Littérature scientifique sur le sujet « ANKRD26 »
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Articles de revues sur le sujet "ANKRD26"
Husnain, Muhammad, Trent Wang, Maikel Valdes, James Hoffman et Lazaros Lekakis. « Multiple Myeloma in a Patient with ANKRD26-Related Thrombocytopenia Successfully Treated with Combination Therapy and Autologous Stem Cell Transplant ». Case Reports in Hematology 2019 (2 juin 2019) : 1–3. http://dx.doi.org/10.1155/2019/9357572.
Texte intégralNecchi, Vittorio, Alessandra Balduini, Patrizia Noris, Serena Barozzi, Patrizia Sommi, Christian di Buduo, Carlo Balduini, Enrico Solcia et Alessandro Pecci. « Ubiquitin/proteasome-rich particulate cytoplasmic structures (PaCSs) in the platelets and megakaryocytes of ANKRD26-related thrombocytopenia ». Thrombosis and Haemostasis 109, no 02 (2013) : 263–71. http://dx.doi.org/10.1160/th12-07-0497.
Texte intégralErdomaeva, Ya A., D. V. Fedorova, P. A. Zharkov, M. A. Kurnikova, S. G. Mann et E. V. Raykina. « ANKRD26-related thrombocytopenia : case report and literature review of inherited thrombocytopenias with predisposition to malignancies ». Pediatric Hematology/Oncology and Immunopathology 18, no 3 (13 septembre 2019) : 54–61. http://dx.doi.org/10.24287/1726-1708-2019-18-3-54-61.
Texte intégralNoris, Patrizia, Silverio Perrotta, Marco Seri, Alessandro Pecci, Chiara Gnan, Giuseppe Loffredo, Nuria Pujol-Moix et al. « Mutations in ANKRD26 are responsible for a frequent form of inherited thrombocytopenia : analysis of 78 patients from 21 families ». Blood 117, no 24 (16 juin 2011) : 6673–80. http://dx.doi.org/10.1182/blood-2011-02-336537.
Texte intégralGuison, Jérôme, Gilles Blaison, Oana Stoica, Remy Hurstel, Marie Favier et Remi Favier. « Idiopathic pulmonary embolism in a case of severe family ANKRD26 thrombocytopenia ». Mediterranean Journal of Hematology and Infectious Diseases 9, no 1 (16 juin 2017) : e2017038. http://dx.doi.org/10.4084/mjhid.2017.038.
Texte intégralKojić, Snežana. « MARP Protein Family : A Possible Role in Molecular Mechanisms of Tumorigenesis ». Journal of Medical Biochemistry 29, no 3 (1 juillet 2010) : 157–64. http://dx.doi.org/10.2478/v10011-010-0024-9.
Texte intégralVincenot, Anne, Marie-Françoise Hurtaud-Roux, Olivier René, Sylvie Binard, Odile Fenneteau et Nicole Schlegel. « ANKRD26 normocytic thrombocytopenia : a family report ». Annales de biologie clinique 74, no 3 (mai 2016) : 317–22. http://dx.doi.org/10.1684/abc.2016.1142.
Texte intégralNoris, Patrizia, Remi Favier, Marie-Christine Alessi, Amy E. Geddis, Shinji Kunishima, Paula G. Heller, Paola Giordano et al. « ANKRD26-related thrombocytopenia and myeloid malignancies ». Blood 122, no 11 (12 septembre 2013) : 1987–89. http://dx.doi.org/10.1182/blood-2013-04-499319.
Texte intégralMorozova, D. S., A. A. Martyanov, M. A. Panteleev, P. A. Zharkov, D. V. Fedorova et A. N. Sveshnikova. « Observation of granulocyte function during ex vivo thrombus formation for patients with ANKRD26-associated thrombocytopenia ». Pediatric Hematology/Oncology and Immunopathology 19, no 1 (28 mars 2020) : 27–34. http://dx.doi.org/10.24287/1726-1708-2020-19-1-27-34.
Texte intégralGnan, Chiara, Patrizia Noris, Felisa C. Molinas, Shinji Kunishima, Paula Graciela Heller, Akihiro Iguchi, Alessandro Pecci et al. « Mutations Identified in Thrombocytopenia THC2 Are Likely to Dysregulate ANKRD26 Expression ». Blood 118, no 21 (18 novembre 2011) : 708. http://dx.doi.org/10.1182/blood.v118.21.708.708.
Texte intégralThèses sur le sujet "ANKRD26"
Donada, Alessandro. « Physiopathological mechanisms of two congenical platelet disorders : filaminopathy-A and ANKRD26-related - Thrombocytopenia 5THC2 ». Thesis, Sorbonne Paris Cité, 2018. https://theses.md.univ-paris-diderot.fr/DONADA_Alessandro_2_complete_2018.zip.
Texte intégralInherited thrombocytopenias are a class of congenital haematological disorders affecting primarily the megakaryocytic lineage and accomunated by a decrease in platelet numbers. Almost 50 different genes have been associated to inherited platelet disorders, and huge differences exist between each disorder, in regard to clinical manifestation and pathobiology. My research interest have been focused on two different congenital thrombocytopenias: Filaminopathy A and Thrombocytopenia 2. The first disease is a X-linked syndrome associated to mutations in the gene FLNA (Filamin A), and patients display a mild to severe macrothrombocytopenia, associated with a lifelong bleeding tendency. The second disorder is an automal dominant condition caused by mutations in the 5’ UTR of the ANKRD26 gene. It is associated with dysmegakaryopoiesis, mild to severe thrombocytopenia and an increased risk to develop myeloid malignancies. To study the physiopathology of those two rare diseases, we have exploited the induced pluripotent stem cell technology to develop several patient specific cell lines. Those experimental tools revealed invaluable for the understanding of the disease physiopathology, and allowed us to describe in great details the molecular mechanisms underlying the reduction in proplatelet formation for Filaminopathy A and the predisposition to leukemia for Thrombocytopenia 2. To perform such studies, we devised a robust differentiation protocol, recapitulating efficiently the haematopoietic differentiation and easily adapted to the in vitro differentiation of multiple cell lineages. Furthermore, we exploited a genome editing technique to introduce efficiently different protein mutants, in order to dissect the molecular role of Filamin A in megakaryopoiesis. In regard of Filaminopathy A, we have been able to describe an original and novel relationship between a membrane integrin (IIb3), Filamin A and a crucial signalling pathway (RhoA) for megakaryopoiesis. Our data support a model where the absence of FLNa induces an abnormal activity of the RhoA pathway, in response to the integrin IIb3 binding to fibrinogen. Concerning the thrombocytopenia 2, we described a novel mechanism that associated the increased expression of ANKRD26 to a deregulated activity of the G-CSF-dependent signalling pathway. This anomaly impacts the normal granulopoiesis and lead to an abnormal amplification of this cell lineage, possibly increasing the risk of acquiring other mutational hits and progress towards a myeloid malignancy.In conclusion, with this work we offer a proof of concept of the potentiality of disease modeling via induced pluripotent stem cells. Our results pave the way for further studies that could advance our understanding of the physiopathology of inherited platelet disorders
Verma, Narendra Kumar. « Ankrd2 modulates NF-kB mediated inflammatory responses during muscle differentiation ». Doctoral thesis, Università degli studi di Padova, 2014. http://hdl.handle.net/11577/3423734.
Texte intégralAbstract (Italiano) La proteina Ankrd2 (Ankyrin repeat domain 2) può interagire sia con proteine del sarcomero sia con proteine nucleari che regolano l’espressione genica e quindi è in grado di trasdurre stimoli di natura diversa in specifiche risposte adattative del muscolo scheletrico. In un’analisi trascrittomica condotta su mioblasti primari (proliferanti o in differenziamento) dove Ankrd2 è stata silenziata o sovra-espressa, abbiamo: a) trovato una correlazione inversa tra i livelli di Ankrd2 e l’espressione di geni pro-infiammatori; b) dimostrato che Ankrd2 agisce da potente repressore della risposta infiammatoria tramite interazione diretta con la subunità p50 del fattore di trascrizione NF-kB. In particolare, abbiamo dimostrato che la chinasi Gsk3ß è il bersaglio privilegiato del dimero di repressione p50:Ankrd2; inoltre, durante il differenziamento miogenico il reclutamento di p50 da parte di Ankrd2 dipende dalla fosforilazione di Ankrd2 mediata dalla chinasi Akt2 in condizioni di stress ossidativo. Stranamente, l’assenza di Ankrd2 influenza in maniera negativa l’espressione di citochine e di geni chiave calcineurina-dipendenti associati al programma di contrazione lenta del muscolo scheletrico. I nostri risultati supportano quindi un modello nel quale alterazioni della proteina Ankrd2 o dei suoi livelli di fosforilazione modulano l’equilibrio tra la risposta infiammatoria fisiologica e patologica nel muscolo scheletrico.
Tachibana, Mitsuhiro. « Ankyrin repeat domain 28 (ANKRD28), a novel binding partner of DOCK180, promotes cell migration by regulating focal adhesion formation ». Kyoto University, 2009. http://hdl.handle.net/2433/124284.
Texte intégralNg, Kung Yau. « ANKRA2 interacts with p35 and is a substrate for Cdk5/p35 / ». View abstract or full-text, 2006. http://library.ust.hk/cgi/db/thesis.pl?BICH%202006%20NG.
Texte intégralRostamirad, Shabnam. « Identification and characterization of a novel retinal protein, ANKRD33, and its interacting partner HPCAL-1 ». Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/27274.
Texte intégralDuffus, Kate. « Investigation of genetic susceptibility to Rheumatoid Arthritis ». Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/investigation-of-genetic-susceptibility-to-rheumatoid-arthritis(edf01c7b-3c46-4c75-8751-6f117291c027).html.
Texte intégralAckermann, Sarah [Verfasser], et Thomas [Akademischer Betreuer] Meyer. « Mutationsanalyse des ANKRD1-Gens bei Patienten mit dilatativer Kardiomyopathie / Sarah Ackermann. Betreuer : Thomas Meyer ». Marburg : Philipps-Universität Marburg, 2012. http://d-nb.info/1021498874/34.
Texte intégralJimenez, Carrera Adriana Patricia [Verfasser]. « Functional characterisation of ANKRD1 and its regulation by RASSF1A and YAP1 signalling / Adriana Patricia Jimenez Carrera ». Gießen : Universitätsbibliothek, 2017. http://d-nb.info/1131551214/34.
Texte intégralPapanikos, Frantzeskos [Verfasser], Attila [Gutachter] Tóth et Konstantinos [Gutachter] Anastasiadis. « The role of two sex chromosome associated proteins, SCML1 and ANKRD31, in gametogenesis in mice / Frantzeskos Papanikos ; Gutachter : Attila Tóth, Konstantinos Anastasiadis ». Dresden : Technische Universität Dresden, 2020. http://d-nb.info/1227196539/34.
Texte intégralLin, Yen-Fan, et 林妍汎. « Inhibition of lung adenocarcinoma metastasis by ANKRD52 ». Thesis, 2017. http://ndltd.ncl.edu.tw/handle/39915447171426219015.
Texte intégralActes de conférences sur le sujet "ANKRD26"
Lee, Ting-Fang, Yen-Fan Lin, Ying-Pu Liu et Cheng-Wen Wu. « Abstract 5508 : ANKRD52 inhibited tumor metastasis in lung adenocarcinoma ». Dans Proceedings : AACR Annual Meeting 2018 ; April 14-18, 2018 ; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-5508.
Texte intégralMohamed, Junaith S., Michael A. Lopez et Aladin M. Boriek. « Anisotropic Mechanical Stretch Up-regulates Ankrd2 Expression Through Two Distinct Signaling Pathways In Skeletal Muscle ». Dans American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6374.
Texte intégralLin, Yen-Fan, Ying-Pu Liu, Ting-Fang Lee et Cheng-Wen Wu. « Abstract 4843 : ANKRD52 inhibited tumor metastasis through dephosphorylation of PAK1 in lung adenocarcinoma ». Dans Proceedings : AACR Annual Meeting 2017 ; April 1-5, 2017 ; Washington, DC. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/1538-7445.am2017-4843.
Texte intégralLee, Ting-Fang, Yin-Pu Liu, Yen-Fan Lin, Chong-Fang Hsu et Cheng-Wen Wu. « Abstract 1782 : ANKRD52 inhibited tumor metastasis through dephosphorylation of PAK1 in lung adenocarcinomas ». Dans Proceedings : AACR Annual Meeting 2019 ; March 29-April 3, 2019 ; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-1782.
Texte intégralLee, Ting-Fang, Yin-Pu Liu, Yen-Fan Lin, Chong-Fang Hsu et Cheng-Wen Wu. « Abstract 1782 : ANKRD52 inhibited tumor metastasis through dephosphorylation of PAK1 in lung adenocarcinomas ». Dans Proceedings : AACR Annual Meeting 2019 ; March 29-April 3, 2019 ; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-1782.
Texte intégral« Differentially methylation of ANKRD53 and GATA3 genes in human miscarriages with trisomy 16 ». Dans Bioinformatics of Genome Regulation and Structure/ Systems Biology. institute of cytology and genetics siberian branch of the russian academy of science, Novosibirsk State University, 2020. http://dx.doi.org/10.18699/bgrs/sb-2020-079.
Texte intégralBoriek, Aladin M., et Junaith S. Mohamed. « Knockdown Of Desmin Protein By SiRNA Up-regulates Ankrd1 Through Akt/NF-kB Signaling Pathway And Turns Ankrd1 Into Mechanosensitive In Human Airway Smooth Muscle Cells ». Dans American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5316.
Texte intégralQian, J., et S. Nan. « 307 The pathogenic mechanisms of systemic lupus erythematosus associated genes pnp, plekhf2 and ankrd44 ». Dans LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.307.
Texte intégralSong, Tianyu Y., Haixin Zhao, Hongjie Fan, Min Long, Chenlu Geng, Xiaoxiao Xie, Yang Liu et al. « Abstract 2154 : Immune pressure selects ANKRD52 mutations for cancer cells to escape T cell-mediated killing ». Dans Proceedings : AACR Annual Meeting 2020 ; April 27-28, 2020 and June 22-24, 2020 ; Philadelphia, PA. American Association for Cancer Research, 2020. http://dx.doi.org/10.1158/1538-7445.am2020-2154.
Texte intégralMa, Jian yang, Xiao Han, Bo Qu et Nan Shen. « 82 Decreased expression of ANKRD44 associates with the overactivation of type I IFN signaling pathway in SLE ». Dans 13th International Congress on Systemic Lupus Erythematosus (LUPUS 2019), San Francisco, California, USA, April 5–8, 2019, Abstract Presentations. Lupus Foundation of America, 2019. http://dx.doi.org/10.1136/lupus-2019-lsm.82.
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