LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 97

Search options

  1. Article ; Online: DDX3 regulates cancer immune surveillance via 3' UTR-mediated cell-surface expression of PD-L1.

    Chen, Hung-Hsi / Yu, Hsin-I / Chang, Jason Jie-Sheng / Li, Chia-Wei / Yang, Muh-Hwa / Hung, Mien-Chie / Tarn, Woan-Yuh

    Cell reports

    2024  Volume 43, Issue 3, Page(s) 113937

    Abstract: Programmed death-1 (PD-1)/PD ligand-1 (PD-L1)-mediated immune escape contributes to cancer development and has been targeted as an anti-cancer strategy. Here, we show that inhibition of the RNA helicase DDX3 increased ... ...

    Abstract Programmed death-1 (PD-1)/PD ligand-1 (PD-L1)-mediated immune escape contributes to cancer development and has been targeted as an anti-cancer strategy. Here, we show that inhibition of the RNA helicase DDX3 increased CD8
    MeSH term(s) Humans ; Carcinoma, Squamous Cell/metabolism ; 3' Untranslated Regions/genetics ; B7-H1 Antigen/metabolism ; Mouth Neoplasms/genetics ; CD8-Positive T-Lymphocytes
    Chemical Substances 3' Untranslated Regions ; B7-H1 Antigen
    Language English
    Publishing date 2024-03-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2024.113937
    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.

  2. Article ; Online: LncRNA HOTAIRM1 functions in DNA double-strand break repair via its association with DNA repair and mRNA surveillance factors.

    Chuang, Tzu-Wei / Su, Chun-Hao / Wu, Pei-Yu / Chang, Yao-Ming / Tarn, Woan-Yuh

    Nucleic acids research

    2023  Volume 51, Issue 7, Page(s) 3166–3184

    Abstract: The eukaryotic exon junction complex component Y14 participates in double-strand break (DSB) repair via its RNA-dependent interaction with the non-homologous end-joining (NHEJ) complex. Using immunoprecipitation-RNA-seq, we identified a set of Y14- ... ...

    Abstract The eukaryotic exon junction complex component Y14 participates in double-strand break (DSB) repair via its RNA-dependent interaction with the non-homologous end-joining (NHEJ) complex. Using immunoprecipitation-RNA-seq, we identified a set of Y14-associated long non-coding RNAs (lncRNAs). The lncRNA HOTAIRM1 serves as a strong candidate that mediates the interaction between Y14 and the NHEJ complex. HOTAIRM1 localized to near ultraviolet laser-induced DNA damage sites. Depletion of HOTAIRM1 delayed the recruitment of DNA damage response and repair factors to DNA lesions and compromised the efficiency of NHEJ-mediated DSB repair. Identification of the HOTAIRM1 interactome revealed a large set of RNA processing factors including mRNA surveillance factors. The surveillance factors Upf1 and SMG6 localized to DNA damage sites in a HOTAIRM1-dependent manner. Depletion of Upf1 or SMG6 increased the level of DSB-induced non-coding transcripts at damaged sites, indicating a pivotal role for Upf1/SMG6-mediated RNA degradation in DNA repair. We conclude that HOTAIRM1 serves as an assembly scaffold for both DNA repair and mRNA surveillance factors that act in concert to repair DSBs.
    MeSH term(s) DNA ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; DNA Repair/genetics ; RNA, Long Noncoding/genetics ; RNA, Messenger/genetics ; Humans ; Cell Line
    Chemical Substances DNA (9007-49-2) ; RNA, Long Noncoding ; RNA, Messenger
    Language English
    Publishing date 2023-03-07
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 186809-3
    ISSN 1362-4962 ; 1362-4954 ; 0301-5610 ; 0305-1048
    ISSN (online) 1362-4962 ; 1362-4954
    ISSN 0301-5610 ; 0305-1048
    DOI 10.1093/nar/gkad143
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 1067: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.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.

  3. Article ; Online: Activation of TrkB signaling mitigates cerebellar anomalies caused by Rbm4-Bdnf deficiency.

    Tsai, Yu-Young / Shen, Chiu-Lun / D, Dhananjaya / Tsai, Ching-Yen / Tarn, Woan-Yuh

    Communications biology

    2023  Volume 6, Issue 1, Page(s) 910

    Abstract: A molecular and functional link between neurotrophin signaling and cerebellar foliation is lacking. Here we show that constitutive knockout of two homologous genes encoding the RNA binding protein RBM4 results in foliation defects at cerebellar lobules ... ...

    Abstract A molecular and functional link between neurotrophin signaling and cerebellar foliation is lacking. Here we show that constitutive knockout of two homologous genes encoding the RNA binding protein RBM4 results in foliation defects at cerebellar lobules VI-VII and delayed motor learning in mice. Moreover, the features of Rbm4 double knockout (dKO), including impaired differentiation of cerebellar granule cells and dendritic arborization of Purkinje cells, are reminiscent of neurotrophin deficiency. Loss of RBM4 indeed reduced brain-derived neurotrophic factor (BDNF). RBM4 promoted the expression of BDNF and full-length TrkB, implicating RBM4 in efficient BDNF-TrkB signaling. Finally, prenatal supplementation with 7,8-dihydroxyflavone, a TrkB agonist, restored granule cell differentiation, Purkinje cell dendritic complexity and foliation-the intercrural fissure in particular-in the neonatal cerebellum of Rbm4dKO mice, which also showed improved motor learning in adulthood. This study provides evidence that prenatal activation of TrkB signaling ameliorates cerebellar malformation caused by BDNF deficiency.
    MeSH term(s) Animals ; Female ; Mice ; Pregnancy ; Brain-Derived Neurotrophic Factor ; Cell Differentiation ; Cerebellum ; Cytoplasmic Granules ; Nervous System Malformations
    Chemical Substances Brain-Derived Neurotrophic Factor ; rbm4 protein, mouse ; Bdnf protein, mouse
    Language English
    Publishing date 2023-09-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-023-05294-z
    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.

    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.

  4. Article ; Online: Co-phase separation of Y14 and RNA in vitro and its implication for DNA repair.

    Yu, Chia-Lin / Chuang, Tzu-Wei / Samuel, Sabrina Yeo / Lou, Yuan-Chao / Tarn, Woan-Yuh

    RNA (New York, N.Y.)

    2023  Volume 29, Issue 7, Page(s) 1007–1019

    Abstract: The multifunctional RNA recognition motif-containing protein Y14/RBM8A participates in mRNA metabolism and is essential for the efficient repair of DNA double-strand breaks (DSBs). Y14 contains highly charged, low-complexity sequences in both the amino- ... ...

    Abstract The multifunctional RNA recognition motif-containing protein Y14/RBM8A participates in mRNA metabolism and is essential for the efficient repair of DNA double-strand breaks (DSBs). Y14 contains highly charged, low-complexity sequences in both the amino- and carboxy-terminal domains. The feature of charge segregation suggests that Y14 may undergo liquid-liquid phase separation (LLPS). Recombinant Y14 formed phase-separated droplets, which were sensitive to pH and salt concentration. Domain mapping suggested that LLPS of Y14 involves multivalent electrostatic interactions and is partly determined by the net charge of its low-complexity regions. Phospho-mimicry of the carboxy-terminal arginine-serine dipeptides of Y14 suppressed phase separation. Moreover, RNA could phase separate into Y14 droplets and modulate Y14 LLPS in a concentration-dependent manner. Finally, the capacity of Y14 in LLPS and coacervation with RNA in vitro correlated with its activity in DSB repair. These results reveal a molecular rule for LLPS of Y14 in vitro and an implication for its co-condensation with RNA in genome stability.
    MeSH term(s) RNA/genetics ; Arginine/chemistry ; Protein Domains ; RNA-Binding Proteins/metabolism ; DNA Repair
    Chemical Substances RNA (63231-63-0) ; Arginine (94ZLA3W45F) ; RNA-Binding Proteins
    Language English
    Publishing date 2023-03-31
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1241540-6
    ISSN 1469-9001 ; 1355-8382
    ISSN (online) 1469-9001
    ISSN 1355-8382
    DOI 10.1261/rna.079514.122
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    In stock of ZB MED Cologne/Königswinter

    Zs.A 4777: 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.

  5. Article ; Online: uORF-mediated translational control: recently elucidated mechanisms and implications in cancer.

    Chen, Hung-Hsi / Tarn, Woan-Yuh

    RNA biology

    2019  Volume 16, Issue 10, Page(s) 1327–1338

    Abstract: Protein synthesis is tightly regulated, and its dysregulation can contribute to the pathology of various diseases, including cancer. Increased or selective translation of mRNAs can promote cancer cell proliferation, metastasis and tumor expansion. ... ...

    Abstract Protein synthesis is tightly regulated, and its dysregulation can contribute to the pathology of various diseases, including cancer. Increased or selective translation of mRNAs can promote cancer cell proliferation, metastasis and tumor expansion. Translational control is one of the most important means for cells to quickly adapt to environmental stresses. Adaptive translation involves various alternative mechanisms of translation initiation. Upstream open reading frames (uORFs) serve as a major regulator of stress-responsive translational control. Since recent advances in omics technologies including ribo-seq have expanded our knowledge of translation, we discuss emerging mechanisms for uORF-mediated translation regulation and its impact on cancer cell biology. A better understanding of dysregulated translational control of uORFs in cancer would facilitate the development of new strategies for cancer therapy.
    MeSH term(s) 5' Flanking Region ; Animals ; Disease Susceptibility ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology ; Open Reading Frames ; Protein Biosynthesis ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Regulatory Sequences, Nucleic Acid ; Stress, Physiological/genetics ; Trans-Activators/metabolism
    Chemical Substances RNA, Messenger ; Trans-Activators
    Language English
    Publishing date 2019-06-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ISSN 1555-8584
    ISSN (online) 1555-8584
    DOI 10.1080/15476286.2019.1632634
    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.

    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.

  6. Article ; Online: p53 Activation in Genetic Disorders: Different Routes to the Same Destination.

    Tsai, Yu-Young / Su, Chun-Hao / Tarn, Woan-Yuh

    International journal of molecular sciences

    2021  Volume 22, Issue 17

    Abstract: The tumor suppressor p53 is critical for preventing neoplastic transformation and tumor progression. Inappropriate activation of p53, however, has been observed in a number of human inherited disorders that most often affect development of the brain, ... ...

    Abstract The tumor suppressor p53 is critical for preventing neoplastic transformation and tumor progression. Inappropriate activation of p53, however, has been observed in a number of human inherited disorders that most often affect development of the brain, craniofacial region, limb skeleton, and hematopoietic system. Genes related to these developmental disorders are essentially involved in transcriptional regulation/chromatin remodeling, rRNA metabolism, DNA damage-repair pathways, telomere maintenance, and centrosome biogenesis. Perturbation of these activities or cellular processes may result in p53 accumulation in cell cultures, animal models, and perhaps humans as well. Mouse models of several p53 activation-associated disorders essentially recapitulate human traits, and inactivation of p53 in these models can alleviate disorder-related phenotypes. In the present review, we focus on how dysfunction of the aforementioned biological processes causes developmental defects via excessive p53 activation. Notably, several disease-related genes exert a pleiotropic effect on those cellular processes, which may modulate the magnitude of p53 activation and establish or disrupt regulatory loops. Finally, we discuss potential therapeutic strategies for genetic disorders associated with p53 misactivation.
    MeSH term(s) Animals ; Cell Transformation, Neoplastic ; Genetic Diseases, Inborn/genetics ; Genetic Diseases, Inborn/pathology ; Humans ; Mutation ; Phenotype ; Signal Transduction ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Tumor Suppressor Protein p53
    Language English
    Publishing date 2021-08-27
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms22179307
    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.

  7. Article ; Online: p53 Activation in Genetic Disorders

    Yu-Young Tsai / Chun-Hao Su / Woan-Yuh Tarn

    International Journal of Molecular Sciences, Vol 22, Iss 9307, p

    Different Routes to the Same Destination

    2021  Volume 9307

    Abstract: The tumor suppressor p53 is critical for preventing neoplastic transformation and tumor progression. Inappropriate activation of p53, however, has been observed in a number of human inherited disorders that most often affect development of the brain, ... ...

    Abstract The tumor suppressor p53 is critical for preventing neoplastic transformation and tumor progression. Inappropriate activation of p53, however, has been observed in a number of human inherited disorders that most often affect development of the brain, craniofacial region, limb skeleton, and hematopoietic system. Genes related to these developmental disorders are essentially involved in transcriptional regulation/chromatin remodeling, rRNA metabolism, DNA damage-repair pathways, telomere maintenance, and centrosome biogenesis. Perturbation of these activities or cellular processes may result in p53 accumulation in cell cultures, animal models, and perhaps humans as well. Mouse models of several p53 activation-associated disorders essentially recapitulate human traits, and inactivation of p53 in these models can alleviate disorder-related phenotypes. In the present review, we focus on how dysfunction of the aforementioned biological processes causes developmental defects via excessive p53 activation. Notably, several disease-related genes exert a pleiotropic effect on those cellular processes, which may modulate the magnitude of p53 activation and establish or disrupt regulatory loops. Finally, we discuss potential therapeutic strategies for genetic disorders associated with p53 misactivation.
    Keywords centrosome ; developmental disorders ; DNA damage repair ; p53 ; ribosome ; telomere ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Subject code 572
    Language English
    Publishing date 2021-08-01T00:00:00Z
    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.

  8. Article: Antisense Oligonucleotide-Based Therapy of Viral Infections.

    Tarn, Woan-Yuh / Cheng, Yun / Ko, Shih-Han / Huang, Li-Min

    Pharmaceutics

    2021  Volume 13, Issue 12

    Abstract: Nucleic acid-based therapeutics have demonstrated their efficacy in the treatment of various diseases and vaccine development. Antisense oligonucleotide (ASO) technology exploits a single-strand short oligonucleotide to either cause target RNA ... ...

    Abstract Nucleic acid-based therapeutics have demonstrated their efficacy in the treatment of various diseases and vaccine development. Antisense oligonucleotide (ASO) technology exploits a single-strand short oligonucleotide to either cause target RNA degradation or sterically block the binding of cellular factors or machineries to the target RNA. Chemical modification or bioconjugation of ASOs can enhance both its pharmacokinetic and pharmacodynamic performance, and it enables customization for a specific clinical purpose. ASO-based therapies have been used for treatment of genetic disorders, cancer and viral infections. In particular, ASOs can be rapidly developed for newly emerging virus and their reemerging variants. This review discusses ASO modifications and delivery options as well as the design of antiviral ASOs. A better understanding of the viral life cycle and virus-host interactions as well as advances in oligonucleotide technology will benefit the development of ASO-based antiviral therapies.
    Language English
    Publishing date 2021-11-26
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527217-2
    ISSN 1999-4923
    ISSN 1999-4923
    DOI 10.3390/pharmaceutics13122015
    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.

  9. Article ; Online: The Y14-p53 regulatory circuit in megakaryocyte differentiation and thrombocytopenia.

    Su, Chun-Hao / Liao, Wei-Ju / Ke, Wei-Chi / Yang, Ruey-Bing / Tarn, Woan-Yuh

    iScience

    2021  Volume 24, Issue 11, Page(s) 103368

    Abstract: Thrombocytopenia-absent radius (TAR) syndrome is caused by RBM8A insufficiency. We generated megakaryocyte- ... ...

    Abstract Thrombocytopenia-absent radius (TAR) syndrome is caused by RBM8A insufficiency. We generated megakaryocyte-specific
    Language English
    Publishing date 2021-10-29
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2021.103368
    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.

    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.

  10. Article: The Host Heat Shock Protein MRJ/DNAJB6 Modulates Virus Infection.

    Ko, Shih-Han / Huang, Li-Min / Tarn, Woan-Yuh

    Frontiers in microbiology

    2019  Volume 10, Page(s) 2885

    Abstract: A variety of pathogens take advantage of cellular heat shock proteins (HSPs) to complete their life cycle and exert pathogenic effects. MRJ (DNAJB6), a member of the heat shock protein 40 family, acts as a molecular chaperone for a wide range of cellular ...

    Abstract A variety of pathogens take advantage of cellular heat shock proteins (HSPs) to complete their life cycle and exert pathogenic effects. MRJ (DNAJB6), a member of the heat shock protein 40 family, acts as a molecular chaperone for a wide range of cellular processes. MRJ mutations are linked to human diseases, such as muscular dystrophy and neurodegenerative diseases. There are two MRJ isoforms generated by alternative use of terminal exons, which differ in their C-terminus. This mini-review summarizes how these two MRJ isoforms participate differentially in viral production and virulence, and the possibility for MRJ as a therapeutic target.
    Language English
    Publishing date 2019-12-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2587354-4
    ISSN 1664-302X
    ISSN 1664-302X
    DOI 10.3389/fmicb.2019.02885
    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