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  1. Article ; Online: Down Syndrome and COVID-19: A Perfect Storm?

    Espinosa, Joaquin M

    Cell reports. Medicine

    2020  Volume 1, Issue 2, Page(s) 100019

    Abstract: People with Down syndrome show signs of chronic immune dysregulation, including a higher prevalence of autoimmune disorders, increased rates of hospitalization during respiratory viral infections, and higher mortality rates from pneumonia and sepsis. At ... ...

    Abstract People with Down syndrome show signs of chronic immune dysregulation, including a higher prevalence of autoimmune disorders, increased rates of hospitalization during respiratory viral infections, and higher mortality rates from pneumonia and sepsis. At the molecular and cellular levels, they show markers of chronic autoinflammation, including interferon hyperactivity, elevated levels of many inflammatory cytokines and chemokines, and changes in diverse immune cell types reminiscent of inflammatory conditions observed in the general population. However, the impact of this immune dysregulation in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and CoV disease of 2019 (COVID-19) remains unknown. This Perspective outlines why individuals with Down syndrome should be considered an at-risk population for severe COVID-19. Specifically, the immune dysregulation caused by trisomy 21 may result in an exacerbated cytokine release syndrome relative to that observed in the euploid population, thus justifying additional monitoring and specialized care for this vulnerable population.
    MeSH term(s) Bacterial Infections/immunology ; COVID-19/immunology ; Coinfection ; Cytokine Release Syndrome/immunology ; Cytokines/immunology ; Cytokines/metabolism ; Down Syndrome/immunology ; Humans ; Inflammation ; Interferons/immunology ; Interferons/metabolism ; SARS-CoV-2
    Chemical Substances Cytokines ; Interferons (9008-11-1)
    Keywords covid19
    Language English
    Publishing date 2020-05-01
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2666-3791
    ISSN (online) 2666-3791
    DOI 10.1016/j.xcrm.2020.100019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Transcriptional control by enhancers: working remotely for improved performance.

    Espinosa, Joaquin M

    Transcription

    2020  Volume 11, Issue 1, Page(s) 1–2

    MeSH term(s) Enhancer Elements, Genetic/genetics ; Humans ; Transcription, Genetic/genetics
    Language English
    Publishing date 2020-02-12
    Publishing country United States
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 2646974-1
    ISSN 2154-1272 ; 2154-1264
    ISSN (online) 2154-1272
    ISSN 2154-1264
    DOI 10.1080/21541264.2020.1724673
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Transcriptional CDKs in the spotlight.

    Espinosa, Joaquin M

    Transcription

    2019  Volume 10, Issue 2, Page(s) 45–46

    MeSH term(s) Animals ; Cyclin-Dependent Kinases/antagonists & inhibitors ; Cyclin-Dependent Kinases/metabolism ; Humans ; Transcription, Genetic/drug effects ; Transcription, Genetic/genetics
    Chemical Substances Cyclin-Dependent Kinases (EC 2.7.11.22)
    Language English
    Publishing date 2019-04-04
    Publishing country United States
    Document type Editorial ; Introductory Journal Article
    ZDB-ID 2646974-1
    ISSN 2154-1272 ; 2154-1264
    ISSN (online) 2154-1272
    ISSN 2154-1264
    DOI 10.1080/21541264.2019.1597479
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Addressing challenges in health care and research for people with Down syndrome.

    Fortea, Juan / McGlinchey, Eimear / Espinosa, Joaquín M / Rafii, Michael S

    Lancet (London, England)

    2024  

    Language English
    Publishing date 2024-03-20
    Publishing country England
    Document type Journal Article
    ZDB-ID 3306-6
    ISSN 1474-547X ; 0023-7507 ; 0140-6736
    ISSN (online) 1474-547X
    ISSN 0023-7507 ; 0140-6736
    DOI 10.1016/S0140-6736(24)00478-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    ab Jg. 2022: Lesesaal (EG)
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  5. Article: Down Syndrome and COVID-19: A Perfect Storm?

    Espinosa, Joaquin M

    Cell Rep Med

    Abstract: People with Down syndrome show signs of chronic immune dysregulation, including a higher prevalence of autoimmune disorders, increased rates of hospitalization during respiratory viral infections, and higher mortality rates from pneumonia and sepsis. At ... ...

    Abstract People with Down syndrome show signs of chronic immune dysregulation, including a higher prevalence of autoimmune disorders, increased rates of hospitalization during respiratory viral infections, and higher mortality rates from pneumonia and sepsis. At the molecular and cellular levels, they show markers of chronic autoinflammation, including interferon hyperactivity, elevated levels of many inflammatory cytokines and chemokines, and changes in diverse immune cell types reminiscent of inflammatory conditions observed in the general population. However, the impact of this immune dysregulation in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and CoV disease of 2019 (COVID-19) remains unknown. This Perspective outlines why individuals with Down syndrome should be considered an at-risk population for severe COVID-19. Specifically, the immune dysregulation caused by trisomy 21 may result in an exacerbated cytokine release syndrome relative to that observed in the euploid population, thus justifying additional monitoring and specialized care for this vulnerable population.
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #306204
    Database COVID19

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  6. Article ; Online: Down Syndrome and COVID-19

    Espinosa, Joaquin M.

    Cell Reports Medicine

    A Perfect Storm?

    2020  Volume 1, Issue 2, Page(s) 100019

    Keywords covid19
    Language English
    Publisher Elsevier BV
    Publishing country us
    Document type Article ; Online
    ISSN 2666-3791
    DOI 10.1016/j.xcrm.2020.100019
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article: On the Origin of lncRNAs: Missing Link Found.

    Espinosa, Joaquín M

    Trends in genetics : TIG

    2017  Volume 33, Issue 10, Page(s) 660–662

    Abstract: Non-coding (nc)RNAs known as enhancer-derived RNAs (eRNAs) and as long ncRNAs (lncRNAs) have received much attention, but their true functional specialization and evolutionary origins remain obscure. The recent characterization of Bloodlinc, an eRNA ... ...

    Abstract Non-coding (nc)RNAs known as enhancer-derived RNAs (eRNAs) and as long ncRNAs (lncRNAs) have received much attention, but their true functional specialization and evolutionary origins remain obscure. The recent characterization of Bloodlinc, an eRNA derived from a super-enhancer that also functions as a lncRNA, suggests that lncRNAs can evolve from eRNAs.
    MeSH term(s) Enhancer Elements, Genetic ; Evolution, Molecular ; Humans ; RNA, Long Noncoding/genetics
    Chemical Substances RNA, Long Noncoding
    Language English
    Publishing date 2017-08-01
    Publishing country England
    Document type Journal Article ; Comment
    ZDB-ID 619240-3
    ISSN 1362-4555 ; 0168-9525 ; 0168-9479
    ISSN (online) 1362-4555
    ISSN 0168-9525 ; 0168-9479
    DOI 10.1016/j.tig.2017.07.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2272: 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)

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  8. Article ; Online: Multi-omics investigation reveals functional specialization of transcriptional cyclin dependent kinases in cancer biology.

    Donovan, Micah G / Galbraith, Matthew D / Espinosa, Joaquin M

    Scientific reports

    2022  Volume 12, Issue 1, Page(s) 22505

    Abstract: Transcriptional addiction is recognized as a valid therapeutic target in cancer, whereby the dependency of cancer cells on oncogenic transcriptional regulators may be pharmacologically exploited. However, a comprehensive understanding of the key factors ... ...

    Abstract Transcriptional addiction is recognized as a valid therapeutic target in cancer, whereby the dependency of cancer cells on oncogenic transcriptional regulators may be pharmacologically exploited. However, a comprehensive understanding of the key factors within the transcriptional machinery that might afford a useful therapeutic window remains elusive. Herein, we present a cross-omics investigation into the functional specialization of the transcriptional cyclin dependent kinases (tCDKs) through analysis of high-content genetic dependency, gene expression, patient survival, and drug response datasets. This analysis revealed specialization among tCDKs in terms of contributions to cancer cell fitness, clinical prognosis, and interaction with oncogenic signaling pathways. CDK7 and CDK9 stand out as the most relevant targets, albeit through distinct mechanisms of oncogenicity and context-dependent contributions to cancer survival and drug sensitivity. Genetic ablation of CDK9, but not CDK7, mimics the effect on cell viability the loss of key components of the transcriptional machinery. Pathway analysis of genetic co-dependency and drug sensitivity data show CDK7 and CDK9 have distinct relationships with major oncogenic signatures, including MYC and E2F targets, oxidative phosphorylation, and the unfolded protein response. Altogether, these results inform the improved design of therapeutic strategies targeting tCDKs in cancer.
    MeSH term(s) Humans ; Cyclin-Dependent Kinases/genetics ; Cyclin-Dependent Kinases/metabolism ; Multiomics ; Signal Transduction ; Neoplasms/genetics ; Cyclins/metabolism
    Chemical Substances Cyclin-Dependent Kinases (EC 2.7.11.22) ; Cyclins
    Language English
    Publishing date 2022-12-28
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-26860-1
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Revisiting lncRNAs: How Do You Know Yours Is Not an eRNA?

    Espinosa, Joaquín M

    Molecular cell

    2016  Volume 62, Issue 1, Page(s) 1–2

    Abstract: Diverse classes of noncoding RNAs have been recently established, but the defining criteria for each class are not always obvious. New research from Paralkar et al. (2016) in this issue of Molecular Cell challenges the distinction between long noncoding ... ...

    Abstract Diverse classes of noncoding RNAs have been recently established, but the defining criteria for each class are not always obvious. New research from Paralkar et al. (2016) in this issue of Molecular Cell challenges the distinction between long noncoding RNAs and enhancer-derived RNAs, and provides an experimental approach to define their mechanism of action.
    MeSH term(s) RNA, Long Noncoding/genetics ; RNA, Untranslated
    Chemical Substances RNA, Long Noncoding ; RNA, Untranslated
    Language English
    Publishing date 2016-04-07
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2016.03.022
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5055: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  10. Article ; Online: PPM1D suppresses p53-dependent transactivation and cell death by inhibiting the Integrated Stress Response.

    Andrysik, Zdenek / Sullivan, Kelly D / Kieft, Jeffrey S / Espinosa, Joaquin M

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 7400

    Abstract: The p53 transcription factor is a master regulator of cellular stress responses inhibited by repressors such as MDM2 and the phosphatase PPM1D. Activation of p53 with pharmacological inhibitors of its repressors is being tested in clinical trials for ... ...

    Abstract The p53 transcription factor is a master regulator of cellular stress responses inhibited by repressors such as MDM2 and the phosphatase PPM1D. Activation of p53 with pharmacological inhibitors of its repressors is being tested in clinical trials for cancer therapy, but efficacy has been limited by poor induction of tumor cell death. We demonstrate that dual inhibition of MDM2 and PPM1D induces apoptosis in multiple cancer cell types via amplification of the p53 transcriptional program through the eIF2α-ATF4 pathway. PPM1D inhibition induces phosphorylation of eIF2α, ATF4 accumulation, and ATF4-dependent enhancement of p53-dependent transactivation upon MDM2 inhibition. Dual inhibition of p53 repressors depletes heme and induces HRI-dependent eIF2α phosphorylation. Pharmacological induction of eIF2α phosphorylation synergizes with MDM2 inhibition to induce cell death and halt tumor growth in mice. These results demonstrate that PPM1D inhibits both the p53 network and the integrated stress response controlled by eIF2α-ATF4, with clear therapeutic implications.
    MeSH term(s) Animals ; Mice ; Apoptosis ; Cell Death ; Eukaryotic Initiation Factor-2/genetics ; Phosphorylation ; Transcription Factors ; Transcriptional Activation ; Tumor Suppressor Protein p53/genetics ; Protein Phosphatase 2C/metabolism ; Neoplasms
    Chemical Substances Eukaryotic Initiation Factor-2 ; Transcription Factors ; Tumor Suppressor Protein p53 ; Ppm1d protein, mouse (EC 3.1.3.16) ; Protein Phosphatase 2C (EC 3.1.3.16)
    Language English
    Publishing date 2022-12-01
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-35089-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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