Relevant bibliographies by topics / NF2/Merlin

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
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Academic literature on the topic 'NF2/Merlin'

Author: Grafiati
Published: 12 October 2024
Last updated: 31 July 2025

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Journal articles on the topic "NF2/Merlin"

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Bashour, Anne-Marie, J. J. Meng, Wallace Ip, Mia MacCollin, and Nancy Ratner. "The Neurofibromatosis Type 2 Gene Product, merlin, Reverses the F-Actin Cytoskeletal Defects in Primary Human Schwannoma Cells." Molecular and Cellular Biology 22, no. 4 (2002): 1150–57. http://dx.doi.org/10.1128/mcb.22.4.1150-1157.2002.

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ABSTRACT Schwannoma tumors, which occur sporadically and in patients with neurofibromatosis, account for 8% of intracranial tumors and can only be treated by surgical removal. Most schwannomas have biallelic mutations in the NF2 tumor suppressor gene. We previously showed that schwannoma-derived Schwann cells exhibit membrane ruffling and aberrant cell spreading when plated onto laminin, indicative of fundamental F-actin cytoskeletal defects. Here we expand these observations to a large group of sporadic and NF2-related tumors and extend them to schwannomatosis-derived tumors. Mutation at NF2
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Eaton, Charlotte, Abrar Choudhury, Timothy Casey-Clyde, Danielle Swaney, Nevan Krogan, and David Raleigh. "CSIG-26. NF2/MERLIN DRIVES MENINGIOMA APOPTOSIS AND SUCEPTIBILITY TO CYTOTOXIC THERAPY." Neuro-Oncology 23, Supplement_6 (2021): vi39. http://dx.doi.org/10.1093/neuonc/noab196.152.

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Abstract BACKGROUND Alterations in NF2 underlie meningioma tumorigenesis, but tumor suppressor functions of the NF2 gene product, Merlin, are incompletely understood in meningiomas. Here we integrate proteomic proximity-labelling mass spectrometry with CRISPR interference (CRISPRi), RNA sequencing, and biochemical approaches to discover Merlin drives meningioma apoptosis and susceptibility to cytotoxic therapy. METHODS RNA sequencing was performed on triplicate M10G meningioma cells stably expressing CRISPRi machinery and either non-targeting control sgRNAs, sgRNAs suppressing NF2, or sgRNAs s
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James, Marianne F., Sangyeul Han, Carolyn Polizzano, et al. "NF2/Merlin Is a Novel Negative Regulator of mTOR Complex 1, and Activation of mTORC1 Is Associated with Meningioma and Schwannoma Growth." Molecular and Cellular Biology 29, no. 15 (2009): 4250–61. http://dx.doi.org/10.1128/mcb.01581-08.

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ABSTRACT Inactivating mutations of the neurofibromatosis 2 (NF2) gene, NF2, result predominantly in benign neurological tumors, schwannomas and meningiomas, in humans; however, mutations in murine Nf2 lead to a broad spectrum of cancerous tumors. The tumor-suppressive function of the NF2 protein, merlin, a membrane-cytoskeleton linker, remains unclear. Here, we identify the mammalian target of rapamycin complex 1 (mTORC1) as a novel mediator of merlin's tumor suppressor activity. Merlin-deficient human meningioma cells and merlin knockdown arachnoidal cells, the nonneoplastic cell counterparts
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Lee, Hansoo, Donghwa Kim, Han C. Dan, et al. "Identification and Characterization of Putative Tumor Suppressor NGB, a GTP-Binding Protein That Interacts with the Neurofibromatosis 2 Protein." Molecular and Cellular Biology 27, no. 6 (2007): 2103–19. http://dx.doi.org/10.1128/mcb.00572-06.

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ABSTRACT Mutations of the neurofibromatosis 2 (NF2) tumor suppressor gene have frequently been detected not only in schwannomas and other central nervous system tumors of NF2 patients but also in their sporadic counterparts and malignant tumors unrelated to the NF2 syndrome such as malignant mesothelioma, indicating a broader role for the NF2 gene in human tumorigenesis. However, the mechanisms by which the NF2 product, merlin or schwannomin, is regulated and controls cell proliferation remain elusive. Here, we identify a novel GTP-binding protein, dubbed NGB (referring to NF2-associated GTP b
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Houshmandi, S. Sean, Ryan J. Emnett, Marco Giovannini, and David H. Gutmann. "The Neurofibromatosis 2 Protein, Merlin, Regulates Glial Cell Growth in an ErbB2- and Src-Dependent Manner." Molecular and Cellular Biology 29, no. 6 (2008): 1472–86. http://dx.doi.org/10.1128/mcb.01392-08.

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ABSTRACT Individuals with the inherited cancer predisposition syndrome neurofibromatosis 2 (NF2) develop several central nervous system (CNS) malignancies, including glial cell neoplasms (ependymomas). Recent studies have suggested that the NF2 protein, merlin (or schwannomin), may regulate receptor tyrosine kinase signaling, intracellular mitogenic growth control pathways, or adherens junction organization in non-nervous-system cell types. For this report, we used glial fibrillary acidic protein conditional knockout mice and derivative glia to determine how merlin regulates CNS glial cell pro
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Xiao, Guang-Hui, Ryan Gallagher, Justin Shetler, et al. "The NF2 Tumor Suppressor Gene Product, Merlin, Inhibits Cell Proliferation and Cell Cycle Progression by Repressing Cyclin D1 Expression." Molecular and Cellular Biology 25, no. 6 (2005): 2384–94. http://dx.doi.org/10.1128/mcb.25.6.2384-2394.2005.

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ABSTRACT Inactivation of the NF2 tumor suppressor gene has been observed in certain benign and malignant tumors. Recent studies have demonstrated that merlin, the product of the NF2 gene, is regulated by Rac/PAK signaling. However, the mechanism by which merlin acts as a tumor suppressor has remained obscure. In this report, we show that adenovirus-mediated expression of merlin in NF2-deficient tumor cells inhibits cell proliferation and arrests cells at G1 phase, concomitant with decreased expression of cyclin D1, inhibition of CDK4 activity, and dephosphorylation of pRB. The effect of merlin
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Kim, Bae-Hoon, Yeon-Ho Chung, Tae-Gyun Woo, et al. "NF2-Related Schwannomatosis (NF2): Molecular Insights and Therapeutic Avenues." International Journal of Molecular Sciences 25, no. 12 (2024): 6558. http://dx.doi.org/10.3390/ijms25126558.

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NF2-related schwannomatosis (NF2) is a genetic syndrome characterized by the growth of benign tumors in the nervous system, particularly bilateral vestibular schwannomas, meningiomas, and ependymomas. This review consolidates the current knowledge on NF2 syndrome, emphasizing the molecular pathology associated with the mutations in the gene of the same name, the NF2 gene, and the subsequent dysfunction of its product, the Merlin protein. Merlin, a tumor suppressor, integrates multiple signaling pathways that regulate cell contact, proliferation, and motility, thereby influencing tumor growth.
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Eaton, Charlotte, Paola Bisignano, and David Raleigh. "CSIG-22. CANCER-ASSOCIATED MISSENSE SINGLE NUCLEOTIDE VARIANTS REGULATE THE STABILITY AND SUBCELLULAR LOCALIZATION OF NF2/MERLIN." Neuro-Oncology 22, Supplement_2 (2020): ii32. http://dx.doi.org/10.1093/neuonc/noaa215.134.

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Abstract BACKGROUND Alterations in the NF2 tumor suppressor gene lead to meningiomas and schwannomas, but the tumor suppressor functions of the NF2 gene product, Merlin, are incompletely understood. To address this problem, we performed a structure-function analysis of Merlin by expressing cancer-associated missense single-nucleotide variants (mSNVs) in primary cancer cells for biochemical and cell biology experiments. METHODS All NF2 mSNVs were assembled from cBioPortal and COSMIC, and modelled on the FERM, a-helical, and C-terminal domains of Merlin (PDB 4ZRJ) using comparative structure pre
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Bachir, Suha, Sanjit Shah, Scott Shapiro, et al. "Neurofibromatosis Type 2 (NF2) and the Implications for Vestibular Schwannoma and Meningioma Pathogenesis." International Journal of Molecular Sciences 22, no. 2 (2021): 690. http://dx.doi.org/10.3390/ijms22020690.

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Patients diagnosed with neurofibromatosis type 2 (NF2) are extremely likely to develop meningiomas, in addition to vestibular schwannomas. Meningiomas are a common primary brain tumor; many NF2 patients suffer from multiple meningiomas. In NF2, patients have mutations in the NF2 gene, specifically with loss of function in a tumor-suppressor protein that has a number of synonymous names, including: Merlin, Neurofibromin 2, and schwannomin. Merlin is a 70 kDa protein that has 10 different isoforms. The Hippo Tumor Suppressor pathway is regulated upstream by Merlin. This pathway is critical in re
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LaJeunesse, Dennis R., Brooke M. McCartney, and Richard G. Fehon. "Structural Analysis of Drosophila Merlin Reveals Functional Domains Important for Growth Control and Subcellular Localization." Journal of Cell Biology 141, no. 7 (1998): 1589–99. http://dx.doi.org/10.1083/jcb.141.7.1589.

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Merlin, the product of the Neurofibromatosis type 2 (NF2) tumor-suppressor gene, is a member of the protein 4.1 superfamily that is most closely related to ezrin, radixin, and moesin (ERM). NF2 is a dominantly inherited disease characterized by the formation of bilateral acoustic schwannomas and other benign tumors associated with the central nervous system. To understand its cellular functions, we are studying a Merlin homologue in Drosophila. As is the case for NF2 tumors, Drosophila cells lacking Merlin function overproliferate relative to their neighbors. Using in vitro mutagenesis, we def
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Dissertations / Theses on the topic "NF2/Merlin"

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Johnson, Kristen C. (Kristen Carrie) 1976. "Analysis of the function of the Nf2 tumor suppressor protein, Merlin." Thesis, Massachusetts Institute of Technology, 2003. http://hdl.handle.net/1721.1/29763.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biology, 2003.<br>Vita.<br>Includes bibliographical references.<br>The Neurofibromatosis type 2 tumor suppressor gene (NF2) is mutated in inherited and sporadically occurring central nervous system tumors. The NF2 encoded protein, merlin, shares close sequence similarity in its amino-terminal domain to members of the band 4.1 family of membrane-cytoskeletal linkers. Similarities between merlin and this family suggest a role for merlin in regulating cytoskeletal function. Thus, NF2 may be a novel type of tumor suppressor gene that
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Schulze, Karin Marlies Marion. "Herstellung rekombinanter Retroviren, In-vitro-Gentransfer und Expressionsanalyse des NF2-Gens Merlin." [S.l. : s.n.], 2001. http://deposit.ddb.de/cgi-bin/dokserv?idn=962345210.

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Chen, Yaxiong. "Characterization of chicken NF2/merlin and its functions in early limb muscle development /." free to MU campus, to others for purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p3115532.

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Mani, Timmy. "The Role of Phosphoinositide Binding in Merlin Function." University of Cincinnati / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1299181100.

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Zhan, Yu. "Mixed Lineage Kinase 3 Signaling in Ovarian Cancer and Neurofibromatosis-2." University of Toledo / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=toledo1310127039.

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Adès, Noémie. "PAK1 and NF2 antagonist functions in regulating central nervous system myelination : from modulation of oligodendrocyte cytoskeleton to myelin sheath formation." Electronic Thesis or Diss., Sorbonne université, 2024. https://accesdistant.sorbonne-universite.fr/login?url=https://theses-intra.sorbonne-universite.fr/2024SORUS197.pdf.

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Dans le système nerveux central, la formation des gaines de myéline par les oligodendrocytes permet une propagation efficace et adaptée des potentiels d'action le long des axones, ainsi qu'un apport métabolique aux neurones. Le processus de myélinisation requière une fine régulation du cytosquelette d'actine des oligodendrocytes. En effet, la première étape de la myélinisation, qu'est l'extension d'un prolongement par les oligodendrocytes pour atteindre un axone, est soutenue par une polymérisation de l'actine. En revanche, l'enroulement de ce prolongement et son étalement autour de l'axone po
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Lyons, Rimmer Jade. "The potential of CRL4-DCAF1 and KSR1 as therapeutic targets in low-grade Merlin-deficient tumours." Thesis, University of Plymouth, 2018. http://hdl.handle.net/10026.1/12833.

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Merlin is a tumour suppressor protein that is frequently mutated or downregulated in cancer. Biallelic Merlin inactivation is causative of tumour formation, including schwannoma, meningioma and ependymoma. These tumours can occur sporadically or as part of the genetic condition Neurofibromatosis type 2 (NF2) and cause significant morbidity. The current treatment options are restricted to surgery and radiotherapy, which are invasive and may cause further tumour development. The activity of both the E3 ubiquitin ligase complex Cullin 4 really interesting new gene (RING) E3 ubiquitin ligase- DNA
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Worseck, Josephine Maria. "Characterization of phosphorylation-dependent interactions involving neurofibromin 2 (NF2, merlin) isoforms and the Parkinson protein 7 (PARK7, DJ1)." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2012. http://dx.doi.org/10.18452/16533.

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Veränderungen in phosphorylierungsabhängigen Signalwegen, Akkumulation von Proteinaggregaten im Gehirn und neuronaler Zelltod sind Neurodegenerationskennzeichen und Indikatoren für überlappende molekulare Mechanismen. Um Einblicke in die involvierten Signalwege zu erhalten, wurde mit Hilfe eines modifizierten Hefe-Zwei-Hybrid (Y2H)-Systems für 71 Proteine, die mit neurologischen Erkrankungen assoziiert sind, proteomweit nach Protein-Protein Interaktionen (PPIs) gesucht. Für 21 dieser Proteine wurden PPIs identifiziert. Das Gesamtnetzwerk besteht aus 79 Proteinen und 90 PPIs von denen 5 phospho
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Sperka, Tobias [Verfasser]. "Ein neuer, regulierter Komplex des NF2-Tumorsuppressor-Genproduktes Merlin mit p190RhoGAP und p120RasGAP / Forschungszentrum Karlsruhe GmbH, Karlsruhe. Tobias Sperka." Karlsruhe : FZKA, 2006. http://d-nb.info/978199979/34.

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Boin, Alizée. "Le rôle de la voie Hippo dans la fonction suppresseur de tumeur associée au gène NF2 et la régulation de Yap par Merlin dans les cellules de Schwann." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112282.

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Les schwannomes sont des tumeurs bénignes se développant à partir d’une hyper-prolifération des cellules de Schwann suite à l’inactivation bi-allélique du gène NF2. Signe pathogonomique d’une pathologie rare et héréditaire, la Neurofibromatose de type 2 (NF2), ils peuvent aussi apparaître de façon sporadique. Hormis la chirurgie ou la radiothérapie, peu d’options pharmacologiques sont proposées aux patients porteurs de schwannomes, principalement à cause du peu de cibles thérapeutiques identifiées. Dans les cellules de Schwann, le phénotype cellulaire associé à la perte NF2 est une perte d’inh
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Books on the topic "NF2/Merlin"

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Cole, Banumathi Kuppusami. Membrane distribution of the NF2 tumor suppressor, Merlin. 2007.

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Morris, Zachary Scott. Regulation of EGFR by the NF2 tumor supressor, Merlin. 2009.

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Book chapters on the topic "NF2/Merlin"

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Mota, Mateus, Rajeev S. Samant, and Lalita A. Shevde. "Merlin (NF2)." In Encyclopedia of Signaling Molecules. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101780.

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Mota, Mateus, Rajeev S. Samant, and Lalita A. Shevde. "Merlin (NF2)." In Encyclopedia of Signaling Molecules. Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101780-1.

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Hanemann, C. O. "Function of Merlin in Genesis of Tumours and Other Symptoms of NF2." In Neurofibromatoses. KARGER, 2008. http://dx.doi.org/10.1159/000126615.

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Takeshima, Hideo, and Hideyuki Saya. "Detection of Binding Proteins of Merlin, the NF2 Tumor Suppressor Gene Product." In Brain Tumor. Springer Japan, 1996. http://dx.doi.org/10.1007/978-4-431-66887-9_28.

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Ren, L., and C. Khanna. "Merlin/NF2 Tumor Suppressor and Ezrin–Radixin–Moesin (ERM) Proteins in Cancer Development and Progression." In Cancer Genome and Tumor Microenvironment. Springer New York, 2009. http://dx.doi.org/10.1007/978-1-4419-0711-0_5.

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Moodley, Manikum, Mary E. Aronow, Karla Robles-Lopez, and Virginia Miraldi Utz. "Ocular Manifestations of Neuro-Oculo-Cutaneous Syndromes." In Genetic Diseases of the Eye, 3rd ed. Oxford University PressNew York, 2025. https://doi.org/10.1093/med/9780197659403.003.0050.

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Abstract In 1923, Van der Hoeve introduced the term “phakomatosis” (from the Greek phakos, meaning birthmark) to include a group of hereditary disorders characterized by hamartomas of the skin, eye, central nervous system (CNS), and other viscera. The phakomatoses later came to include other diseases, such as von Hippel-Lindau disease, Sturge-Weber syndrome, ataxia-telangiectasia (Louis-Bar syndrome), and Wyburn-Mason syndrome. Overlapping clinical features, such as pheochromocytoma in neurofibromatosis (NF) type 1 and von Hippel-Lindau disease, persuaded the medical world initially to unite t
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Conference papers on the topic "NF2/Merlin"

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Papadas, T., S. Nikou, H. Papadaki, and G. Tsinias. "Immunhistochemischer Nachweis von NF2/Merlin und LATS1 beim Larynxkarzinom." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1685895.

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Papadas, T., S. Nikou, H. Papadaki, and G. Tsinias. "Immunohistochemical expression of NF2/Merlin and LATS1 in laryngeal carcinoma." In Abstract- und Posterband – 90. Jahresversammlung der Deutschen Gesellschaft für HNO-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn – Digitalisierung in der HNO-Heilkunde. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1686041.

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Yi, Chunling, and Joseph Kissil. "Abstract 1128: The tumor suppressive function of Merlin/Nf2 is mediated by a novel tight junction-associated protein complex." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-1128.

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Cocciadiferro, Letizia, Vitale Miceli, Orazia M. Granata, and Giuseppe Carruba. "Abstract 1852: Merlin/NF2 is associated with elevated aromatase expression and estrogen formation in human liver tissues and liver cancer cells: An unifying model for hepatocellular carcinoma development and progression." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-1852.

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Reports on the topic "NF2/Merlin"

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Ramesh, Vijaya, and Anat Stemmer-Rachamimov. Role of Merlin/NF2 in mTOR Signaling and Meningioma Growth. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada566365.

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Derewenda, Zygmunt W. Structure-Function Relationships in Merlin, the Product of the NF2 Causal Gene. Defense Technical Information Center, 2004. http://dx.doi.org/10.21236/ada429527.

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Yogesha, Sollepura. Structure-Guided Insights into the Function of Merlin in Neurofibromatosis 2 (NF2). Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada608430.

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Yogesha, Sollepura. Structure-Guided Insights into the Function of Merlin in Neurofibromatosis 2 (NF2). Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada542511.

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McClatchey, Andrea I. Utilization of a NF2-Mutant Mouse Strain to Investigate the Cellular and Molecular Function of the NF2 Tumor Suppressor, Merlin. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada399194.

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McClatchey, Andrea I. Utilization of a Nf2-Mutant Mouse strain to Investigate the Cellular and Molecular Function of the NF2 Tumor Suppressor, Merlin. Defense Technical Information Center, 2002. http://dx.doi.org/10.21236/ada412822.

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McClatchey, Andrea I. Utilization of a NF2-Mutant Mouse Strain to Investigate the Cellular and Molecular Function of the NF2 Tumor Suppressor Merlin. Defense Technical Information Center, 2003. http://dx.doi.org/10.21236/ada420954.

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Tomoda, Toshifumi, and Michael E. Barish. Novel Role of Merlin Tumor Suppressor in Autophagy and its Implication in Treating NF2-Associated Tumors. Defense Technical Information Center, 2014. http://dx.doi.org/10.21236/ada608945.

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Tomoda, Toshifumi, Jr Jhung, Hirota Donald, and Yuki. Novel Role of Merlin Tumor Suppressor in Autophagy and its Implication in Treating NF2-Associated Tumors. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada563285.

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Barish, Michael E., Toshifumi Tomoda, Akiko Sumitomo, and Yuki Hirota. Novel Role of Merlin Tumor Suppressor in Autophagy and its Implication in Treating NF2-Associated Tumors. Defense Technical Information Center, 2013. http://dx.doi.org/10.21236/ada592192.

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