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  1. Article ; Online: P-TEFb promotes cell survival upon p53 activation by suppressing intrinsic apoptosis pathway.

    Wang, Zhijia / Mačáková, Monika / Bugai, Andrii / Kuznetsov, Sergey G / Hassinen, Antti / Lenasi, Tina / Potdar, Swapnil / Friedel, Caroline C / Barborič, Matjaž

    Nucleic acids research

    2023  Volume 51, Issue 4, Page(s) 1687–1706

    Abstract: Positive transcription elongation factor b (P-TEFb) is the crucial player in RNA polymerase II (Pol II) pause release that has emerged as a promising target in cancer. Because single-agent therapy may fail to deliver durable clinical response, targeting ... ...

    Abstract Positive transcription elongation factor b (P-TEFb) is the crucial player in RNA polymerase II (Pol II) pause release that has emerged as a promising target in cancer. Because single-agent therapy may fail to deliver durable clinical response, targeting of P-TEFb shall benefit when deployed as a combination therapy. We screened a comprehensive oncology library and identified clinically relevant antimetabolites and Mouse double minute 2 homolog (MDM2) inhibitors as top compounds eliciting p53-dependent death of colorectal cancer cells in synergy with selective inhibitors of P-TEFb. While the targeting of P-TEFb augments apoptosis by anti-metabolite 5-fluorouracil, it switches the fate of cancer cells by the non-genotoxic MDM2 inhibitor Nutlin-3a from cell-cycle arrest to apoptosis. Mechanistically, the fate switching is enabled by the induction of p53-dependent pro-apoptotic genes and repression of P-TEFb-dependent pro-survival genes of the PI3K-AKT signaling cascade, which stimulates caspase 9 and intrinsic apoptosis pathway in BAX/BAK-dependent manner. Finally, combination treatments trigger apoptosis of cancer cell spheroids. Together, co-targeting of P-TEFb and suppressors of intrinsic apoptosis could become a viable strategy to eliminate cancer cells.
    MeSH term(s) Apoptosis ; Cell Line, Tumor ; Cell Survival ; Phosphatidylinositol 3-Kinases/metabolism ; Positive Transcriptional Elongation Factor B/antagonists & inhibitors ; Positive Transcriptional Elongation Factor B/metabolism ; Proto-Oncogene Proteins c-mdm2/genetics ; Tumor Suppressor Protein p53/genetics ; Humans
    Chemical Substances Phosphatidylinositol 3-Kinases (EC 2.7.1.-) ; Positive Transcriptional Elongation Factor B (EC 2.7.11.-) ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27) ; Tumor Suppressor Protein p53 ; MDM2 protein, human (EC 2.3.2.27)
    Language English
    Publishing date 2023-02-01
    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/gkad001
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    Zs.A 1067: Show issues Location:
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  2. Article ; Online: Response to: The GPRC5A frameshift variant c.183del is not associated with increased breast cancer risk in BRCA1 mutation carriers.

    Bulanova, Daria R / Helenius, Mikko / Sokolenko, Anna P / Kuznetsov, Sergey G / Imyanitov, Evgeny N

    International journal of cancer

    2019  Volume 144, Issue 7, Page(s) 1758–1760

    MeSH term(s) BRCA1 Protein/genetics ; BRCA2 Protein/genetics ; Breast ; Breast Neoplasms ; Humans ; Mutation ; Receptors, G-Protein-Coupled
    Chemical Substances BRCA1 Protein ; BRCA2 Protein ; GPRC5A protein, human ; Receptors, G-Protein-Coupled
    Language English
    Publishing date 2019-01-06
    Publishing country United States
    Document type Letter ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.32013
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    Zs.MO 576: Show issues

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  3. Article ; Online: Resolving RAD51C function in late stages of homologous recombination.

    Sharan, Shyam K / Kuznetsov, Sergey G

    Cell division

    2007  Volume 2, Page(s) 15

    Abstract: DNA double strand breaks are efficiently repaired by homologous recombination. One of the last steps of this process is resolution of Holliday junctions that are formed at the sites of genetic exchange between homologous DNA. Although various resolvases ... ...

    Abstract DNA double strand breaks are efficiently repaired by homologous recombination. One of the last steps of this process is resolution of Holliday junctions that are formed at the sites of genetic exchange between homologous DNA. Although various resolvases with Holliday junctions processing activity have been identified in bacteriophages, bacteria and archaebacteria, eukaryotic resolvases have been elusive. Recent biochemical evidence has revealed that RAD51C and XRCC3, members of the RAD51-like protein family, are involved in Holliday junction resolution in mammalian cells. However, purified recombinant RAD51C and XRCC3 proteins have not shown any Holliday junction resolution activity. In addition, these proteins did not reveal the presence of a nuclease domain, which raises doubts about their ability to function as a resolvase. Furthermore, oocytes from infertile Rad51C mutant mice exhibit precocious separation of sister chromatids at metaphase II, a phenotype that reflects a defect in sister chromatid cohesion, not a lack of Holliday junction resolution. Here we discuss a model to explain how a Holliday junction resolution defect can lead to sister chromatid separation in mouse oocytes. We also describe other recent in vitro and in vivo evidence supporting a late role for RAD51C in homologous recombination in mammalian cells, which is likely to be resolution of the Holliday junction.
    Language English
    Publishing date 2007-06-04
    Publishing country England
    Document type Editorial
    ZDB-ID 2236097-9
    ISSN 1747-1028 ; 1747-1028
    ISSN (online) 1747-1028
    ISSN 1747-1028
    DOI 10.1186/1747-1028-2-15
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  4. Article ; Online: Functional analysis of human BRCA2 variants using a mouse embryonic stem cell-based assay.

    Kuznetsov, Sergey G / Chang, Suhwan / Sharan, Shyam K

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

    2010  Volume 653, Page(s) 259–280

    Abstract: We describe here a comprehensive and reliable assay to test the functional significance of variants of unknown clinical significance (VUS) identified in the human breast cancer susceptibility gene, BRCA2. The assay is based on the ability of human BRCA2 ... ...

    Abstract We describe here a comprehensive and reliable assay to test the functional significance of variants of unknown clinical significance (VUS) identified in the human breast cancer susceptibility gene, BRCA2. The assay is based on the ability of human BRCA2 to complement the loss of endogenous Brca2 in mouse embryonic stem cells. The procedure involves generation of a desired mutation in BRCA2 present in a bacterial artificial chromosome (BAC) and the introduction of the BAC into ES cells engineered for the assay. These ES cells have one null and one conditional allele of Brca2. First, the effect of the BRCA2 variants on the viability of ES cells is tested by Cre-mediated deletion of the conditional allele. Subsequently, variants that result in viable ES cells are examined for their effect on known functions of BRCA2 using a variety of functional assays such as sensitivity to genotoxic agents, in vivo and in vitro proliferation, effect on homologous recombination and genomic stability. The method described herein allows for the analysis of three to five sequence variants within 2-3 months. This approach can also be used for functional analysis of variants identified in other human disease genes that result in a phenotype detectable in ES cells.
    MeSH term(s) Animals ; BRCA2 Protein/genetics ; BRCA2 Protein/physiology ; Biological Assay/methods ; Embryonic Stem Cells/metabolism ; Embryonic Stem Cells/physiology ; Genetic Techniques ; Genetic Variation/physiology ; Humans ; Mice ; Mutant Proteins/genetics ; Mutant Proteins/physiology ; Phenotype
    Chemical Substances BRCA2 Protein ; BRCA2 protein, human ; Mutant Proteins
    Language English
    Publishing date 2010-08-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-60761-759-4_16
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  5. Article ; Online: Orphan G protein-coupled receptor GPRC5A modulates integrin β1-mediated epithelial cell adhesion.

    Bulanova, Daria R / Akimov, Yevhen A / Rokka, Anne / Laajala, Teemu D / Aittokallio, Tero / Kouvonen, Petri / Pellinen, Teijo / Kuznetsov, Sergey G

    Cell adhesion & migration

    2017  Volume 11, Issue 5-6, Page(s) 434–446

    Abstract: G-Protein Coupled Receptor (GPCR), Class C, Group 5, Member A (GPRC5A) has been implicated in several malignancies. The underlying mechanisms, however, remain poorly understood. Using a panel of human cell lines, we demonstrate that CRISPR/Cas9-mediated ... ...

    Abstract G-Protein Coupled Receptor (GPCR), Class C, Group 5, Member A (GPRC5A) has been implicated in several malignancies. The underlying mechanisms, however, remain poorly understood. Using a panel of human cell lines, we demonstrate that CRISPR/Cas9-mediated knockout and RNAi-mediated depletion of GPRC5A impairs cell adhesion to integrin substrates: collagens I and IV, fibronectin, as well as to extracellular matrix proteins derived from the Engelbreth-Holm-Swarm (EHS) mouse sarcoma (Matrigel). Consistent with the phenotype, knock-out of GPRC5A correlated with a reduced integrin β1 (ITGB1) protein expression, impaired phosphorylation of the focal adhesion kinase (FAK), and lower activity of small GTPases RhoA and Rac1. Furthermore, we provide the first evidence for a direct interaction between GPRC5A and a receptor tyrosine kinase EphA2, an upstream regulator of FAK, although its contribution to the observed adhesion phenotype is unclear. Our findings reveal an unprecedented role for GPRC5A in regulation of the ITGB1-mediated cell adhesion and it's downstream signaling, thus indicating a potential novel role for GPRC5A in human epithelial cancers.
    MeSH term(s) CRISPR-Cas Systems/genetics ; CRISPR-Cas Systems/physiology ; Cell Adhesion/genetics ; Cell Adhesion/physiology ; Cell Line, Tumor ; Cell Movement/genetics ; Cell Movement/physiology ; Epithelial Cells/cytology ; Epithelial Cells/metabolism ; HeLa Cells ; Humans ; Immunoblotting ; Immunoprecipitation ; Integrin beta1/genetics ; Integrin beta1/metabolism ; MCF-7 Cells ; RNA Interference ; Receptors, G-Protein-Coupled/genetics ; Receptors, G-Protein-Coupled/metabolism ; Signal Transduction/genetics ; Signal Transduction/physiology ; Tandem Mass Spectrometry
    Chemical Substances GPRC5A protein, human ; Integrin beta1 ; Receptors, G-Protein-Coupled
    Language English
    Publishing date 2017-02-06
    Publishing country United States
    Document type Journal Article
    ISSN 1933-6926
    ISSN (online) 1933-6926
    DOI 10.1080/19336918.2016.1245264
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  6. Article ; Online: Resolving RAD51C function in late stages of homologous recombination

    Kuznetsov Sergey G / Sharan Shyam K

    Cell Division, Vol 2, Iss 1, p

    2007  Volume 15

    Abstract: Abstract DNA double strand breaks are efficiently repaired by homologous recombination. One of the last steps of this process is resolution of Holliday junctions that are formed at the sites of genetic exchange between homologous DNA. Although various ... ...

    Abstract Abstract DNA double strand breaks are efficiently repaired by homologous recombination. One of the last steps of this process is resolution of Holliday junctions that are formed at the sites of genetic exchange between homologous DNA. Although various resolvases with Holliday junctions processing activity have been identified in bacteriophages, bacteria and archaebacteria, eukaryotic resolvases have been elusive. Recent biochemical evidence has revealed that RAD51C and XRCC3, members of the RAD51-like protein family, are involved in Holliday junction resolution in mammalian cells. However, purified recombinant RAD51C and XRCC3 proteins have not shown any Holliday junction resolution activity. In addition, these proteins did not reveal the presence of a nuclease domain, which raises doubts about their ability to function as a resolvase. Furthermore, oocytes from infertile Rad51C mutant mice exhibit precocious separation of sister chromatids at metaphase II, a phenotype that reflects a defect in sister chromatid cohesion, not a lack of Holliday junction resolution. Here we discuss a model to explain how a Holliday junction resolution defect can lead to sister chromatid separation in mouse oocytes. We also describe other recent in vitro and in vivo evidence supporting a late role for RAD51C in homologous recombination in mammalian cells, which is likely to be resolution of the Holliday junction.
    Keywords Cytology ; QH573-671 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Cytology ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
    Subject code 612
    Language English
    Publishing date 2007-06-01T00:00:00Z
    Publisher BioMed Central
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  7. Article ; Online: Mouse embryonic stem cell-based functional assay to evaluate mutations in BRCA2.

    Kuznetsov, Sergey G / Liu, Pentao / Sharan, Shyam K

    Nature medicine

    2008  Volume 14, Issue 8, Page(s) 875–881

    Abstract: Individuals with mutations in breast cancer susceptibility genes BRCA1 and BRCA2 have up to an 80% risk of developing breast cancer by the age of 70. Sequencing-based genetic tests are now available to identify mutation carriers in an effort to reduce ... ...

    Abstract Individuals with mutations in breast cancer susceptibility genes BRCA1 and BRCA2 have up to an 80% risk of developing breast cancer by the age of 70. Sequencing-based genetic tests are now available to identify mutation carriers in an effort to reduce mortality through prevention and early diagnosis. However, lack of a suitable functional assay hinders the risk assessment of more than 1,900 BRCA1 and BRCA2 variants in the Breast Cancer Information Core database that do not clearly disrupt the gene product. We have established a simple, versatile and reliable assay to test for the functional significance of mutations in BRCA2 using mouse embryonic stem cells (ES cells) and bacterial artificial chromosomes and have used it to classify 17 sequence variants. The assay is based on the ability of human BRCA2 to complement the loss of endogenous Brca2 in mouse ES cells. This technique may also serve as a paradigm for functional analysis of mutations found in other genes linked to human diseases.
    MeSH term(s) Animals ; BRCA2 Protein/genetics ; Breast Neoplasms/genetics ; Breast Neoplasms/metabolism ; Embryonic Stem Cells/cytology ; Gene Expression Regulation, Neoplastic ; Genes, BRCA1 ; Genes, BRCA2 ; Genetic Techniques ; Genetic Variation ; Karyotyping ; Mice ; Mutation ; Phenotype ; RNA Splicing ; Transgenes
    Chemical Substances BRCA2 Protein
    Language English
    Publishing date 2008-07-06
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1220066-9
    ISSN 1546-170X ; 1078-8956
    ISSN (online) 1546-170X
    ISSN 1078-8956
    DOI 10.1038/nm.1719
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4212: Show issues Location:
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    Zs.MG 39: Show issues

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  8. Article ; Online: Loss of Rad51c accelerates tumourigenesis in sebaceous glands of Trp53-mutant mice.

    Tumiati, Manuela / Hemmes, Annabrita / Uusivirta, Sanna / Koopal, Sonja / Kankainen, Matti / Lehtonen, Eero / Kuznetsov, Sergey G

    The Journal of pathology

    2015  Volume 235, Issue 1, Page(s) 136–146

    Abstract: Germline mutations in RAD51C predispose to breast and ovarian cancers. However, the mechanism of RAD51C-mediated carcinogenesis is poorly understood. We previously reported a first-generation Rad51c-knock-out mouse model, in which a spontaneous loss of ... ...

    Abstract Germline mutations in RAD51C predispose to breast and ovarian cancers. However, the mechanism of RAD51C-mediated carcinogenesis is poorly understood. We previously reported a first-generation Rad51c-knock-out mouse model, in which a spontaneous loss of both Rad51c and Trp53 together resulted in a high incidence of sebaceous carcinomas, particularly in preputial glands. Here we describe a second-generation mouse model, in which Rad51c is deleted, alone or together with Trp53, in sebaceous glands, using Cre-mediated recombination. We demonstrate that deletion of Rad51c alone is not sufficient to drive tumourigenesis and may only cause keratinization of preputial sebocytes. However, deletion of Rad51c together with Trp53 leads to tumour development at around 6 months of age, compared to 11 months for single Trp53-mutant mice. Preputial glands of double-mutant mice are also characterized by increased levels of cell proliferation and DNA damage and form multiple hyperplasias, detectable as early as 2 months of age. Our results reveal a critical synergy between Rad51c and Trp53 in tumour progression and provide a predictable in vivo model system for studying mechanisms of Rad51c-mediated carcinogenesis.
    MeSH term(s) Animals ; Carcinogenesis/genetics ; Cell Transformation, Neoplastic/genetics ; Female ; Mice ; Mice, Knockout ; Mice, Transgenic ; Mutation/genetics ; Ovarian Neoplasms/genetics ; Ovarian Neoplasms/pathology ; Rad51 Recombinase/genetics ; Sebaceous Glands/metabolism ; Sebaceous Glands/pathology ; Tumor Suppressor Protein p53/genetics
    Chemical Substances RAD51C protein, mouse ; Tumor Suppressor Protein p53 ; Rad51 Recombinase (EC 2.7.7.-)
    Language English
    Publishing date 2015-01
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3119-7
    ISSN 1096-9896 ; 0022-3417
    ISSN (online) 1096-9896
    ISSN 0022-3417
    DOI 10.1002/path.4455
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    Ud II Zs.12: Show issues Location:
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  9. Article ; Online: Loss of Rad51c leads to embryonic lethality and modulation of Trp53-dependent tumorigenesis in mice.

    Kuznetsov, Sergey G / Haines, Diana C / Martin, Betty K / Sharan, Shyam K

    Cancer research

    2009  Volume 69, Issue 3, Page(s) 863–872

    Abstract: RecA/Rad51 protein family members (Rad51, Rad51b, Rad51c, Rad51d, Xrcc2, and Xrcc3) are essential for DNA repair by homologous recombination, and their role in cancers has been anticipated. Here we provide the first direct evidence for a tumor suppressor ...

    Abstract RecA/Rad51 protein family members (Rad51, Rad51b, Rad51c, Rad51d, Xrcc2, and Xrcc3) are essential for DNA repair by homologous recombination, and their role in cancers has been anticipated. Here we provide the first direct evidence for a tumor suppressor function for a member of the Rad51 family. We show that Rad51c deficiency leads to early embryonic lethality, which can be delayed on a Trp53-null background. To uncover the role of Rad51c in tumorigenesis, we have exploited the fact that Rad51c and Trp53 are both closely located on the mouse chromosome 11. We have generated double heterozygous (DH) mice carrying mutant alleles of both genes either on different (DH-trans) or on the same chromosome (DH-cis), the latter allowing for a deletion of wild-type alleles of both genes by loss of heterozygosity. DH-trans mice, in contrast to DH-cis, developed tumors with latency and spectrum similar to Trp53 heterozygous mice. Strikingly, Rad51c mutation in DH-cis mice promoted the development of tumors of specialized sebaceous glands and suppressed tumors characteristic of Trp53 mutation. In addition, DH-cis females developed tumors significantly earlier than any other group.
    MeSH term(s) Adenocarcinoma, Sebaceous/genetics ; Alleles ; Animals ; Cell Transformation, Neoplastic/genetics ; DNA-Binding Proteins ; Embryonic Development/genetics ; Embryonic Stem Cells/cytology ; Embryonic Stem Cells/physiology ; Female ; Genes, Tumor Suppressor ; Loss of Heterozygosity ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Rad51 Recombinase/deficiency ; Rad51 Recombinase/genetics ; Sebaceous Gland Neoplasms/genetics ; Sex Factors ; Tumor Suppressor Protein p53/genetics
    Chemical Substances DNA-Binding Proteins ; RAD51C protein, mouse ; Tumor Suppressor Protein p53 ; Rad51 Recombinase (EC 2.7.7.-)
    Language English
    Publishing date 2009-01-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-08-3057
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  10. Article ; Online: Recombineering: a homologous recombination-based method of genetic engineering.

    Sharan, Shyam K / Thomason, Lynn C / Kuznetsov, Sergey G / Court, Donald L

    Nature protocols

    2009  Volume 4, Issue 2, Page(s) 206–223

    Abstract: Recombineering is an efficient method of in vivo genetic engineering applicable to chromosomal as well as episomal replicons in Escherichia coli. This method circumvents the need for most standard in vitro cloning techniques. Recombineering allows ... ...

    Abstract Recombineering is an efficient method of in vivo genetic engineering applicable to chromosomal as well as episomal replicons in Escherichia coli. This method circumvents the need for most standard in vitro cloning techniques. Recombineering allows construction of DNA molecules with precise junctions without constraints being imposed by restriction enzyme site location. Bacteriophage homologous recombination proteins catalyze these recombineering reactions using double- and single-stranded linear DNA substrates, so-called targeting constructs, introduced by electroporation. Gene knockouts, deletions and point mutations are readily made, gene tags can be inserted and regions of bacterial artificial chromosomes or the E. coli genome can be subcloned by gene retrieval using recombineering. Most of these constructs can be made within about 1 week's time.
    MeSH term(s) DNA, Bacterial/genetics ; Escherichia coli/genetics ; Escherichia coli/metabolism ; Gene Expression Regulation, Bacterial/physiology ; Genetic Engineering/methods ; Plasmids/genetics ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism
    Chemical Substances DNA, Bacterial ; Recombinant Proteins
    Language English
    Publishing date 2009-01-30
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2244966-8
    ISSN 1750-2799 ; 1754-2189
    ISSN (online) 1750-2799
    ISSN 1754-2189
    DOI 10.1038/nprot.2008.227
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