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  1. Article ; Online: Understanding on CRISPR/Cas9 mediated cutting-edge approaches for cancer therapeutics.

    Bhattacharjee, Rudrarup / Das Roy, Lopamudra / Choudhury, Amarendranath

    Discover. Oncology

    2022  Volume 13, Issue 1, Page(s) 45

    Abstract: The research focus on CRISPR/Cas9 has gained substantial concentration since the discovery of 'an unusual repeat sequence' reported by Ishino et al. (J Bacteriol 169:5429-5433, 1987) and the journey comprises the recent Nobel Prize award (2020), ... ...

    Abstract The research focus on CRISPR/Cas9 has gained substantial concentration since the discovery of 'an unusual repeat sequence' reported by Ishino et al. (J Bacteriol 169:5429-5433, 1987) and the journey comprises the recent Nobel Prize award (2020), conferred to Emmanuelle Charpentier and Jennifer Doudna. Cumulatively, the CRISPR has a short, compact, and most discussed success of its application in becoming one of the most versatile and paradigm shifting technologies of Biological Research. Today, the CRISPR/Cas9 genome editing system is almost ubiquitously utilized in many facets of biological research where its tremendous gene manipulation capability has been harnessed to create miracles. From 2012, the CRISPR/Cas 9 system has been showcased in almost 15,000 research articles in the PubMed database, till date. Backed by some strong molecular evidence, the CRISPR system has been utilized in a few clinical trials targeted towards various pathologies. While the area covered by CRISPR is cosmic, this review will focus mostly on the utilization of CRISPR/Cas9 technology in the field of cancer therapy.
    Language English
    Publishing date 2022-06-08
    Publishing country United States
    Document type Journal Article
    ISSN 2730-6011
    ISSN (online) 2730-6011
    DOI 10.1007/s12672-022-00509-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Multiomic analysis implicates nuclear hormone receptor signalling in clustering epilepsy.

    de Nys, Rebekah / van Eyk, Clare L / Ritchie, Tarin / Møller, Rikke S / Scheffer, Ingrid E / Marini, Carla / Bhattacharjee, Rudrarup / Kumar, Raman / Gecz, Jozef

    Translational psychiatry

    2024  Volume 14, Issue 1, Page(s) 65

    Abstract: Clustering Epilepsy (CE) is an epileptic disorder with neurological comorbidities caused by heterozygous variants of the X chromosome gene Protocadherin 19 (PCDH19). Recent studies have implicated dysregulation of the Nuclear Hormone Receptor (NHR) ... ...

    Abstract Clustering Epilepsy (CE) is an epileptic disorder with neurological comorbidities caused by heterozygous variants of the X chromosome gene Protocadherin 19 (PCDH19). Recent studies have implicated dysregulation of the Nuclear Hormone Receptor (NHR) pathway in CE pathogenesis. To obtain a comprehensive overview of the impact and mechanisms of loss of PCDH19 function in CE pathogenesis, we have performed epigenomic, transcriptomic and proteomic analysis of CE relevant models. Our studies identified differential regulation and expression of Androgen Receptor (AR) and its targets in CE patient skin fibroblasts. Furthermore, our cell culture assays revealed the repression of PCDH19 expression mediated through ERα and the co-regulator FOXA1. We also identified a protein-protein interaction between PCDH19 and AR, expanding upon the intrinsic link between PCDH19 and the NHR pathway. Together, these results point to a novel mechanism of NHR signaling in the pathogenesis of CE that can be explored for potential therapeutic options.
    MeSH term(s) Humans ; Cadherins/genetics ; Protocadherins ; Multiomics ; Proteomics ; Epilepsy/genetics ; Cluster Analysis
    Chemical Substances Cadherins ; Protocadherins ; PCDH19 protein, human
    Language English
    Publishing date 2024-01-27
    Publishing country United States
    Document type Review ; Journal Article
    ZDB-ID 2609311-X
    ISSN 2158-3188 ; 2158-3188
    ISSN (online) 2158-3188
    ISSN 2158-3188
    DOI 10.1038/s41398-024-02783-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Proteomic analysis of the developing mammalian brain links PCDH19 to the Wnt/β-catenin signalling pathway.

    de Nys, Rebekah / Gardner, Alison / van Eyk, Clare / Mincheva-Tasheva, Stefka / Thomas, Paul / Bhattacharjee, Rudrarup / Jolly, Lachlan / Martinez-Garay, Isabel / Fox, Ian W J / Kamath, Karthik Shantharam / Kumar, Raman / Gecz, Jozef

    Molecular psychiatry

    2024  

    Abstract: Clustering Epilepsy (CE) is a neurological disorder caused by pathogenic variants of the Protocadherin 19 (PCDH19) gene. PCDH19 encodes a protein involved in cell adhesion and Estrogen Receptor α mediated-gene regulation. To gain further insights into ... ...

    Abstract Clustering Epilepsy (CE) is a neurological disorder caused by pathogenic variants of the Protocadherin 19 (PCDH19) gene. PCDH19 encodes a protein involved in cell adhesion and Estrogen Receptor α mediated-gene regulation. To gain further insights into the molecular role of PCDH19 in the brain, we investigated the PCDH19 interactome in the developing mouse hippocampus and cortex. Combined with a meta-analysis of all reported PCDH19 interacting proteins, our results show that PCDH19 interacts with proteins involved in actin, microtubule, and gene regulation. We report CAPZA1, αN-catenin and, importantly, β-catenin as novel PCDH19 interacting proteins. Furthermore, we show that PCDH19 is a regulator of β-catenin transcriptional activity, and that this pathway is disrupted in CE individuals. Overall, our results support the involvement of PCDH19 in the cytoskeletal network and point to signalling pathways where PCDH19 plays critical roles.
    Language English
    Publishing date 2024-03-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 1330655-8
    ISSN 1476-5578 ; 1359-4184
    ISSN (online) 1476-5578
    ISSN 1359-4184
    DOI 10.1038/s41380-024-02482-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4812: 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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  4. Article ; Online: Controlling Intestinal Infections and Digestive Disorders Using Probiotics.

    Kumar, Sanjeev / Ahmad, Md Faruque / Nath, Priyakshi / Roy, Rubina / Bhattacharjee, Rudrarup / Shama, Eman / Gahatraj, Indira / Sehrawat, Manisha / Dasriya, Vaishali / Dhillon, Harmeet Singh / Puniya, Monica / Samtiya, Mrinal / Dhewa, Tejpal / Aluko, Rotimi E / Khedkar, Gulab D / Raposo, António / Puniya, Anil Kumar

    Journal of medicinal food

    2023  Volume 26, Issue 10, Page(s) 705–720

    Abstract: After consumption, probiotics provide health benefits to the host. Probiotics and their metabolites have therapeutic and nutritional properties that help to alleviate gastrointestinal, neurological, and cardiovascular problems. Probiotics strengthen host ...

    Abstract After consumption, probiotics provide health benefits to the host. Probiotics and their metabolites have therapeutic and nutritional properties that help to alleviate gastrointestinal, neurological, and cardiovascular problems. Probiotics strengthen host immunity through various mechanisms, including improved gut barrier function, receptor site blocking, competitive exclusion of pathogens, and the production of bioactive molecules. Emerging evidence suggests that intestinal bowel diseases can be fatal, but regular probiotic consumption can alleviate disease symptoms. The use and detailed description of the health benefits of probiotics to consumers in terms of reducing intestinal infection, inflammation, and digestive disorders are discussed in this review. The well-designed and controlled studies that examined the use of probiotics to reduce life-threatening activities caused by intestinal bowel diseases are also covered. This review discussed the active principles and potency of probiotics as evidenced by the known effects on host health, in addition to providing information on the mechanism of action.
    MeSH term(s) Humans ; Probiotics/therapeutic use ; Probiotics/metabolism ; Inflammation
    Language English
    Publishing date 2023-08-30
    Publishing country United States
    Document type Review ; Journal Article
    ZDB-ID 1427365-2
    ISSN 1557-7600 ; 1096-620X
    ISSN (online) 1557-7600
    ISSN 1096-620X
    DOI 10.1089/jmf.2023.0062
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5916: 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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  5. Article ; Online: Compromised transcription-mRNA export factor THOC2 causes R-loop accumulation, DNA damage and adverse neurodevelopment.

    Bhattacharjee, Rudrarup / Jolly, Lachlan A / Corbett, Mark A / Wee, Ing Chee / Rao, Sushma R / Gardner, Alison E / Ritchie, Tarin / van Hugte, Eline J H / Ciptasari, Ummi / Piltz, Sandra / Noll, Jacqueline E / Nazri, Nazzmer / van Eyk, Clare L / White, Melissa / Fornarino, Dani / Poulton, Cathryn / Baynam, Gareth / Collins-Praino, Lyndsey E / Snel, Marten F /
    Nadif Kasri, Nael / Hemsley, Kim M / Thomas, Paul Q / Kumar, Raman / Gecz, Jozef

    Nature communications

    2024  Volume 15, Issue 1, Page(s) 1210

    Abstract: We implicated the X-chromosome THOC2 gene, which encodes the largest subunit of the highly-conserved TREX (Transcription-Export) complex, in a clinically complex neurodevelopmental disorder with intellectual disability as the core phenotype. To study the ...

    Abstract We implicated the X-chromosome THOC2 gene, which encodes the largest subunit of the highly-conserved TREX (Transcription-Export) complex, in a clinically complex neurodevelopmental disorder with intellectual disability as the core phenotype. To study the molecular pathology of this essential eukaryotic gene, we generated a mouse model based on a hypomorphic Thoc2 exon 37-38 deletion variant of a patient with ID, speech delay, hypotonia, and microcephaly. The Thoc2 exon 37-38 deletion male (Thoc2
    MeSH term(s) Humans ; Male ; Mice ; Animals ; Transcription Factors/metabolism ; R-Loop Structures ; Active Transport, Cell Nucleus ; Intellectual Disability/genetics ; DNA Damage ; Phenotype ; RNA, Messenger/metabolism
    Chemical Substances Transcription Factors ; RNA, Messenger
    Language English
    Publishing date 2024-02-08
    Publishing country England
    Document type Journal Article
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-024-45121-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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