrosine Phosphatases, Non-Receptor/genetics ; Protein Tyrosine Phosphatases, Non-Receptor/metabolism ; Transcription Factors/chemistry ; Transcription Factors/metabolism ; Tumor Suppressor Proteins/metabolism ; Ubiquitin-Protein Ligases/chemistry ; Ubiquitin-Protein Ligases/genetics ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitination
    Chemical Substances ATG14 protein, human ; Adaptor Proteins, Vesicular Transport ; Autophagy-Related Proteins ; Beclin-1 ; PI3KCA protein, human ; Transcription Factors ; Tumor Suppressor Proteins ; UVRAG protein, human ; NHLRC1 protein, human (EC 2.3.2.27) ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; Protein Tyrosine Phosphatases, Non-Receptor (EC 3.1.3.48) ; EPM2A protein, human (EC 3.1.3.48.)
    Language English
    Publishing date 2019-11-21
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    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.2019.118613
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.247: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top