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  1. Book ; Online ; E-Book: Transcription and translation in health and disease

    Sethi, Gautam / Garg, Manoj / Pandey, Amit Kumar

    2023  

    Author's details edited by Gautam Sethi, Manoj Garg, Amit Kumar Pandey
    Keywords Medical care/Translating ; Transcription
    Subject code 362.1
    Language English
    Size 1 Online-Ressource (xv, 399 Seiten), Illustrationen
    Publisher Elsevier Academic Press
    Publishing place London
    Publishing country Great Britain
    Document type Book ; Online ; E-Book
    Remark Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
    HBZ-ID HT021879567
    ISBN 978-0-323-99522-1 ; 9780323995214 ; 0-323-99522-5 ; 0323995217
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: Jarisch‒Herxheimer reaction.

    Gautam, Manjyot / Sethi, Sahil / Nadkarni, Nitin J

    Indian journal of sexually transmitted diseases and AIDS

    2023  Volume 44, Issue 1, Page(s) 79–81

    Abstract: Syphilis is caused by a spirochete, ...

    Abstract Syphilis is caused by a spirochete,
    Language English
    Publishing date 2023-06-06
    Publishing country India
    Document type Case Reports
    ZDB-ID 2622183-4
    ISSN 2589-0565 ; 2589-0565
    ISSN (online) 2589-0565
    ISSN 2589-0565
    DOI 10.4103/ijstd.ijstd_107_22
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Transmembrane protein 25 abrogates monomeric EGFR-driven STAT3 activation in triple-negative breast cancer.

    Mohan, Chakrabhavi Dhananjaya / Rangappa, Kanchugarakoppal S / Sethi, Gautam

    MedComm

    2024  Volume 5, Issue 4, Page(s) e492

    Abstract: In wild-type cells, TMEM25 physically associates with EGFR monomer and suppresses the EGFR-mediated STAT3 phosphorylation, which results in the sequestration of unphosphorylated STAT3 in the cytoplasm. In ... ...

    Abstract In wild-type cells, TMEM25 physically associates with EGFR monomer and suppresses the EGFR-mediated STAT3 phosphorylation, which results in the sequestration of unphosphorylated STAT3 in the cytoplasm. In TMEM
    Language English
    Publishing date 2024-03-26
    Publishing country China
    Document type Journal Article
    ISSN 2688-2663
    ISSN (online) 2688-2663
    DOI 10.1002/mco2.492
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Long noncoding RNAs induced control of ferroptosis: Implications in cancer progression and treatment.

    Shi, Wei / Sethi, Gautam

    Journal of cellular physiology

    2023  Volume 238, Issue 5, Page(s) 880–895

    Abstract: A novel kind of nonapoptotic, iron-dependent cell death brought on by lipid peroxidation is known as ferroptosis. Numerous pathological processes, including neurotoxicity, neurological disorders, ischemia-reperfusion damage, and particularly cancer, have ...

    Abstract A novel kind of nonapoptotic, iron-dependent cell death brought on by lipid peroxidation is known as ferroptosis. Numerous pathological processes, including neurotoxicity, neurological disorders, ischemia-reperfusion damage, and particularly cancer, have been demonstrated to be influenced by changes in the ferroptosis-regulating network. Recent studies have established the critical roles that ferroptosis can play in cancer development and the evolution of resistance to standard chemoradiotherapy, thus suggesting that ferroptosis may be a feasible therapeutic strategy for cancer management. Gene expression may be regulated at the transcriptional and posttranscriptional levels by long noncoding RNAs (lncRNAs). They have been implicated in tumorigenesis. Some lncRNAs participate in the biological process of ferroptosis, which represents an exciting alternative to regulate ferroptosis as a means of cancer therapy. Even though there is evidence that lncRNAs have a mechanistic role in the ferroptosis of cancer cells, research on the mechanism and potential treatments for these lncRNAs is still lacking. We elucidate the potential mechanisms by which lncRNAs modulate ferroptosis in cancer and examine the promise and challenges of employing lncRNAs as novel therapeutic targets in cancer.
    MeSH term(s) Humans ; Carcinogenesis ; Cell Transformation, Neoplastic ; Ferroptosis/genetics ; Neoplasms/genetics ; RNA, Long Noncoding/genetics
    Chemical Substances RNA, Long Noncoding
    Language English
    Publishing date 2023-03-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.30992
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    Uc I Zs.212: Show issues Location:
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  5. Article ; Online: Telomerase and hallmarks of cancer: An intricate interplay governing cancer cell evolution.

    Kumar, Naveen / Sethi, Gautam

    Cancer letters

    2023  Volume 578, Page(s) 216459

    Abstract: Transformed cells must acquire specific characteristics to be malignant. Weinberg and Hanahan characterize these characteristics as cancer hallmarks. Though these features are independently driven, substantial signaling crosstalk in transformed cells ... ...

    Abstract Transformed cells must acquire specific characteristics to be malignant. Weinberg and Hanahan characterize these characteristics as cancer hallmarks. Though these features are independently driven, substantial signaling crosstalk in transformed cells efficiently promotes these feature acquisitions. Telomerase is an enzyme complex that maintains telomere length. However, its main component, Telomere reverse transcriptase (TERT), has been found to interact with various signaling molecules like cMYC, NF-kB, BRG1 and cooperate in transcription and metabolic reprogramming, acting as a strong proponent of malignant features such as cell death resistance, sustained proliferation, angiogenesis activation, and metastasis, among others. It allows cells to avoid replicative senescence and achieve endless replicative potential. This review summarizes both the canonical and noncanonical functions of TERT and discusses how they promote cancer hallmarks. Understanding the role of Telomerase in promoting cancer hallmarks provides vital insight into the underlying mechanism of cancer genesis and progression and telomerase intervention as a possible therapeutic target for cancer treatment. More investigation into the precise molecular mechanisms of telomerase-mediated impacts on cancer hallmarks will contribute to developing more focused and customized cancer treatment methods.
    MeSH term(s) Humans ; Telomerase/genetics ; Telomerase/metabolism ; Neoplasms/metabolism ; Signal Transduction ; NF-kappa B/metabolism ; Telomere/metabolism
    Chemical Substances Telomerase (EC 2.7.7.49) ; NF-kappa B
    Language English
    Publishing date 2023-10-19
    Publishing country Ireland
    Document type Review ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2023.216459
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    Zs.A 1177: Show issues Location:
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  6. Article ; Online: Featuring the special issue guest editor.

    Garg, Manoj / Sethi, Gautam

    Cancer letters

    2021  Volume 505, Page(s) 73–74

    Language English
    Publishing date 2021-02-18
    Publishing country Ireland
    Document type Editorial
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2021.01.033
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  7. Article ; Online: Cannabidiol activates MAPK pathway to induce apoptosis, paraptosis, and autophagy in colorectal cancer cells.

    Kim, Na Young / Mohan, Chakrabhavi Dhananjaya / Sethi, Gautam / Ahn, Kwang Seok

    Journal of cellular biochemistry

    2024  Volume 125, Issue 4, Page(s) e30537

    Abstract: Mitogen-activated protein kinase (MAPK) activation by natural compounds is known to be involved in the induction of apoptosis, paraptosis, and autophagy. Cannabidiol (CBD), a bioactive compound found in Cannabis sativa, is endowed with many ... ...

    Abstract Mitogen-activated protein kinase (MAPK) activation by natural compounds is known to be involved in the induction of apoptosis, paraptosis, and autophagy. Cannabidiol (CBD), a bioactive compound found in Cannabis sativa, is endowed with many pharmacological activities. We investigated the cytotoxic effect of CBD in a panel of colorectal cancer (CRC) cells (HT-29, SW480, HCT-116, and HCT-15). CBD induced significant cytotoxicity as evidenced by the results of MTT  assay, live-dead assay, and flow cytometric analysis. Since CBD displayed cytotoxicity against CRC cells, we examined the effect of CBD on apoptosis, paraptosis, and autophagy. CBD decreased the expression of antiapoptotic proteins and increased the Annexin-V-positive as well as TUNEL-positive cells suggesting that CBD induces apoptosis. CBD increased the expression of ATF4 (activating transcription factor 4) and CHOP (CCAAT/enhancer-binding protein homologous protein), elevated endoplasmic reticulum stress, and enhanced reactive oxygen species levels indicating that CBD also promotes paraptosis. CBD also induced the expression of Atg7, phospho-Beclin-1, and LC3 suggesting that CBD also accelerates autophagy. Since, the MAPK pathway is a common cascade that is involved in the regulation of apoptosis, paraptosis, and autophagy, we investigated the effect of CBD on the activation of JNK, p38, and ERK pathways. CBD activated all the forms of MAPK proteins and pharmacological inhibition of these proteins reverted the observed effects. Our findings implied that CBD could induce CRC cell death by activating apoptosis, paraptosis, and autophagy through the activation of the MAPK pathway.
    MeSH term(s) Humans ; Mitogen-Activated Protein Kinases/metabolism ; Cannabidiol/pharmacology ; Cell Line, Tumor ; Paraptosis ; Apoptosis ; Autophagy ; Colorectal Neoplasms/drug therapy
    Chemical Substances Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; Cannabidiol (19GBJ60SN5)
    Language English
    Publishing date 2024-02-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 392402-6
    ISSN 1097-4644 ; 0730-2312
    ISSN (online) 1097-4644
    ISSN 0730-2312
    DOI 10.1002/jcb.30537
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    Zs.A 1114: Show issues Location:
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  8. Article ; Online: Emerging role of long non-coding RNA (lncRNA) in human malignancies: A unique opportunity for precision medicine.

    Garg, Manoj / Sethi, Gautam

    Cancer letters

    2021  Volume 519, Page(s) 1

    MeSH term(s) Humans ; Neoplasms/genetics ; Precision Medicine ; RNA, Long Noncoding/genetics
    Chemical Substances RNA, Long Noncoding
    Language English
    Publishing date 2021-06-18
    Publishing country Ireland
    Document type Editorial
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2021.01.032
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    Zs.A 1177: Show issues Location:
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  9. Article ; Online: Autophagy machinery in glioblastoma: The prospect of cell death crosstalk and drug resistance with bioinformatics analysis.

    Qin, Yi / Xiong, Shengjun / Ren, Jun / Sethi, Gautam

    Cancer letters

    2023  Volume 580, Page(s) 216482

    Abstract: Brain tumors are common malignancies with high mortality and morbidity in which glioblastoma (GB) is a grade IV astrocytoma with heterogeneous nature. The conventional therapeutics for the GB mainly include surgery and chemotherapy, however their ... ...

    Abstract Brain tumors are common malignancies with high mortality and morbidity in which glioblastoma (GB) is a grade IV astrocytoma with heterogeneous nature. The conventional therapeutics for the GB mainly include surgery and chemotherapy, however their efficacy has been compromised due to the aggressiveness of tumor cells. The dysregulation of cell death mechanisms, especially autophagy has been reported as a factor causing difficulties in cancer therapy. As a mechanism contributing to cell homeostasis, the autophagy process is hijacked by tumor cells for the purpose of aggravating cancer progression and drug resistance. The autophagy function is context-dependent and its role can be lethal or protective in cancer. The aim of the current paper is to highlight the role of autophagy in the regulation of GB progression. The cytotoxic function of autophagy can promote apoptosis and ferroptosis in GB cells and vice versa. Autophagy dysregulation can cause drug resistance and radioresistance in GB. Moreover, stemness can be regulated by autophagy and overall growth as well as metastasis are affected by autophagy. The various interventions including administration of synthetic/natural products and nanoplatforms can target autophagy. Therefore, autophagy can act as a promising target in GB therapy.
    MeSH term(s) Humans ; Glioblastoma/drug therapy ; Glioblastoma/genetics ; Glioblastoma/metabolism ; Autophagy ; Cell Death ; Brain Neoplasms/drug therapy ; Brain Neoplasms/genetics ; Brain Neoplasms/pathology ; Drug Resistance ; Computational Biology ; Cell Line, Tumor
    Language English
    Publishing date 2023-11-17
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2023.216482
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1177: Show issues Location:
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  10. Article ; Online: Want of Wnt in Parkinson's disease: Could sFRP disrupt interplay between Nurr1 and Wnt signaling?

    Gamit, Naisarg / Dharmarajan, Arun / Sethi, Gautam / Warrier, Sudha

    Biochemical pharmacology

    2023  Volume 212, Page(s) 115566

    Abstract: Nuclear receptor related 1 (Nurr1) is a transcription factor known to regulate the development and maintenance of midbrain dopaminergic (mDA) neurons. Reports have confirmed that defect or obliteration of Nurr1 results in neurodegeneration and motor ... ...

    Abstract Nuclear receptor related 1 (Nurr1) is a transcription factor known to regulate the development and maintenance of midbrain dopaminergic (mDA) neurons. Reports have confirmed that defect or obliteration of Nurr1 results in neurodegeneration and motor function impairment leading to Parkinson's disease (PD). Studies have also indicated that Nurr1 regulates the expression of alpha-synuclein (α-SYN) and mutations in Nurr1 cause α-SYN overexpression, thereby increasing the risk of PD. Nurr1 is modulated via various pathways including Wnt signaling pathway which is known to play an important role in neurogenesis, and deregulation of it contributes to PD pathogenesis. Both Wnt/β-catenin dependent and independent pathways are implicated in the activation of Nurr1 and subsequent downregulation of α-SYN. This review highlights the interaction between Nurr1 and Wnt signaling pathways in mDA neuronal development. We further hypothesize how modulation of Wnt signaling pathway by its antagonist, secreted frizzled related proteins (sFRPs) could be a potential route to treat PD.
    MeSH term(s) Humans ; Parkinson Disease/genetics ; Parkinson Disease/metabolism ; Wnt Signaling Pathway/physiology ; Dopaminergic Neurons/metabolism ; Transcription Factors/metabolism ; Receptors, Cytoplasmic and Nuclear/metabolism
    Chemical Substances Transcription Factors ; Receptors, Cytoplasmic and Nuclear
    Language English
    Publishing date 2023-04-22
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 208787-x
    ISSN 1873-2968 ; 0006-2952
    ISSN (online) 1873-2968
    ISSN 0006-2952
    DOI 10.1016/j.bcp.2023.115566
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