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Artículos de revistas sobre el tema "NF2/Merlin"

Autor: Grafiati

Publicado: 12 de octubre de 2024

Última modificación: 31 de julio de 2025

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Pachter, Jonathan A., Irina M. Shapiro, David T. Weaver, et al. "Sensitivity of malignant mesothelioma lacking Merlin to the FAK inhibitor VS-6063: Evaluation of merlin/NF2 status in clinical samples." Journal of Clinical Oncology 31, no. 15_suppl (2013): e18541-e18541. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e18541.

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e18541 Background: Malignant pleural mesothelioma (MPM) is an aggressive tumor in the pleural lining of the lung often resulting from prior exposure to asbestos. MPM patients are usually diagnosed at an advanced stage of disease and the prognosis is poor. Median survival after diagnosis is 9 to 12 months and standard-of-care agents such as cisplatin and pemetrexed have only a modest impact on median survival time for MPM patients. New therapeutic modalities are urgently needed to improve the prognosis of MPM patients. 40-50% of MPM patients exhibit homozygous disruption of the NF2 tumor suppre

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12

Pećina-Šlaus, Nives. "Merlin, the NF2 Gene Product." Pathology & Oncology Research 19, no. 3 (2013): 365–73. http://dx.doi.org/10.1007/s12253-013-9644-y.

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13

Xiao, Guang-Hui, Jonathan Chernoff, and Joseph R. Testa. "NF2: The wizardry of merlin." Genes, Chromosomes and Cancer 38, no. 4 (2003): 389–99. http://dx.doi.org/10.1002/gcc.10282.

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14

Maxwell, Marius, Sarah D. Shih, Theofanis Galanopoulos, E. Tessa Hedley-Whyte, and G. Rees Cosgrove. "Familial meningioma: analysis of expression of neurofibromatosis 2 protein Merlin." Journal of Neurosurgery 88, no. 3 (1998): 562–69. http://dx.doi.org/10.3171/jns.1998.88.3.0562.

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✓ Meningiomas are primarily benign brain tumors thought to arise through multistep tumorigenesis, involving both the activation of oncogenes and the loss of tumor suppressor genes. The recently isolated neurofibromatosis 2 (NF2) tumor suppressor gene has been found to be mutated in a large proportion of meningiomas. Almost all cases of familial meningioma occur in association with NF2. Familial meningioma in isolation from NF2 (sporadic) is exceedingly rare, with only 14 reports since 1959. The authors report the existence of a family lacking any stigmata of NF2, in which two members had spina

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15

LaJeunesse, Dennis R., Brooke M. McCartney, and Richard G. Fehon. "A Systematic Screen for Dominant Second-Site Modifiers of Merlin/NF2 Phenotypes Reveals an Interaction With blistered/DSRF and scribbler." Genetics 158, no. 2 (2001): 667–79. http://dx.doi.org/10.1093/genetics/158.2.667.

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Abstract Merlin, the Drosophila homologue of the human tumor suppressor gene Neurofibromatosis 2 (NF2), is required for the regulation of cell proliferation and differentiation. To better understand the cellular functions of the NF2 gene product, Merlin, recent work has concentrated on identifying proteins with which it interacts either physically or functionally. In this article, we describe genetic screens designed to isolate second-site modifiers of Merlin phenotypes from which we have identified five multiallelic complementation groups that modify both loss-of-function and dominant-negativ

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16

Ikeda, Keiro, Yoshinaga Saeki, Charo Gonzalez-Agosti, Vijaya Ramesh, and E. Antonio Chiocca. "Inhibition of NF2-negative and NF2-positive primary human meningioma cell proliferation by overexpression of merlin due to vector-mediated gene transfer." Journal of Neurosurgery 91, no. 1 (1999): 85–92. http://dx.doi.org/10.3171/jns.1999.91.1.0085.

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Object. The absence of in vitro models of neurofibromatosis Type 2 (NF2)—defective meningiomas has limited investigative efforts to study the biological effects of this gene in the pathogenesis of these tumors. The goals of this report are to show that gene transfer vectors can efficiently express the wild-type NF2 transgene into primary meningioma cells and to determine effects on cellular proliferation.Methods. In this study, the authors have compared the transducing capacities of a retrovirus, an adenovirus, and a herpes simplex virus amplicon vector for use in primary human meningioma cell

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17

Lee, Sungho, Patrick J. Karas, Caroline C. Hadley, et al. "The Role of Merlin/NF2 Loss in Meningioma Biology." Cancers 11, no. 11 (2019): 1633. http://dx.doi.org/10.3390/cancers11111633.

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Mutations in the neurofibromin 2 (NF2) gene were among the first genetic alterations implicated in meningioma tumorigenesis, based on analysis of neurofibromatosis type 2 (NF2) patients who not only develop vestibular schwannomas but later have a high incidence of meningiomas. The NF2 gene product, merlin, is a tumor suppressor that is thought to link the actin cytoskeleton with plasma membrane proteins and mediate contact-dependent inhibition of proliferation. However, the early recognition of the crucial role of NF2 mutations in the pathogenesis of the majority of meningiomas has not yet tra

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18

Benton, Dorothy, Hoi Yee Chow, Sofiia Karchugina, and Jonathan Chernoff. "Synergistic effect of PAK and Hippo pathway inhibitor combination in NF2-deficient Schwannoma." PLOS ONE 19, no. 7 (2024): e0305121. http://dx.doi.org/10.1371/journal.pone.0305121.

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Neurofibromatosis type 2 is a genetic disorder that results in the formation and progressive growth of schwannomas, ependymomas, and/or meningiomas. The NF2 gene encodes the Merlin protein, which links cell cortical elements to the actin cytoskeleton and regulates a number of key enzymes including Group I p21-activated kinases (PAKs), the Hippo-pathway kinase LATS, and mTORC. While PAK1 and PAK2 directly bind Merlin and transmit proliferation and survival signals when Merlin is mutated or absent, inhibition of Group 1 PAKs alone has not proven sufficient to completely stop the growth of NF2-de

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19

Curto, Marcello, Banumathi K. Cole, Dominique Lallemand, Ching-Hui Liu, and Andrea I. McClatchey. "Contact-dependent inhibition of EGFR signaling by Nf2/Merlin." Journal of Cell Biology 177, no. 5 (2007): 893–903. http://dx.doi.org/10.1083/jcb.200703010.

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The neurofibromatosis type 2 (NF2) tumor suppressor, Merlin, is a membrane/cytoskeleton-associated protein that mediates contact-dependent inhibition of proliferation. Here we show that upon cell–cell contact Merlin coordinates the processes of adherens junction stabilization and negative regulation of epidermal growth factor receptor (EGFR) signaling by restraining the EGFR into a membrane compartment from which it can neither signal nor be internalized. In confluent Nf2−/− cells, EGFR activation persists, driving continued proliferation that is halted by specific EGFR inhibitors. These studi

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20

Hennigan, Robert F., Jonathan S. Fletcher, Steven Guard, and Nancy Ratner. "Proximity biotinylation identifies a set of conformation-specific interactions between Merlin and cell junction proteins." Science Signaling 12, no. 578 (2019): eaau8749. http://dx.doi.org/10.1126/scisignal.aau8749.

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Neurofibromatosis type 2 is an inherited, neoplastic disease associated with schwannomas, meningiomas, and ependymomas and that is caused by inactivation of the tumor suppressor gene NF2. The NF2 gene product, Merlin, has no intrinsic catalytic activity; its tumor suppressor function is mediated through the proteins with which it interacts. We used proximity biotinylation followed by mass spectrometry and direct binding assays to identify proteins that associated with wild-type and various mutant forms of Merlin in immortalized Schwann cells. We defined a set of 52 proteins in close proximity

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21

Hawley, Eric, Jeffrey Gehlhausen, Sofiia Karchugina, et al. "PAK1 inhibition reduces tumor size and extends the lifespan of mice in a genetically engineered mouse model of Neurofibromatosis Type 2 (NF2)." Human Molecular Genetics 30, no. 17 (2021): 1607–17. http://dx.doi.org/10.1093/hmg/ddab106.

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Abstract Neurofibromatosis Type II (NF2) is an autosomal dominant cancer predisposition syndrome in which germline haploinsufficiency at the NF2 gene confers a greatly increased propensity for tumor development arising from tissues of neural crest derived origin. NF2 encodes the tumor suppressor, Merlin, and its biochemical function is incompletely understood. One well-established function of Merlin is as a negative regulator of group A serine/threonine p21-activated kinases (PAKs). In these studies we explore the role of PAK1 and its closely related paralog, PAK2, both pharmacologically and g

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Sughrue, Michael E., Andrea H. Yeung, Martin J. Rutkowski, Steven W. Cheung, and Andrew T. Parsa. "Molecular biology of familial and sporadic vestibular schwannomas: implications for novel therapeutics." Journal of Neurosurgery 114, no. 2 (2011): 359–66. http://dx.doi.org/10.3171/2009.10.jns091135.

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Vestibular schwannomas (VSs) are benign tumors arising from the sheath of cranial nerve VIII. The pathogenesis underlying most familial and sporadic VSs has been linked to a mutation in a single gene, the neurofibromin 2 (NF2) gene located on chromosome 22, band q11–13.1. In this review, the authors summarized what is known about the epidemiology of NF2 mutations and patients with VSs. The authors also discuss the function of the NF2 gene product, merlin, and describe the known and hypothetical effects of genetic mutations that lead to merlin dysfunction on a broad variety of cellular and hist

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23

Gronholm, M., M. Sainio, F. Zhao, L. Heiska, A. Vaheri, and O. Carpen. "Homotypic and heterotypic interaction of the neurofibromatosis 2 tumor suppressor protein merlin and the ERM protein ezrin." Journal of Cell Science 112, no. 6 (1999): 895–904. http://dx.doi.org/10.1242/jcs.112.6.895.

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Ezrin, radixin and moesin (ERM) are homologous proteins, which are linkers between plasma membrane components and the actin-containing cytoskeleton. The ERM protein family members associate with each other in a homotypic and heterotypic manner. The neurofibromatosis 2 (NF2) tumor suppressor protein merlin (schwannomin) is structurally related to ERM members. Merlin is involved in tumorigenesis of NF2-associated and sporadic schwannomas and meningiomas, but the tumor suppressor mechanism is poorly understood. We have studied the ability of merlin to self-associate and bind ezrin. Ezrin was coim

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24

Eaton, Charlotte, S. John Liu, Calixto-Hope Lucas, et al. "CSIG-37. MERLIN S13 DEPHOSPHORYLATION DRIVES MENINGIOMA WNT SIGNALLING AND CELL PROLIFERATION." Neuro-Oncology 24, Supplement_7 (2022): vii47. http://dx.doi.org/10.1093/neuonc/noac209.186.

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Abstract How Merlin-intact meningiomas arise in the absence of NF2/Merlin inactivation is incompletely understood. Here, we integrate single-cell RNA sequencing of 86,000 cells from meningioma xenografts with APEX2 proteomic proximity-labelling mass spectrometry and functional biochemical approaches to discover Merlin Serine 13 (S13) dephosphorylation drives meningioma Wnt signalling and cell proliferation. Cell biology, molecular biology, and biochemical techniques were used to validate Merlin functions in meningioma cells or xenografts using wildtype Merlin constructs or Merlin constructs en

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25

Yekeduz, Emre, Marc Machaalani, Stephanie E. Siegmund, et al. "Association of clinical characterization of renal cell carcinoma (RCC) with merlin protein deficiency and biallelic loss of NF2 ." Journal of Clinical Oncology 43, no. 5_suppl (2025): 506. https://doi.org/10.1200/jco.2025.43.5_suppl.506.

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506 Background: Neurofibromin-2 (NF2) is a tumor suppressor gene that encodes the scaffolding protein merlin and is commonly mutated in rare RCC subtypes: unclassified (uRCC), papillary (pRCC), collecting duct carcinoma (CDCA), and the emerging entity, biphasic hyalinizing psammomatous (BHP-RCC). Merlin loss/deficiency by immunohistochemistry (IHC) was recently demonstrated as a reliable surrogate marker of NF2 genomic alterations (GAs). We report the first clinical outcomes of RCC patients (pts) with merlin-deficiency/biallelic loss of NF2, treated with immune checkpoint inhibitor (ICI) and v

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Gonzalez, Maria Alejandra, Joseph Kissil, and Scott Troutman. "Abstract LB326: Combined inhibition of BRD4 and FAK1 as a novel therapeutic strategy for neurofibromatosis type 2 related schwannomas." Cancer Research 83, no. 8_Supplement (2023): LB326. http://dx.doi.org/10.1158/1538-7445.am2023-lb326.

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Abstract Neurofibromatosis type 2 (NF2) is a rare disorder that is inherited in an autosomal-dominant manner and is attributed to the loss of heterozygosity (LOH) of the NF2 gene, which encodes for the tumor suppressor protein Merlin. Patients affected by the disease develop vestibular schwannomas (VS), meningiomas, and ependymomas resulting in high morbidity and premature mortality. To date, neurofibromatosis type 2 has no FDA-approved drug-based treatment. Merlin plays a central role in mediating cell contact inhibition (CI) of proliferation. Loss of Merlin leads to abnormal activation of mu

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Short, Ben. "Merlin casts its spell on the cortical cytoskeleton." Journal of Cell Biology 211, no. 2 (2015): 207. http://dx.doi.org/10.1083/jcb.2112if.

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Gerardo-Ramírez, Monserrat, Vanessa Giam, Diana Becker, et al. "Deletion of Cd44 Inhibits Metastasis Formation of Liver Cancer in Nf2-Mutant Mice." Cells 12, no. 9 (2023): 1257. http://dx.doi.org/10.3390/cells12091257.

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Primary liver cancer is the third leading cause of cancer-related death worldwide. An increasing body of evidence suggests that the Hippo tumor suppressor pathway plays a critical role in restricting cell proliferation and determining cell fate during physiological and pathological processes in the liver. Merlin (Moesin-Ezrin-Radixin-like protein) encoded by the NF2 (neurofibromatosis type 2) gene is an upstream regulator of the Hippo signaling pathway. Targeting of Merlin to the plasma membrane seems to be crucial for its major tumor-suppressive functions; this is facilitated by interactions

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Карандашева, К. О., Е. С. Макашова, А. А. Мартьянова, К. И. Аношкин, С. В. Золотова, and В. В. Стрельников. "Clinical and molecular genetic features of neurofibromatosis type." Nauchno-prakticheskii zhurnal «Medicinskaia genetika, no. 10 (October 29, 2021): 3–12. http://dx.doi.org/10.25557/2073-7998.2021.10.3-12.

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Нейрофиброматоз 2 типа - редкое генетическое заболевание, этиологическим фактором развития которого являются мутации в гене-онкосупрессоре NF2, кодирующем белок мерлин. В обзоре подробно описаны структура, функции и посттрансляционные модификации мерлина, освещены клинические особенности нейрофиброматоза 2 типа, известные клинико-генетические корреляции, а также представлена информация о сайтах связывания мерлина и о функциональном вкладе расположенных в них мутаций, что закладывает базис персонализированной терапии нейрофиброматоза 2 типа. Neurofibromatosis type 2 is a rare genetic disorder c

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Moesslacher, Christina S., Elisabeth Auernig, Jonathan Woodsmith, et al. "Missense variant interaction scanning reveals a critical role of the FERM domain for tumor suppressor protein NF2 conformation and function." Life Science Alliance 6, no. 8 (2023): e202302043. http://dx.doi.org/10.26508/lsa.202302043.

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NF2 (moesin–ezrin–radixin-like [MERLIN] tumor suppressor) is frequently inactivated in cancer, where its NF2 tumor suppressor functionality is tightly coupled to protein conformation. How NF2 conformation is regulated and how NF2 conformation influences tumor suppressor activity is a largely open question. Here, we systematically characterized three NF2 conformation-dependent protein interactions utilizing deep mutational scanning interaction perturbation analyses. We identified two regions in NF2 with clustered mutations which affected conformation-dependent protein interactions. NF2 variants

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Srotyr, Marie, Liyam Laraba, Glenn M. Harper, et al. "Use of a new mouse schwannoma tumour model to monitor changes in peripheral nerve morphology in Merlin null Schwann cells." Neuro-Oncology 23, Supplement_4 (2021): iv7—iv8. http://dx.doi.org/10.1093/neuonc/noab195.014.

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Abstract Aims Our lab is interested in signals that trigger schwannoma tumour formation and we have previously shown that peripheral nerve injury triggers tumour formation in nerves with Schwann cell-specific loss of the Merlin (NF2) tumour suppressor. The Ras/Raf/MAPK/ERK pathway activity in myelinating Schwann cells is involved in nerve regeneration, causing demyelination and recruitment of inflammatory cells in areas of nerve damage, as well as dedifferentiation of myelinating Schwann cells into a repair-competent state. We have used a mouse model expressing a tamoxifen-inducible Raf-Kinase

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Roehrig, Anne E., Kristina Klupsch, Juan A. Oses-Prieto, et al. "Cell-cell adhesion regulates Merlin/NF2 interaction with the PAF complex." PLOS ONE 16, no. 8 (2021): e0254697. http://dx.doi.org/10.1371/journal.pone.0254697.

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The PAF complex (PAFC) coordinates transcription elongation and mRNA processing and its CDC73/parafibromin subunit functions as a tumour suppressor. The NF2/Merlin tumour suppressor functions both at the cell cortex and nucleus and is a key mediator of contact inhibition but the molecular mechanisms remain unclear. In this study we have used affinity proteomics to identify novel Merlin interacting proteins and show that Merlin forms a complex with multiple proteins involved in RNA processing including the PAFC and the CHD1 chromatin remodeller. Tumour-derived inactivating mutations in both Mer

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Woodhouse, Evyn, Liyam Laraba, Charlotte Lespade, Marie Srotyr, Alison C. Lloyd, and David B. Parkinson. "Activation of MAPK/ERK signalling in Merlin-null Schwann cells leads to increased and sustained immune cell infiltration in the peripheral nervous system." Neuro-Oncology 23, Supplement_4 (2021): iv8. http://dx.doi.org/10.1093/neuonc/noab195.017.

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Abstract Aims Previous work has shown that increased numbers of macrophages are associated with more rapid schwannoma tumour growth and we are interested in signals that control entry of macrophages and other immune cells into these tumours. Activation of the Raf-kinase domain and the Raf/MEK/ERK pathway within Schwann cells has been observed to induce an inflammatory response in peripheral nerves in the absence of injury. Activation of an inducible Raf-kinase transgene in Schwann cells allows modelling of acute demyelination of peripheral nerves without nerve injury. This Raf-oestrogen recept

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Hennigan, Robert F., Lauren A. Foster, Mary F. Chaiken, et al. "Fluorescence Resonance Energy Transfer Analysis of Merlin Conformational Changes." Molecular and Cellular Biology 30, no. 1 (2009): 54–67. http://dx.doi.org/10.1128/mcb.00248-09.

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ABSTRACT Neurofibromatosis type 2 is an inherited autosomal disorder caused by biallelic inactivation of the NF2 tumor suppressor gene. The NF2 gene encodes a 70-kDa protein, merlin, which is a member of the ezrin-radixin-moesin (ERM) family. ERM proteins are believed to be regulated by a transition between a closed conformation, formed by binding of their N-terminal FERM domain and C-terminal tail domain (CTD), and an open conformation, in which the two domains do not interact. Previous work suggests that the tumor suppressor function of merlin is similarly regulated and that only the closed

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Chiang, Ming-Fu, Shur-Tzu Chen, Chen-Peng Lo, Chun-I. Sze, Nan-Shan Chang, and Yu-Jen Chen. "Expression of WW Domain-Containing Oxidoreductase WOX1 in Human Nervous System Tumors." Analytical Cellular Pathology 36, no. 5-6 (2013): 133–47. http://dx.doi.org/10.1155/2013/945156.

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Background and ObjectiveS: We aimed to evaluate the expression levels of the tumor suppressor WOX1 in nervous system tumors and its co-expression with p53 and neurofibromatosis type 2/merlin (NF2) tumor suppressor gene products.Methods: Immunohistochemistry, western blotting andin situhybridization were used for WOX1 protein and WWOX mRNA expression. Immunofluorescence and electron microscopical immunohistochemistry were performed for colocalization of gene products.Results: WOX1 expression is low in normal cortical neurons, mainly on the axon fibers, whereas there is moderate to high immunore

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Guerrero, P. A., W. Yin, L. Camacho, and D. Marchetti. "Oncogenic role of Merlin/NF2 in glioblastoma." Oncogene 34, no. 20 (2014): 2621–30. http://dx.doi.org/10.1038/onc.2014.185.

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McCartney, B. M., and R. G. Fehon. "Distinct cellular and subcellular patterns of expression imply distinct functions for the Drosophila homologues of moesin and the neurofibromatosis 2 tumor suppressor, merlin." Journal of Cell Biology 133, no. 4 (1996): 843–52. http://dx.doi.org/10.1083/jcb.133.4.843.

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Interest in members of the protein 4.1 super-family, which includes the ezrin-radixin-moesin (ERM) group, has been stimulated recently by the discovery that the human neurofibromatosis 2 (NF2) tumor suppressor gene encodes an ERM-like protein, merlin. Although many proteins in this family are thought to act by linking the actin-based cytoskeleton to transmembrane proteins, the cellular functions of merlin have not been defined. To investigate the cellular and developmental functions of these proteins, we have identified and characterized Drosophila homologues of moesin (Dmoesin) and of the NF2

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López-Lago, Miguel A., Tomoyo Okada, Miguel M. Murillo, Nick Socci, and Filippo G. Giancotti. "Loss of the Tumor Suppressor Gene NF2, Encoding Merlin, Constitutively Activates Integrin-Dependent mTORC1 Signaling." Molecular and Cellular Biology 29, no. 15 (2009): 4235–49. http://dx.doi.org/10.1128/mcb.01578-08.

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ABSTRACT Integrin signaling promotes, through p21-activated kinase, phosphorylation and inactivation of the tumor suppressor merlin, thus removing a block to mitogenesis in normal cells. However, the biochemical function of merlin and the effector pathways critical for the pathogenesis of malignant mesothelioma and other NF2-related malignancies are not known. We report that integrin-specific signaling promotes activation of mTORC1 and cap-dependent mRNA translation. Depletion of merlin rescues mTORC1 signaling in cells deprived of anchorage to a permissive extracellular matrix, suggesting tha

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Chiasson-MacKenzie, Christine, Zachary S. Morris, Quentin Baca, et al. "NF2/Merlin mediates contact-dependent inhibition of EGFR mobility and internalization via cortical actomyosin." Journal of Cell Biology 211, no. 2 (2015): 391–405. http://dx.doi.org/10.1083/jcb.201503081.

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The proliferation of normal cells is inhibited at confluence, but the molecular basis of this phenomenon, known as contact-dependent inhibition of proliferation, is unclear. We previously identified the neurofibromatosis type 2 (NF2) tumor suppressor Merlin as a critical mediator of contact-dependent inhibition of proliferation and specifically found that Merlin inhibits the internalization of, and signaling from, the epidermal growth factor receptor (EGFR) in response to cell contact. Merlin is closely related to the membrane–cytoskeleton linking proteins Ezrin, Radixin, and Moesin, and local

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Petrilli, A. M., and C. Fernández-Valle. "Role of Merlin/NF2 inactivation in tumor biology." Oncogene 35, no. 5 (2015): 537–48. http://dx.doi.org/10.1038/onc.2015.125.

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Smole, Zlatko, Claudio R. Thoma, Kathryn T. Applegate, et al. "Tumor Suppressor NF2/Merlin Is a Microtubule Stabilizer." Cancer Research 74, no. 1 (2013): 353–62. http://dx.doi.org/10.1158/0008-5472.can-13-1334.

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Thurneysen, Claudio, Isabelle Opitz, Stefanie Kurtz, Walter Weder, Rolf A. Stahel, and Emanuela Felley-Bosco. "Functional inactivation of NF2/merlin in human mesothelioma." Lung Cancer 64, no. 2 (2009): 140–47. http://dx.doi.org/10.1016/j.lungcan.2008.08.014.

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Martin, Spencer D., Simon Cheung, and Andrew Churg. "Immunohistochemical Demonstration of Merlin/NF2 Loss in Mesothelioma." Modern Pathology 36, no. 1 (2023): 100036. http://dx.doi.org/10.1016/j.modpat.2022.100036.

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Cole, Banumathi K., Marcello Curto, Annie W. Chan, and Andrea I. McClatchey. "Localization to the Cortical Cytoskeleton Is Necessary for Nf2/Merlin-Dependent Epidermal Growth Factor Receptor Silencing." Molecular and Cellular Biology 28, no. 4 (2007): 1274–84. http://dx.doi.org/10.1128/mcb.01139-07.

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ABSTRACT Merlin, the product of the NF2 tumor suppressor gene, is closely related to the ERM (ezrin, radixin, moesin) proteins, which provide anchorage between membrane proteins and the underlying cortical cytoskeleton; all four proteins are members of the band 4.1 superfamily. Despite their similarity, the subcellular distributions and functional properties of merlin and the ERM proteins are largely distinct. Upon cell-cell contact merlin prevents internalization of and signaling from the epidermal growth factor receptor (EGFR) by sequestering it into an insoluble membrane compartment. Here w

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Sainio, M., F. Zhao, L. Heiska, et al. "Neurofibromatosis 2 tumor suppressor protein colocalizes with ezrin and CD44 and associates with actin-containing cytoskeleton." Journal of Cell Science 110, no. 18 (1997): 2249–60. http://dx.doi.org/10.1242/jcs.110.18.2249.

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Neurofibromatosis 2 (NF2) protein (merlin; schwannomin) is a tumor suppressor involved in tumorigenesis of NF2-associated and sporadic schwannomas and meningiomas. The protein shares the domain structure of three homologous proteins: ezrin, radixin and moesin (ERM). ERM proteins function as membrane organizers and may act as linkers between plasma membrane molecules, such as CD44 and ICAM-2, and the cytoskeleton. We analyzed the distribution and effects of transfected NF2 protein in COS-1, CHO and 293 cells, and endogenous NF2 protein in U251 glioma cells. The distribution was compared to ezri

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Jindal, Hitesh K., Kazumi Yoshinaga, Pil-Soo Seo, et al. "Purification of the NF2 Tumor Suppressor Protein from Human Erythrocytes." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 33, no. 4 (2006): 394–402. http://dx.doi.org/10.1017/s0317167100005357.

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Background:Neurofibromatosis type 2 (NF2) is an autosomal dominant disease predisposing individuals to the risk of developing tumors of cranial and spinal nerves. The NF2 tumor suppressor protein, known as Merlin/Schwanomin, is a member of the protein 4.1 superfamily that function as links between the cytoskeleton and the plasma membrane.Methods:Upon selective extraction of membrane-associated proteins from erythrocyte plasma membrane (ghosts) using low ionic strength solution, the bulk of NF2 protein remains associated with the spectrin-actin depleted inside-out-vesicles. Western blot analysi

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Hennigan, Robert F., Craig S. Thomson, Kye Stachowski, Nicolas Nassar, and Nancy Ratner. "Merlin tumor suppressor function is regulated by PIP2-mediated dimerization." PLOS ONE 18, no. 2 (2023): e0281876. http://dx.doi.org/10.1371/journal.pone.0281876.

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Neurofibromatosis Type 2 is an inherited disease characterized by Schwann cell tumors of cranial and peripheral nerves. The NF2 gene encodes Merlin, a member of the ERM family consisting of an N-terminal FERM domain, a central α-helical region, and a C-terminal domain. Changes in the intermolecular FERM-CTD interaction allow Merlin to transition between an open, FERM accessible conformation and a closed, FERM-inaccessible conformation, modulating Merlin activity. Merlin has been shown to dimerize, but the regulation and function Merlin dimerization is not clear. We used a nanobody based bindin

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NEILL, Graham W., та Mark R. CROMPTON. "Binding of the merlin-I product of the neurofibromatosis type 2 tumour suppressor gene to a novel site in β-fodrin is regulated by association between merlin domains". Biochemical Journal 358, № 3 (2001): 727–35. http://dx.doi.org/10.1042/bj3580727.

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The mechanism underlying the tumour-suppressor activity of the neurofibromatosis type 2 (NF2) gene product, merlin, is largely undefined but there is evidence that the biological function of the protein might be mediated partly through interactions with the cytoskeleton. Merlin is expressed predominantly as two isoforms that differ at their C-termini owing to alternative splicing of exon 16. By expressing merlin isoform I as bait in a yeast two-hybrid screen, we isolated a clone encoding a region of the cytoskeletal protein β-fodrin. Confirmation of the merlin–fodrin interaction was provided b

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Belliveau, Michael J., Mohini Lutchman, Jaime O. Claudio, Claude Marineau, and Guy A. Rouleau. "Schwannomin: new insights into this member of the band 4.1 superfamily." Biochemistry and Cell Biology 73, no. 9-10 (1995): 733–37. http://dx.doi.org/10.1139/o95-081.

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Neurofibromatosis type 2 (NF2) is an autosomal dominant disease characterized by the development of central nervous system tumours. The NF2 gene was recently cloned and found to encode a protein, schwannomin (or merlin), with homology to the band 4.1 superfamily. This superfamily of proteins includes ezrin, moesin, radixin, and talin, as well as several protein tyrosine phosphatases. How does a cytoskeleton-associated protein act as a tumour suppressor? While this fundamental question remains unanswered, recent studies have begun to address key questions regarding the function of schwannomin.

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Fong, Brendan, Garni Barkhoudarian, Patrick Pezeshkian, Andrew T. Parsa, Quinton Gopen, and Isaac Yang. "The molecular biology and novel treatments of vestibular schwannomas." Journal of Neurosurgery 115, no. 5 (2011): 906–14. http://dx.doi.org/10.3171/2011.6.jns11131.

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Vestibular schwannomas are histopathologically benign tumors arising from the Schwann cell sheath surrounding the vestibular branch of cranial nerve VIII and are related to the NF2 gene and its product merlin. Merlin acts as a tumor suppressor and as a mediator of contact inhibition. Thus, deficiencies in both NF2 genes lead to vestibular schwannoma development. Recently, there have been major advances in our knowledge of the molecular biology of vestibular schwannomas as well as the development of novel therapies for its treatment. In this article the authors comprehensively review the recent

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