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  1. Book ; Online: Amyotrophic Lateral Sclerosis : Recent Advances and Therapeutic Challenges

    Hegde, Muralidhar L.

    2020  

    Keywords Neurology & clinical neurophysiology
    Size 1 electronic resource (160 pages)
    Publisher IntechOpen
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021049658
    ISBN 9781838805821 ; 1838805826
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: Introduction to The Special Issue: Novel Molecular Pathways and Therapeutic Challenges in Neurodegenerative Diseases.

    Kosagisharaf, Jagannatha Rao / Hegde, Muralidhar L

    Journal of Alzheimer's disease : JAD

    2023  Volume 94, Issue s1, Page(s) S3–S7

    MeSH term(s) Humans ; Neurodegenerative Diseases/therapy ; Neurodegenerative Diseases/drug therapy
    Language English
    Publishing date 2023-07-02
    Publishing country Netherlands
    Document type Introductory Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1440127-7
    ISSN 1875-8908 ; 1387-2877
    ISSN (online) 1875-8908
    ISSN 1387-2877
    DOI 10.3233/JAD-230622
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6084: 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)

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  3. Article ; Online: Characterizing the Repair of DNA Double-Strand Breaks: A Review of Surrogate Plasmid-Based Reporter Methods.

    Dutta, Arijit / Mitra, Joy / Hegde, Pavana M / Mitra, Sankar / Hegde, Muralidhar L

    Methods in molecular biology (Clifton, N.J.)

    2023  Volume 2701, Page(s) 173–182

    Abstract: DNA double-strand breaks (DSBs) are the most lethal genomic lesions that are induced endogenously during physiological reactions as well as by external stimuli and genotoxicants. DSBs are repaired in mammalian cells via one of three well-studied pathways ...

    Abstract DNA double-strand breaks (DSBs) are the most lethal genomic lesions that are induced endogenously during physiological reactions as well as by external stimuli and genotoxicants. DSBs are repaired in mammalian cells via one of three well-studied pathways depending on the cell cycle status and/or the nature of the break. First, the homologous recombination (HR) pathway utilizes the duplicated sister chromatid as a template in S/G
    MeSH term(s) Animals ; Humans ; DNA Breaks, Double-Stranded ; Reactive Oxygen Species ; DNA End-Joining Repair ; DNA/metabolism ; Plasmids/genetics ; DNA Repair ; Mammals/metabolism
    Chemical Substances Reactive Oxygen Species ; DNA (9007-49-2)
    Language English
    Publishing date 2023-07-28
    Publishing country United States
    Document type Review ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-3373-1_11
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Editorial: The self-renewal and reprogramming of cancer stem cells and their crosstalk with the immune microenvironment.

    Li, Chong / Rao, Jayanth Kosagisharaf / Emani, Lakshmi Sowmya / Kosagisharaf, Rao Jagannatha / Hegde, Muralidhar L

    Frontiers in cell and developmental biology

    2022  Volume 10, Page(s) 1024761

    Language English
    Publishing date 2022-11-11
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2022.1024761
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: Endogenous TDP-43 mislocalization in a novel knock-in mouse model reveals DNA repair impairment, inflammation, and neuronal senescence.

    Mitra, Joy / Dharmalingam, Prakash / Kodavati, Manohar / Guerrero, Erika N / Rao, K S / Garruto, Ralph M / Hegde, Muralidhar L

    Research square

    2024  

    Abstract: TDP-43 mislocalization and aggregation are key pathological features of motor neuron diseases (MND) including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). However, transgenic hTDP-43 WT or ΔNLS-overexpression animal models ... ...

    Abstract TDP-43 mislocalization and aggregation are key pathological features of motor neuron diseases (MND) including amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). However, transgenic hTDP-43 WT or ΔNLS-overexpression animal models mainly capture late-stages TDP-43 proteinopathy, and do not provide a complete understanding of early motor neuron-specific pathology during pre-symptomatic phases. We have now addressed this shortcoming by generating a new endogenous knock-in (KI) mouse model using a combination of CRISPR/Cas9 and FLEX Cre-switch strategy for the conditional expression of a mislocalized Tdp-43ΔNLS variant of mouse Tdp-43. This variant is either expressed conditionally in whole mice or specifically in the motor neurons. The mice exhibit loss of nuclear Tdp-43 concomitant with its cytosolic accumulation and aggregation in targeted cells, leading to increased DNA double-strand breaks (DSBs), signs of inflammation and DNA damage-associated cellular senescence. Notably, unlike WT Tdp43 which functionally interacts with Xrcc4 and DNA Ligase 4, the key DSB repair proteins in the non-homologous end-joining (NHEJ) pathway, the Tdp-43ΔNLS mutant sequesters them into cytosolic aggregates, exacerbating neuronal damage in mice brain. The mutant mice also exhibit myogenic degeneration in limb muscles and distinct motor deficits, consistent with the characteristics of MND. Our findings reveal progressive degenerative mechanisms in motor neurons expressing endogenous Tdp-43ΔNLS mutant, independent of TDP-43 overexpression or other confounding etiological factors. Thus, this unique Tdp-43 KI mouse model, which displays key molecular and phenotypic features of Tdp-43 proteinopathy, offers a significant opportunity to further characterize the early-stage progression of MND and also opens avenues for developing DNA repair-targeted approaches for treating TDP-43 pathology-linked neurodegenerative diseases.
    Language English
    Publishing date 2024-03-20
    Publishing country United States
    Document type Preprint
    DOI 10.21203/rs.3.rs-3879966/v2
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Correction: The Role of the Mammalian DNA End-processing Enzyme Polynucleotide Kinase 3'-Phosphatase in Spinocerebellar Ataxia Type 3 Pathogenesis.

    Chatterjee, Arpita / Saha, Saikat / Chakraborty, Anirban / Silva-Fernandes, Anabela / Mandal, Santi M / Neves-Carvalho, Andreia / Liu, Yongping / Pandita, Raj K / Hegde, Muralidhar L / Hegde, Pavana M / Boldogh, Istvan / Ashizawa, Tetsuo / Koeppen, Arnulf H / Pandita, Tej K / Maciel, Patricia / Sarkar, Partha S / Hazra, Tapas K

    PLoS genetics

    2024  Volume 20, Issue 1, Page(s) e1011124

    Abstract: This corrects the article DOI: 10.1371/journal.pgen.1004749.]. ...

    Abstract [This corrects the article DOI: 10.1371/journal.pgen.1004749.].
    Language English
    Publishing date 2024-01-18
    Publishing country United States
    Document type Published Erratum
    ZDB-ID 2186725-2
    ISSN 1553-7404 ; 1553-7390
    ISSN (online) 1553-7404
    ISSN 1553-7390
    DOI 10.1371/journal.pgen.1011124
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: DNA Double-Strand Breaks as Pathogenic Lesions in Neurological Disorders.

    Provasek, Vincent E / Mitra, Joy / Malojirao, Vikas H / Hegde, Muralidhar L

    International journal of molecular sciences

    2022  Volume 23, Issue 9

    Abstract: The damage and repair of DNA is a continuous process required to maintain genomic integrity. DNA double-strand breaks (DSBs) are the most lethal type of DNA damage and require timely repair by dedicated machinery. DSB repair is uniquely important to ... ...

    Abstract The damage and repair of DNA is a continuous process required to maintain genomic integrity. DNA double-strand breaks (DSBs) are the most lethal type of DNA damage and require timely repair by dedicated machinery. DSB repair is uniquely important to nondividing, post-mitotic cells of the central nervous system (CNS). These long-lived cells must rely on the intact genome for a lifetime while maintaining high metabolic activity. When these mechanisms fail, the loss of certain neuronal populations upset delicate neural networks required for higher cognition and disrupt vital motor functions. Mammalian cells engage with several different strategies to recognize and repair chromosomal DSBs based on the cellular context and cell cycle phase, including homologous recombination (HR)/homology-directed repair (HDR), microhomology-mediated end-joining (MMEJ), and the classic non-homologous end-joining (NHEJ). In addition to these repair pathways, a growing body of evidence has emphasized the importance of DNA damage response (DDR) signaling, and the involvement of heterogeneous nuclear ribonucleoprotein (hnRNP) family proteins in the repair of neuronal DSBs, many of which are linked to age-associated neurological disorders. In this review, we describe contemporary research characterizing the mechanistic roles of these non-canonical proteins in neuronal DSB repair, as well as their contributions to the etiopathogenesis of selected common neurological diseases.
    MeSH term(s) Animals ; DNA/genetics ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; DNA Repair ; Mammals/genetics ; Nervous System Diseases/genetics ; Recombinational DNA Repair
    Chemical Substances DNA (9007-49-2)
    Language English
    Publishing date 2022-04-22
    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/ijms23094653
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: Molecular characterization of neuroprotective activities of plant based products could revive their utilization and lead discovery of new drug candidates for brain diseases.

    Hegde, Muralidhar L

    Journal of pharmacy & bioallied sciences

    2014  Volume 6, Issue 2, Page(s) 63–64

    Language English
    Publishing date 2014-02-28
    Publishing country India
    Document type Journal Article
    ZDB-ID 2573569-X
    ISSN 0975-7406 ; 0976-4879
    ISSN (online) 0975-7406
    ISSN 0976-4879
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: A Commentary on TDP-43 and DNA Damage Response in Amyotrophic Lateral Sclerosis.

    Mitra, Joy / Hegde, Muralidhar L

    Journal of experimental neuroscience

    2019  Volume 13, Page(s) 1179069519880166

    Abstract: Amyotrophic lateral sclerosis (ALS) is a devastating, motor neuron degenerative disease without any cure. About 95% of the ALS patients feature abnormalities in the RNA/DNA-binding protein, TDP-43, involving its nucleo-cytoplasmic mislocalization in ... ...

    Abstract Amyotrophic lateral sclerosis (ALS) is a devastating, motor neuron degenerative disease without any cure. About 95% of the ALS patients feature abnormalities in the RNA/DNA-binding protein, TDP-43, involving its nucleo-cytoplasmic mislocalization in spinal motor neurons. How TDP-43 pathology triggers neuronal apoptosis remains unclear. In a recent study, we reported for the first time that TDP-43 participates in the DNA damage response (DDR) in neurons, and its nuclear clearance in spinal motor neurons caused DNA double-strand break (DSB) repair defects in ALS. We documented that TDP-43 was a key component of the non-homologous end joining (NHEJ) pathway of DSB repair, which is likely the major pathway for repair of DSBs in post-mitotic neurons. We have also uncovered molecular insights into the role of TDP-43 in DSB repair and showed that TDP-43 acts as a scaffold in recruiting the XRCC4/DNA Ligase 4 complex at DSB damage sites and thus regulates a critical rate-limiting function in DSB repair. Significant DSB accumulation in the genomes of TDP-43-depleted, human neural stem cell-derived motor neurons as well as in ALS patient spinal cords with TDP-43 pathology, strongly supported a TDP-43 involvement in genome maintenance and toxicity-induced genome repair defects in ALS. In this commentary, we highlight our findings that have uncovered a link between TDP-43 pathology and impaired DNA repair and suggest potential possibilities for DNA repair-targeted therapies for TDP-43-ALS.
    Language English
    Publishing date 2019-10-10
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2659991-0
    ISSN 1179-0695
    ISSN 1179-0695
    DOI 10.1177/1179069519880166
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: New Mechanisms of DNA Repair Defects in Fused in Sarcoma-Associated Neurodegeneration: Stage Set for DNA Repair-Based Therapeutics?

    Wang, Haibo / Hegde, Muralidhar L

    Journal of experimental neuroscience

    2019  Volume 13, Page(s) 1179069519856358

    Abstract: Genome damage and defective DNA repair are etiologically linked to several neurodegenerative disorders, including fused in sarcoma (FUS)-associated amyotrophic lateral sclerosis (ALS). However, the underlying mechanisms remain enigmatic, which is a ... ...

    Abstract Genome damage and defective DNA repair are etiologically linked to several neurodegenerative disorders, including fused in sarcoma (FUS)-associated amyotrophic lateral sclerosis (ALS). However, the underlying mechanisms remain enigmatic, which is a roadblock for exploiting genome repair-targeted therapies. Our recent studies identified defects in DNA nick ligation and oxidative damage repair caused by mutations in the RNA/DNA-binding protein FUS in familial ALS patients. In healthy neurons, FUS protects the genome by facilitating PARP1-dependent recruitment of XRCC1/DNA Ligase IIIα (LigIII) to oxidized genome sites and activating LigIII via direct interaction. This is a critical step in the repair of oxidative genome damage, a foremost challenge for postmitotic neurons due to their high oxygen consumption. We discovered that mutant FUS significantly inhibited the recruitment of XRCC1/LigIII to DNA strand breaks, causing defects in DNA ligation during the repair of oxidative DNA damage, which contributed to neurodegeneration. While the FUS loss of function was responsible for the repair defects, increased oxidative genome damage due to mutant FUS aggregation could exacerbate the phenomenon. We highlight how these new molecular insights into previously undescribed DNA repair defect linked to FUS-associated neurodegeneration could provide an important opportunity for exploring DNA repair-based therapeutic avenues.
    Language English
    Publishing date 2019-06-10
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2659991-0
    ISSN 1179-0695
    ISSN 1179-0695
    DOI 10.1177/1179069519856358
    Database MEDical Literature Analysis and Retrieval System OnLINE

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