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  1. Article ; Online: The interaction between invariant Natural Killer T cells and the mucosal microbiota.

    Hapil, Fatma Zehra / Wingender, Gerhard

    Immunology

    2018  Volume 155, Issue 2, Page(s) 164–175

    Abstract: The surface of mammalian bodies is colonized by a multitude of microbial organisms, which under normal conditions support the host and are considered beneficial commensals. This requires, however, that the composition of the commensal microbiota is ... ...

    Abstract The surface of mammalian bodies is colonized by a multitude of microbial organisms, which under normal conditions support the host and are considered beneficial commensals. This requires, however, that the composition of the commensal microbiota is tightly controlled and regulated. The host immune system plays an important role in the maintenance of this microbiota composition. Here we focus on the contribution of one particular immune cell type, invariant Natural Killer T (iNKT) cells, in this process. The iNKT cells are a unique subset of T cells characterized by two main features. First, they express an invariant T-cell receptor that recognizes glycolipid antigens presented by CD1d, a non-polymorphic major histocompatibility complex class I-like molecule. Second, iNKT cells develop as effector/memory cells and swiftly exert effector functions, like cytokine production and cytotoxicity, after activation. We outline the influence that the mucosal microbiota can have on iNKT cells, and how iNKT cells contribute to the maintenance of the microbiota composition.
    MeSH term(s) Animals ; Gastrointestinal Microbiome/immunology ; Host-Pathogen Interactions/immunology ; Humans ; Immune System ; Intestinal Mucosa/immunology ; Intestinal Mucosa/metabolism ; Intestinal Mucosa/microbiology ; Microbiota ; Mucous Membrane/immunology ; Mucous Membrane/metabolism ; Mucous Membrane/microbiology ; Natural Killer T-Cells/immunology ; Natural Killer T-Cells/metabolism ; Respiratory Mucosa/immunology ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/microbiology
    Language English
    Publishing date 2018-07-11
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80124-0
    ISSN 1365-2567 ; 0019-2805 ; 0953-4954
    ISSN (online) 1365-2567
    ISSN 0019-2805 ; 0953-4954
    DOI 10.1111/imm.12958
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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  2. Article ; Online: Positive regulation of TNFR1 signaling via SH3 recognition motif.

    Çopuroğlu, Fatma Ece / Hapil, Fatma Zehra / Yoldaş, Şükran Burçak / Özeş, Osman Nidai

    Turkish journal of biology = Turk biyoloji dergisi

    2021  Volume 45, Issue 1, Page(s) 171–179

    Abstract: TNF is a pleiotropic cytokine and shows its biological function by binding to its receptors called TNFR1 and TNFR2. While TNFR1 induces apoptosis by activation of caspase-8 via the "death domain", it also activates IKKα/β, MKK3/6, MKK4/7 by activation of ...

    Abstract TNF is a pleiotropic cytokine and shows its biological function by binding to its receptors called TNFR1 and TNFR2. While TNFR1 induces apoptosis by activation of caspase-8 via the "death domain", it also activates IKKα/β, MKK3/6, MKK4/7 by activation of TAK1. Although the TNFR1 signaling pathway is known by in large, it is not known how AKT and MAPKs p38, ERK1/2, and JNK1/2 are activated. The presence of a proline-rich PPAP region, (P448PAP451, a binding site for the SH3 domain-containing proteins) very close to the C-terminus promoted us to determine whether this region has any role in the TNFR1 signal transduction. To test this, the codons of P448 and P451 were changed to that of Alanin, GCG, via site-directed mutagenesis, and this plasmid was named as TNFR1-SH3-P/A. Subsequently, ectopically expressed the wild type TNFR1 and TNFR1-SH3-P/A in 293T cells and determined the levels of TNF-α-mediated phosphorylations of ERK, p38, JNK and AKT, NF-kB, and caspase-8 activation. While ectopic expression of our mutant diminished TNFα-mediated phosphorylations of p38, JNK, ERK and AKT, it increased NF-kB, and caspase-8 activations. In conclusion, TNFα-mediated ERK, AKT, JNK, p38 activations are affected by TNFR1 SH3 domain modifications.
    Language English
    Publishing date 2021-04-20
    Publishing country Turkey
    Document type Journal Article
    ZDB-ID 2046470-8
    ISSN 1303-6092 ; 1300-0152
    ISSN (online) 1303-6092
    ISSN 1300-0152
    DOI 10.3906/biy-2010-28
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Negative Regulation of TNFR1 Signaling Via PKA-Mediated Phosphorylation of TNFR1.

    Hapil, Fatma Zehra / Çopuroğlu, Fatma Ece / Ertosun, Mustafa Gökhan / Mert, Ufuk / Özeş, Derya / Özeş, Osman Nidai

    Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research

    2020  Volume 40, Issue 5, Page(s) 225–235

    Abstract: Tumor necrosis factor alpha (TNF-α) plays a paramount role in homeostasis by inducing tumor cytotoxicity and activating immune system. The signaling complexes formed by TNFR1 to activate JNK, p38, and nuclear factor-kappa B pathways and to subsequently ... ...

    Abstract Tumor necrosis factor alpha (TNF-α) plays a paramount role in homeostasis by inducing tumor cytotoxicity and activating immune system. The signaling complexes formed by TNFR1 to activate JNK, p38, and nuclear factor-kappa B pathways and to subsequently induce apoptosis and necroptosis are well known. However, this "canonical TNF-α signaling" does not explain how ERK, AKT, and STAT3 can be activated by TNF-α. In addition, little to nothing is known about negative regulation of TNFR1 signaling. Because cyclic AMP-activated kinase (PKA) shows anti-TNF and anti-inflammatory activities, we postulated that PKA might affect TNF-α signaling by directly phosphorylating TNFR1. In line with this, we identified 2 putative PKA-phosphorylation motifs RRRT
    MeSH term(s) Cells, Cultured ; Cyclic AMP-Dependent Protein Kinases/metabolism ; HEK293 Cells ; Humans ; Phosphorylation ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Signal Transduction
    Chemical Substances Receptors, Tumor Necrosis Factor, Type I ; Cyclic AMP-Dependent Protein Kinases (EC 2.7.11.11)
    Language English
    Publishing date 2020-03-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1226675-9
    ISSN 1557-7465 ; 1079-9907
    ISSN (online) 1557-7465
    ISSN 1079-9907
    DOI 10.1089/jir.2019.0128
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1748: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: E2F1 transcription factor and its impact on growth factor and cytokine signaling.

    Ertosun, Mustafa Gokhan / Hapil, Fatma Zehra / Osman Nidai, Ozes

    Cytokine & growth factor reviews

    2016  Volume 31, Page(s) 17–25

    Abstract: E2F1 is a transcription factor involved in cell cycle regulation and apoptosis. The transactivation capacity of E2F1 is regulated by pRb. In its hypophosphorylated form, pRb binds and inactivates DNA binding and transactivating functions of E2F1. The ... ...

    Abstract E2F1 is a transcription factor involved in cell cycle regulation and apoptosis. The transactivation capacity of E2F1 is regulated by pRb. In its hypophosphorylated form, pRb binds and inactivates DNA binding and transactivating functions of E2F1. The growth factor stimulation of cells leads to activation of CDKs (cyclin dependent kinases), which in turn phosphorylate Rb and hyperphosphorylated Rb is released from E2F1 or E2F1/DP complex, and free E2F1 can induce transcription of several genes involved in cell cycle entry, induction or inhibition of apoptosis. Thus, growth factors and cytokines generally utilize E2F1 to direct cells to either fate. Furthermore, E2F1 regulates expressions of various cytokines and growth factor receptors, establishing positive or negative feedback mechanisms. This review focuses on the relationship between E2F1 transcription factor and cytokines (IL-1, IL-2, IL-3, IL-6, TGF-beta, G-CSF, LIF), growth factors (EGF, KGF, VEGF, IGF, FGF, PDGF, HGF, NGF), and interferons (IFN-α, IFN-β and IFN-γ).
    MeSH term(s) Animals ; E2F1 Transcription Factor/metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Signal Transduction
    Chemical Substances E2F1 Transcription Factor ; E2F1 protein, human ; Intercellular Signaling Peptides and Proteins
    Language English
    Publishing date 2016
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 1330534-7
    ISSN 1879-0305 ; 1359-6101
    ISSN (online) 1879-0305
    ISSN 1359-6101
    DOI 10.1016/j.cytogfr.2016.02.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2653: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
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  5. Article: Identification of novel mutations of Insulin Receptor Substrate 1 (IRS1) in tumor samples of non-small cell lung cancer (NSCLC): Implications for aberrant insulin signaling in development of cancer.

    Gorgisen, Gokhan / Hapil, Fatma Zehra / Yilmaz, Ozlem / Cetin, Zafer / Pehlivanoglu, Suray / Ozbudak, Irem Hicran / Erdogan, Abdullah / Ozes, Osman Nidai

    Genetics and molecular biology

    2019  Volume 42, Issue 1, Page(s) 15–25

    Abstract: Lung cancer is the leading cause of cancer-related death, and NSCLC constitutes nearly 85%-90% of all cases. The IRS proteins function as adaptors and transmit signals from multiple receptors. Upon binding of insulin to the insulin receptor (IR), IRS1 is ...

    Abstract Lung cancer is the leading cause of cancer-related death, and NSCLC constitutes nearly 85%-90% of all cases. The IRS proteins function as adaptors and transmit signals from multiple receptors. Upon binding of insulin to the insulin receptor (IR), IRS1 is phosphorylated at several YXXM motifs creating docking sites for the binding of PI3Kp85, which activates AKT kinase. Therefore, we thought that gain of function mutantions of IRS1 could be related to development of lung cancer. In line with this, we wanted determine whether the IRS1 gene was mutated in the coding regions surrounding YXXM motifs. We sequenced the coding regions surrounding YXXM motifs of IRS1 using tumor samples of 42 NSCLC patients and 40 matching controls and found heterozygote p.S668T mutation in nine of 42 samples and four of nine also had the p.D674H mutation. We generated IRS1 expression vectors harboring p.S668T, p.D674H and double mutants. Expression of the mutants differentially affected insulin-induced phosphorylation of IRS1, AKT, ERK, and STAT3. Also, our mutants induced proliferation, glucose uptake, inhibited the migration of 293T cells and affected the responsiveness of the cells to cisplatin and radiation. Our results suggest that these novel mutations play a role in the phenotype of lung cancer.
    Language English
    Publishing date 2019-02-25
    Publishing country Brazil
    Document type Journal Article
    ZDB-ID 1445712-x
    ISSN 1678-4685 ; 1415-4757
    ISSN (online) 1678-4685
    ISSN 1415-4757
    DOI 10.1590/1678-4685-gmb-2017-0307
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3079: Show issues Location:
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  6. Article: Progress and harmonization of gene editing to treat human diseases: Proceeding of COST Action CA21113 GenE-HumDi.

    Cavazza, Alessia / Hendel, Ayal / Bak, Rasmus O / Rio, Paula / Güell, Marc / Lainšček, Duško / Arechavala-Gomeza, Virginia / Peng, Ling / Hapil, Fatma Zehra / Harvey, Joshua / Ortega, Francisco G / Gonzalez-Martinez, Coral / Lederer, Carsten W / Mikkelsen, Kasper / Gasiunas, Giedrius / Kalter, Nechama / Gonçalves, Manuel A F V / Petersen, Julie / Garanto, Alejandro /
    Montoliu, Lluis / Maresca, Marcello / Seemann, Stefan E / Gorodkin, Jan / Mazini, Loubna / Sanchez, Rosario / Rodriguez-Madoz, Juan R / Maldonado-Pérez, Noelia / Laura, Torella / Schmueck-Henneresse, Michael / Maccalli, Cristina / Grünewald, Julian / Carmona, Gloria / Kachamakova-Trojanowska, Neli / Miccio, Annarita / Martin, Francisco / Turchiano, Giandomenico / Cathomen, Toni / Luo, Yonglun / Tsai, Shengdar Q / Benabdellah, Karim

    Molecular therapy. Nucleic acids

    2023  Volume 34, Page(s) 102066

    Abstract: The European Cooperation in Science and Technology (COST) is an intergovernmental organization dedicated to funding and coordinating scientific and technological research in Europe, fostering collaboration among researchers and institutions across ... ...

    Abstract The European Cooperation in Science and Technology (COST) is an intergovernmental organization dedicated to funding and coordinating scientific and technological research in Europe, fostering collaboration among researchers and institutions across countries. Recently, COST Action funded the "Genome Editing to treat Human Diseases" (GenE-HumDi) network, uniting various stakeholders such as pharmaceutical companies, academic institutions, regulatory agencies, biotech firms, and patient advocacy groups. GenE-HumDi's primary objective is to expedite the application of genome editing for therapeutic purposes in treating human diseases. To achieve this goal, GenE-HumDi is organized in several working groups, each focusing on specific aspects. These groups aim to enhance genome editing technologies, assess delivery systems, address safety concerns, promote clinical translation, and develop regulatory guidelines. The network seeks to establish standard procedures and guidelines for these areas to standardize scientific practices and facilitate knowledge sharing. Furthermore, GenE-HumDi aims to communicate its findings to the public in accessible yet rigorous language, emphasizing genome editing's potential to revolutionize the treatment of many human diseases. The inaugural GenE-HumDi meeting, held in Granada, Spain, in March 2023, featured presentations from experts in the field, discussing recent breakthroughs in delivery methods, safety measures, clinical translation, and regulatory aspects related to gene editing.
    Language English
    Publishing date 2023-10-29
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2662631-7
    ISSN 2162-2531
    ISSN 2162-2531
    DOI 10.1016/j.omtn.2023.102066
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article: Odour intensity learning in fruit flies.

    Yarali, Ayse / Ehser, Sabrina / Hapil, Fatma Zehra / Huang, Ju / Gerber, Bertram

    Proceedings. Biological sciences

    2009  Volume 276, Issue 1672, Page(s) 3413–3420

    Abstract: Animals' behaviour towards odours depends on both odour quality and odour intensity. While neuronal coding of odour quality is fairly well studied, how odour intensity is treated by olfactory systems is less clear. Here we study odour intensity ... ...

    Abstract Animals' behaviour towards odours depends on both odour quality and odour intensity. While neuronal coding of odour quality is fairly well studied, how odour intensity is treated by olfactory systems is less clear. Here we study odour intensity processing at the behavioural level, using the fruit fly Drosophila melanogaster. We trained flies by pairing a MEDIUM intensity of an odour with electric shock, and then, at a following test phase, measured flies' conditioned avoidance of either this previously trained MEDIUM intensity or a LOWer or a HIGHer intensity. With respect to 3-octanol, n-amylacetate and 4-methylcyclohexanol, we found that conditioned avoidance is strongest when training and test intensities match, speaking for intensity-specific memories. With respect to a fourth odour, benzaldehyde, on the other hand, we found no such intensity specificity. These results form the basis for further studies of odour intensity processing at the behavioural, neuronal and molecular level.
    MeSH term(s) Animals ; Behavior, Animal/physiology ; Conditioning, Psychological/physiology ; Drosophila melanogaster/physiology ; Learning/physiology ; Odorants
    Language English
    Publishing date 2009-07-08
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 209242-6
    ISSN 1471-2954 ; 0962-8452 ; 0080-4649 ; 0950-1193
    ISSN (online) 1471-2954
    ISSN 0962-8452 ; 0080-4649 ; 0950-1193
    DOI 10.1098/rspb.2009.0705
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1364: Show issues Location:
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