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  1. Article ; Online: Novel oncogenic transcriptional targets of mutant p53 in esophageal squamous cell carcinoma.

    George, Sara A / Kotapalli, Viswakalyan / Ramaswamy, Pandilla / Kumar, Raju / Gowrishankar, Swarnalata / Uppin, Shantveer G / Bashyam, Murali D

    Journal of cellular biochemistry

    2024  Volume 125, Issue 4, Page(s) e30534

    Abstract: Missense mutations in the DNA binding domain of p53 are observed frequently in esophageal squamous cell carcinoma (ESCC). Recent studies have revealed the potentially oncogenic transcriptional networks regulated by mutant p53 proteins. However, majority ... ...

    Abstract Missense mutations in the DNA binding domain of p53 are observed frequently in esophageal squamous cell carcinoma (ESCC). Recent studies have revealed the potentially oncogenic transcriptional networks regulated by mutant p53 proteins. However, majority of these studies have focused on common "hotspot" p53 mutations while rarer mutations are poorly characterized. In this study, we report the characterization of rare, "non-hotspot" p53 mutations from ESCC. In vitro tumorigenic assays performed following ectopic-expression of certain "non-hotspot" mutant p53 proteins caused enhancement of oncogenic properties in squamous carcinoma cell lines. Genome-wide transcript profiling of ESCC tumor samples stratified for p53 status, revealed several genes exhibiting elevated transcript levels in tumors harboring mutant p53. Of these, ARF6, C1QBP, and TRIM23 were studied further. Reverse transcription-quantitative PCR (RT-qPCR) performed on RNA isolated from ESCC tumors revealed significant correlation of TP53 transcript levels with those of the three target genes. Ectopic expression of wild-type and several mutant p53 forms followed by RT-qPCR, chromatin affinity-purification (ChAP), and promoter-luciferase assays indicated the exclusive recruitment of p53 mutants-P190T and P278L, to the target genes leading to the activation of expression. Several functional assays following knockdown of the target genes revealed a significant suppression of tumorigenicity in squamous carcinoma cell lines. Rescue experiments confirmed the specificity of the knockdown. The tumorigenic effects of the genes were confirmed in nude mice xenograft assays. This study has therefore identified novel oncogenic targets of "non-hotspot" mutant p53 proteins relevant for ESCC besides validating the functional heterogeneity of the spectrum of tumor-specific p53 mutations.
    MeSH term(s) Animals ; Mice ; Humans ; Esophageal Squamous Cell Carcinoma/genetics ; Esophageal Squamous Cell Carcinoma/pathology ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism ; Esophageal Neoplasms/pathology ; Mice, Nude ; Carcinoma, Squamous Cell/metabolism ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Cell Proliferation ; GTP-Binding Proteins/genetics ; Carrier Proteins/genetics ; Mitochondrial Proteins/genetics
    Chemical Substances Tumor Suppressor Protein p53 ; TRIM23 protein, human ; GTP-Binding Proteins (EC 3.6.1.-) ; C1QBP protein, human ; Carrier Proteins ; Mitochondrial Proteins
    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.30534
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1114: Show issues Location:
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  2. Article ; Online: Multiple oncogenic roles of nuclear beta-catenin.

    Kumar, Raju / Bashyam, Murali D

    Journal of biosciences

    2018  Volume 42, Issue 4, Page(s) 695–707

    Abstract: β-Catenin is essential for embryonic development and required for cell renewal/regeneration in adult life. Cellular β-catenin exists in three different pools: membranous, cytoplasmic and nuclear. In this review, we focus on functions of the nuclear pool ... ...

    Abstract β-Catenin is essential for embryonic development and required for cell renewal/regeneration in adult life. Cellular β-catenin exists in three different pools: membranous, cytoplasmic and nuclear. In this review, we focus on functions of the nuclear pool in relation to tumorigenesis. In the nucleus, beta-catenin functions as both activator and repressor of transcription in a context-dependent manner. It promotes cell proliferation and supports tumour growth by enhancing angiogenesis. β-Catenin-mediated signalling regulates cancer cell metabolism and is associated with tumour-initiating cells in multiple malignancies. In addition, it functions as both pro- and anti-apoptotic factor besides acting to inhibit recruitment of inflammatory anti-tumour T-cells. Thus, β-catenin appears to possess a multifaceted nuclear function that may significantly impact tumour initiation and progression.
    MeSH term(s) Cell Nucleus/immunology ; Cell Nucleus/metabolism ; Cell Proliferation ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/immunology ; Cell Transformation, Neoplastic/pathology ; Epithelial-Mesenchymal Transition/genetics ; Epithelial-Mesenchymal Transition/immunology ; Gene Expression Regulation, Neoplastic ; Humans ; Neoplasm Proteins/genetics ; Neoplasm Proteins/immunology ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplastic Stem Cells/immunology ; Neoplastic Stem Cells/pathology ; Neovascularization, Pathologic/genetics ; Neovascularization, Pathologic/immunology ; Neovascularization, Pathologic/pathology ; Signal Transduction ; T-Lymphocytes/immunology ; T-Lymphocytes/pathology ; beta Catenin/genetics ; beta Catenin/immunology
    Chemical Substances CTNNB1 protein, human ; Neoplasm Proteins ; beta Catenin
    Language English
    Publishing date 2018-01-18
    Publishing country India
    Document type Journal Article ; Review
    ZDB-ID 756157-x
    ISSN 0973-7138 ; 0250-5991
    ISSN (online) 0973-7138
    ISSN 0250-5991
    DOI 10.1007/s12038-017-9710-9
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1907: Show issues Location:
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  3. Article ; Online: SMARCD1 is a transcriptional target of specific non-hotspot mutant p53 forms.

    Adduri, Raju S R / George, Sara A / Kavadipula, Padmavathi / Bashyam, Murali D

    Journal of cellular physiology

    2019  Volume 235, Issue 5, Page(s) 4559–4570

    Abstract: Though primarily a tumor suppressor, TP53 harboring specific missense mutations located in the region encoding the DNA binding domain exhibits a gain of function by transcriptional activation of oncogenes. We performed microarray-based messenger RNA ... ...

    Abstract Though primarily a tumor suppressor, TP53 harboring specific missense mutations located in the region encoding the DNA binding domain exhibits a gain of function by transcriptional activation of oncogenes. We performed microarray-based messenger RNA profiling of squamous cell carcinoma of the oral tongue (SCCOT) and identified significant elevation of SMARCD1 in samples exhibiting p53 nuclear stabilization. Activation of SMARCD1 by mutant p53 was confirmed by evaluation of additional tongue cancer samples as well as The Cancer Genome Atlas expression datasets. SMARCD1 knockdown in HNSCC cells resulted in a significant reduction in several tumorigenic characteristics including cell viability, ability to form colonies in liquid and solid media and cell migration. We identified significantly increased SMARCD1 transcript levels in tumor versus matched normal samples in SCCOT as well as in other cancer types. Increased SMARCD1 expression predicted poor survival in HNSCC tumors harboring missense p53 mutations. Our results suggest SMARCD1 to be a novel transcriptional target of mutant p53.
    MeSH term(s) Cell Line, Tumor ; Cell Movement ; Cell Proliferation ; Chromosomal Proteins, Non-Histone/genetics ; Chromosomal Proteins, Non-Histone/metabolism ; Databases, Genetic ; Gene Expression Regulation, Neoplastic ; Humans ; Mouth Neoplasms/genetics ; Mouth Neoplasms/metabolism ; Mouth Neoplasms/pathology ; Mutation ; RNA-Binding Proteins/genetics ; RNA-Binding Proteins/metabolism ; Signal Transduction ; Squamous Cell Carcinoma of Head and Neck/genetics ; Squamous Cell Carcinoma of Head and Neck/metabolism ; Squamous Cell Carcinoma of Head and Neck/pathology ; Transcription, Genetic ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Chromosomal Proteins, Non-Histone ; RNA-Binding Proteins ; SMARCD1 protein, human ; TP53 protein, human ; Tumor Suppressor Protein p53 ; ZMAT3 protein, human
    Language English
    Publishing date 2019-10-21
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3116-1
    ISSN 1097-4652 ; 0021-9541
    ISSN (online) 1097-4652
    ISSN 0021-9541
    DOI 10.1002/jcp.29332
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    Uc I Zs.212: Show issues Location:
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  4. Article ; Online: Nonsense-mediated decay: linking a basic cellular process to human disease.

    Bashyam, Murali D

    Expert review of molecular diagnostics

    2009  Volume 9, Issue 4, Page(s) 299–303

    MeSH term(s) Animals ; Codon, Nonsense/genetics ; Genetic Diseases, Inborn/genetics ; Humans ; Introns ; Mammals ; Protein Biosynthesis ; RNA, Messenger/genetics ; Terminator Regions, Genetic/genetics
    Chemical Substances Codon, Nonsense ; RNA, Messenger
    Language English
    Publishing date 2009-05
    Publishing country England
    Document type Editorial ; Research Support, Non-U.S. Gov't
    ZDB-ID 2112530-2
    ISSN 1744-8352 ; 1473-7159
    ISSN (online) 1744-8352
    ISSN 1473-7159
    DOI 10.1586/erm.09.18
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    Zs.A 6073: Show issues Location:
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  5. Article ; Online: A novel EDARADD 5'-splice site mutation resulting in activation of two alternate cryptic 5'-splice sites causes autosomal recessive Hypohidrotic Ectodermal Dysplasia.

    Chaudhary, Ajay K / Girisha, Katta M / Bashyam, Murali D

    American journal of medical genetics. Part A

    2016  Volume 170, Issue 6, Page(s) 1639–1641

    MeSH term(s) Ectodermal Dysplasia, Hypohidrotic, Autosomal Recessive/genetics ; Female ; Humans ; Male ; Pedigree ; RNA Splicing
    Language English
    Publishing date 2016-03-15
    Publishing country United States
    Document type Case Reports ; Letter ; Research Support, Non-U.S. Gov't
    ZDB-ID 1493479-6
    ISSN 1552-4833 ; 1552-4825
    ISSN (online) 1552-4833
    ISSN 1552-4825
    DOI 10.1002/ajmg.a.37607
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  6. Article: Multiple oncogenic roles of nuclear β-catenin

    Kumar, Raju / Murali D Bashyam

    Journal of biosciences. 2017 Dec., v. 42, no. 4

    2017  

    Abstract: β-Catenin is essential for embryonic development and required for cell renewal/regeneration in adult life. Cellular β-catenin exists in three different pools: membranous, cytoplasmic and nuclear. In this review, we focus on functions of the nuclear ... ...

    Abstract β-Catenin is essential for embryonic development and required for cell renewal/regeneration in adult life. Cellular β-catenin exists in three different pools: membranous, cytoplasmic and nuclear. In this review, we focus on functions of the nuclear pool in relation to tumorigenesis. In the nucleus, β-catenin functions as both activator and repressor of transcription in a context-dependent manner. It promotes cell proliferation and supports tumour growth by enhancing angiogenesis. β-Catenin-mediated signalling regulates cancer cell metabolism and is associated with tumour-initiating cells in multiple malignancies. In addition, it functions as both pro- and anti-apoptotic factor besides acting to inhibit recruitment of inflammatory anti-tumour T-cells. Thus, β-catenin appears to possess a multifaceted nuclear function that may significantly impact tumour initiation and progression.
    Keywords adults ; angiogenesis ; beta catenin ; carcinogenesis ; cell proliferation ; embryogenesis ; metabolism ; neoplasms ; T-lymphocytes
    Language English
    Dates of publication 2017-12
    Size p. 695-707.
    Publishing place Springer India
    Document type Article
    Note Review
    ZDB-ID 756157-x
    ISSN 0973-7138 ; 0250-5991
    ISSN (online) 0973-7138
    ISSN 0250-5991
    DOI 10.1007/s12038-017-9710-9
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    In stock of ZB MED Bonn / Germany

    Z 5290: Show issues

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  7. Article ; Online: Studies on nonsense mediated decay reveal novel therapeutic options for genetic diseases.

    Bashyam, Murali D

    Recent patents on DNA & gene sequences

    2008  Volume 3, Issue 1, Page(s) 7–15

    Abstract: Scientific breakthroughs have often led to commercially viable patents mainly in the field of engineering. Commercialization in the field of medicine has been restricted mostly to machinery and engineering on the one hand and therapeutic drugs for common ...

    Abstract Scientific breakthroughs have often led to commercially viable patents mainly in the field of engineering. Commercialization in the field of medicine has been restricted mostly to machinery and engineering on the one hand and therapeutic drugs for common chronic ailments such as cough, cold, headache, etc, on the other. Sequencing of the human genome has attracted the attention of pharmaceutical companies and now biotechnology has become a goldmine for commercialization of products and processes. Recent advances in our understanding of basic biological processes have resulted in the opening of new avenues for treatment of human genetic diseases, especially single gene disorders. A significant proportion of human genetic disorders have been shown to be caused due to degradation of transcripts for specific genes through a process called nonsense mediated decay (NMD). The modulation of NMD provides a viable therapeutic option for treatment of several genetic disorders and therefore has been a good prospect for patenting and commercialization. In this review the molecular basis for NMD and attempts to treat genetic diseases which result from NMD are discussed.
    MeSH term(s) Animals ; Codon, Nonsense/genetics ; Gene Targeting/methods ; Genetic Diseases, Inborn/genetics ; Genetic Diseases, Inborn/therapy ; Genetic Therapy/legislation & jurisprudence ; Genetic Therapy/methods ; Humans ; Models, Biological ; Patents as Topic ; Protein Biosynthesis/physiology ; RNA/biosynthesis ; RNA Stability/genetics ; RNA Stability/physiology
    Chemical Substances Codon, Nonsense ; RNA (63231-63-0)
    Language English
    Publishing date 2008-02-29
    Publishing country United Arab Emirates
    Document type Journal Article ; Review
    ISSN 2212-3431
    ISSN (online) 2212-3431
    DOI 10.2174/187221509787236219
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: A novel large deletion that encompasses EDA and the downstream gene AWAT2 causes X-linked hypohidrotic/anhidrotic ectodermal dysplasia.

    Chaudhary, Ajay K / Sankar, V H / Bashyam, Murali D

    Journal of dermatological science

    2016  Volume 84, Issue 1, Page(s) 105–107

    MeSH term(s) 3' Untranslated Regions ; 5' Untranslated Regions ; Acyltransferases/genetics ; Cytoplasm/metabolism ; Ectodermal Dysplasia 1, Anhidrotic/genetics ; Ectodysplasins/genetics ; Edar Receptor/metabolism ; Family Health ; Female ; Gene Deletion ; Humans ; Hypohidrosis/genetics ; India ; Infant ; Male ; Mutation ; NF-kappa B/metabolism ; Pedigree ; Recombination, Genetic ; Sequence Deletion ; Signal Transduction
    Chemical Substances 3' Untranslated Regions ; 5' Untranslated Regions ; EDA protein, human ; Ectodysplasins ; Edar Receptor ; NF-kappa B ; Acyltransferases (EC 2.3.-) ; AWAT2 protein, human (EC 2.3.1.-)
    Language English
    Publishing date 2016-10
    Publishing country Netherlands
    Document type Letter
    ZDB-ID 1024446-3
    ISSN 1873-569X ; 0923-1811
    ISSN (online) 1873-569X
    ISSN 0923-1811
    DOI 10.1016/j.jdermsci.2016.06.012
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2870: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  9. Article ; Online: Hormonal regulation of gluconeogenic gene transcription in the liver.

    Yabaluri, Nirmala / Bashyam, Murali D

    Journal of biosciences

    2010  Volume 35, Issue 3, Page(s) 473–484

    Abstract: Glucose homeostasis in mammals is achieved by the actions of counterregulatory hormones, namely insulin, glucagon and glucocorticoids. Glucose levels in the circulation are regulated by the liver, the metabolic centre which produces glucose when it is ... ...

    Abstract Glucose homeostasis in mammals is achieved by the actions of counterregulatory hormones, namely insulin, glucagon and glucocorticoids. Glucose levels in the circulation are regulated by the liver, the metabolic centre which produces glucose when it is scarce in the blood. This process is catalysed by two rate-limiting enzymes, phosphoenolpyruvate carboxykinase (PEPCK) and glucose-6-phosphatase (G6Pase) whose gene expression is regulated by hormones. Hormone response units (HRUs) present in the two genes integrate signals from various signalling pathways triggered by hormones. How such domains are arranged in the regulatory region of these two genes, how this complex regulation is accomplished and the latest advancements in the field are discussed in this review.
    MeSH term(s) Animals ; Gene Expression Regulation ; Gluconeogenesis ; Glucose-6-Phosphatase/genetics ; Glucose-6-Phosphatase/metabolism ; Hormones/metabolism ; Humans ; Liver/enzymology ; Liver/growth & development ; Phosphoenolpyruvate Carboxykinase (GTP)/genetics ; Phosphoenolpyruvate Carboxykinase (GTP)/metabolism
    Chemical Substances Hormones ; Glucose-6-Phosphatase (EC 3.1.3.9) ; Phosphoenolpyruvate Carboxykinase (GTP) (EC 4.1.1.32)
    Language English
    Publishing date 2010-09-08
    Publishing country India
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 756157-x
    ISSN 0973-7138 ; 0250-5991
    ISSN (online) 0973-7138
    ISSN 0250-5991
    DOI 10.1007/s12038-010-0052-0
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1907: Show issues Location:
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  10. Article: Understanding cancer metastasis: an urgent need for using differential gene expression analysis.

    Bashyam, Murali D

    Cancer

    2002  Volume 94, Issue 6, Page(s) 1821–1829

    Abstract: Cancer is a multistep process and occurs as a result of the loss of control of cell division, leading to the initial tumor formation, which is followed by metastatic spread. Recent years have witnessed a vast improvement in the understanding of the ... ...

    Abstract Cancer is a multistep process and occurs as a result of the loss of control of cell division, leading to the initial tumor formation, which is followed by metastatic spread. Recent years have witnessed a vast improvement in the understanding of the molecular mechanisms regulating cell division and their links to tumorigenesis. The process of metastasis involves an intricate interplay between cell adhesion, proteolysis, migration, and angiogenesis. However, there is little knowledge of how these events are coordinately regulated in the tumor cell. Given that the uncontrolled spread of the tumor to distant organs is usually lethal, a study of the molecular mechanisms regulating metastasis assumes great significance. Recently, several technologies have been developed for analyzing differential gene expression. The current review discusses the importance of these technologies in the molecular analyses of metastasis.
    MeSH term(s) Cell Adhesion/genetics ; DNA, Neoplasm/analysis ; Gene Expression Regulation, Neoplastic ; Humans ; In Situ Hybridization ; Matrix Metalloproteinases/biosynthesis ; Neoplasm Metastasis/genetics ; Oligonucleotide Array Sequence Analysis
    Chemical Substances DNA, Neoplasm ; Matrix Metalloproteinases (EC 3.4.24.-)
    Language English
    Publishing date 2002-03-15
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 1429-1
    ISSN 1097-0142 ; 0008-543X ; 1934-662X
    ISSN (online) 1097-0142
    ISSN 0008-543X ; 1934-662X
    DOI 10.1002/cncr.10362
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