LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 5 of total 5

Search options

  1. Article: Notch Inhibition Enhances Morphological Reprogramming of microRNA-Induced Human Neurons.

    Burbach, Kyle F / Yoo, Andrew S

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Although the importance of Notch signaling in brain development is well-known, its specific contribution to cellular reprogramming remains less defined. Here, we use microRNA-induced neurons that are directly reprogrammed from human fibroblasts to ... ...

    Abstract Although the importance of Notch signaling in brain development is well-known, its specific contribution to cellular reprogramming remains less defined. Here, we use microRNA-induced neurons that are directly reprogrammed from human fibroblasts to determine how Notch signaling contributes to neuronal identity. We found that inhibiting Notch signaling led to an increase in neurite extension, while activating Notch signaling had the opposite effect. Surprisingly, Notch inhibition during the first week of reprogramming was both necessary and sufficient to enhance neurite outgrowth at a later timepoint. This timeframe is when the reprogramming miRNAs, miR-9/9* and miR-124, primarily induce a post-mitotic state and erase fibroblast identity. Accordingly, transcriptomic analysis showed that the effect of Notch inhibition was likely due to improvements in fibroblast fate erasure and silencing of anti-neuronal genes. To this effect, we identify
    Language English
    Publishing date 2024-01-12
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.12.575384
    Database MEDical Literature Analysis and Retrieval System 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.

  2. Article: SAK3 confers neuroprotection in the neurodegeneration model of X-linked Dystonia-Parkinsonism.

    Aryal, Shivani / Chen, Shawei / Burbach, Kyle F / Yang, Yan / Capano, Lucia S / Kim, Woo Kyung / Bragg, D Cristopher / Yoo, Andrew

    Research square

    2024  

    Abstract: Background X-linked Dystonia-Parkinsonism(XDP) is an adult-onset neurodegenerative disorder that results in the loss of striatal medium spiny neurons (MSNs). XDP is associated with disease-specific mutations in and around ... ...

    Abstract Background X-linked Dystonia-Parkinsonism(XDP) is an adult-onset neurodegenerative disorder that results in the loss of striatal medium spiny neurons (MSNs). XDP is associated with disease-specific mutations in and around the
    Language English
    Publishing date 2024-04-25
    Publishing country United States
    Document type Preprint
    DOI 10.21203/rs.3.rs-4068432/v1
    Database MEDical Literature Analysis and Retrieval System 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.

  3. Article ; Online: Recapitulation of endogenous 4R tau expression and formation of insoluble tau in directly reprogrammed human neurons.

    Capano, Lucia S / Sato, Chihiro / Ficulle, Elena / Yu, Anan / Horie, Kanta / Kwon, Ji-Sun / Burbach, Kyle F / Barthélemy, Nicolas R / Fox, Susan G / Karch, Celeste M / Bateman, Randall J / Houlden, Henry / Morimoto, Richard I / Holtzman, David M / Duff, Karen E / Yoo, Andrew S

    Cell stem cell

    2022  Volume 29, Issue 6, Page(s) 918–932.e8

    Abstract: Tau is a microtubule-binding protein expressed in neurons, and the equal ratios between 4-repeat (4R) and 3-repeat (3R) isoforms are maintained in normal adult brain function. Dysregulation of 3R:4R ratio causes tauopathy, and human neurons that ... ...

    Abstract Tau is a microtubule-binding protein expressed in neurons, and the equal ratios between 4-repeat (4R) and 3-repeat (3R) isoforms are maintained in normal adult brain function. Dysregulation of 3R:4R ratio causes tauopathy, and human neurons that recapitulate tau isoforms in health and disease will provide a platform for elucidating pathogenic processes involving tau pathology. We carried out extensive characterizations of tau isoforms expressed in human neurons derived by microRNA-induced neuronal reprogramming of adult fibroblasts. Transcript and protein analyses showed that miR neurons expressed all six isoforms with the 3R:4R isoform ratio equivalent to that detected in human adult brains. Also, miR neurons derived from familial tauopathy patients with a 3R:4R ratio altering mutation showed increased 4R tau and the formation of insoluble tau with seeding activity. Our results collectively demonstrate the utility of miRNA-induced neuronal reprogramming to recapitulate endogenous tau regulation comparable with the adult brain in health and disease.
    MeSH term(s) Adult ; Humans ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Neurons/metabolism ; Protein Isoforms/metabolism ; Tauopathies/metabolism ; Tauopathies/pathology ; tau Proteins/metabolism
    Chemical Substances MicroRNAs ; Protein Isoforms ; tau Proteins
    Language English
    Publishing date 2022-04-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2022.04.018
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 6589: 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)
    Zs.MG 75: Show issues

    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 ; Online: Deconstructing Stepwise Fate Conversion of Human Fibroblasts to Neurons by MicroRNAs.

    Cates, Kitra / McCoy, Matthew J / Kwon, Ji-Sun / Liu, Yangjian / Abernathy, Daniel G / Zhang, Bo / Liu, Shaopeng / Gontarz, Paul / Kim, Woo Kyung / Chen, Shawei / Kong, Wenjun / Ho, Joshua N / Burbach, Kyle F / Gabel, Harrison W / Morris, Samantha A / Yoo, Andrew S

    Cell stem cell

    2020  Volume 28, Issue 1, Page(s) 127–140.e9

    Abstract: Cell-fate conversion generally requires reprogramming effectors to both introduce fate programs of the target cell type and erase the identity of starting cell population. Here, we reveal insights into the activity of microRNAs miR-9/ ... ...

    Abstract Cell-fate conversion generally requires reprogramming effectors to both introduce fate programs of the target cell type and erase the identity of starting cell population. Here, we reveal insights into the activity of microRNAs miR-9/9
    MeSH term(s) Cell Differentiation ; Cellular Reprogramming/genetics ; Chromatin ; Fibroblasts ; Humans ; MicroRNAs/genetics ; Transcription Factors/genetics
    Chemical Substances Chromatin ; MicroRNAs ; Transcription Factors
    Language English
    Publishing date 2020-09-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2375354-7
    ISSN 1875-9777 ; 1934-5909
    ISSN (online) 1875-9777
    ISSN 1934-5909
    DOI 10.1016/j.stem.2020.08.015
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 6589: 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)
    Zs.MG 75: Show issues

    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: Psychedelics Promote Structural and Functional Neural Plasticity.

    Ly, Calvin / Greb, Alexandra C / Cameron, Lindsay P / Wong, Jonathan M / Barragan, Eden V / Wilson, Paige C / Burbach, Kyle F / Soltanzadeh Zarandi, Sina / Sood, Alexander / Paddy, Michael R / Duim, Whitney C / Dennis, Megan Y / McAllister, A Kimberley / Ori-McKenney, Kassandra M / Gray, John A / Olson, David E

    Cell reports

    2018  Volume 23, Issue 11, Page(s) 3170–3182

    Abstract: Atrophy of neurons in the prefrontal cortex (PFC) plays a key role in the pathophysiology of depression and related disorders. The ability to promote both structural and functional plasticity in the PFC has been hypothesized to underlie the fast-acting ... ...

    Abstract Atrophy of neurons in the prefrontal cortex (PFC) plays a key role in the pathophysiology of depression and related disorders. The ability to promote both structural and functional plasticity in the PFC has been hypothesized to underlie the fast-acting antidepressant properties of the dissociative anesthetic ketamine. Here, we report that, like ketamine, serotonergic psychedelics are capable of robustly increasing neuritogenesis and/or spinogenesis both in vitro and in vivo. These changes in neuronal structure are accompanied by increased synapse number and function, as measured by fluorescence microscopy and electrophysiology. The structural changes induced by psychedelics appear to result from stimulation of the TrkB, mTOR, and 5-HT2A signaling pathways and could possibly explain the clinical effectiveness of these compounds. Our results underscore the therapeutic potential of psychedelics and, importantly, identify several lead scaffolds for medicinal chemistry efforts focused on developing plasticity-promoting compounds as safe, effective, and fast-acting treatments for depression and related disorders.
    MeSH term(s) Animals ; Antidepressive Agents/pharmacology ; Brain-Derived Neurotrophic Factor/pharmacology ; Cells, Cultured ; Cerebral Cortex/cytology ; Cerebral Cortex/metabolism ; Female ; Male ; Microscopy, Fluorescence ; Neurogenesis/drug effects ; Neuronal Plasticity/drug effects ; Rats ; Rats, Sprague-Dawley ; Receptor, Serotonin, 5-HT2A/metabolism ; Receptor, trkB/metabolism ; Signal Transduction/drug effects ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances Antidepressive Agents ; Brain-Derived Neurotrophic Factor ; Receptor, Serotonin, 5-HT2A ; mTOR protein, rat (EC 2.7.1.1) ; Ntrk2 protein, rat (EC 2.7.10.1) ; Receptor, trkB (EC 2.7.10.1) ; TOR Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2018-02-13
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2018.05.022
    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.

To top