Relevant bibliographies by topics / MS4A4E

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Academic literature on the topic 'MS4A4E'

Author: Grafiati
Published: 4 June 2021
Last updated: 7 February 2022

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Journal articles on the topic "MS4A4E"

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Sun, Lei, Yanli Zhang, and Chao Zhang. "Distinct expression and prognostic value of MS4A in gastric cancer." Open Medicine 13, no. 1 (May 9, 2018): 178–88. http://dx.doi.org/10.1515/med-2018-0028.

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AbstractGastric cancer has high malignancy and early metastasis, which lead to poor survival rate. In this study, we assessed the expressions and prognostic values of MS4A family, a newly recently discovered family, by two online dataset, GEPIA and Kaplan Meier-plotter. From these results eight members, MS4A2, MS4A6, MS4A7, MS4A8, MS4A14, MS4A15, TMEM176A and TMEM176B showed positive expression in gastric cancer or normal tissues, and these genes were screened for further analysis of prognostic values. We observed that low mRNA expressions of MS4A2, MS4A7, MS4A14, MS4A15, TMEM176A and TMEM176B were correlated with better overall survival (OS) in all gastric cancer patients, while high mRNA expression of MS4A6 was observed to be associated with good prognosis. MS4A8’s high mRNA level was correlated to better OS in diffuse gastric cancer patients. Further, we estimated prognostic values of MS4A family in gastric cancer patients with different clinic-pathological features, including clinical stages, differentiation level, lymph node status and HER2 status. Our results indicate that these eight MS4A members can estimate prognosis in patients with different pathological groups. In conclusion, MS4A family members are potential biomarkers, and may contribute to tumor progression in gastric cancer.
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Barber, Robert C. "The Genetics of Alzheimer’s Disease." Scientifica 2012 (2012): 1–14. http://dx.doi.org/10.6064/2012/246210.

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Alzheimer’s disease is a progressive, neurodegenerative disease that represents a growing global health crisis. Two major forms of the disease exist: early onset (familial) and late onset (sporadic). Early onset Alzheimer’s is rare, accounting for less than 5% of disease burden. It is inherited in Mendelian dominant fashion and is caused by mutations in three genes (APP,PSEN1, andPSEN2). Late onset Alzheimer’s is common among individuals over 65 years of age. Heritability of this form of the disease is high (79%), but the etiology is driven by a combination of genetic and environmental factors. A large number of genes have been implicated in the development of late onset Alzheimer’s. Examples that have been confirmed by multiple studies includeABCA7,APOE,BIN1,CD2AP,CD33,CLU,CR1,EPHA1,MS4A4A/MS4A4E/MS4A6E,PICALM, andSORL1. Despite tremendous progress over the past three decades, roughly half of the heritability for the late onset of the disease remains unidentified. Finding the remaining genetic factors that contribute to the development of late onset Alzheimer’s disease holds the potential to provide novel targets for treatment and prevention, leading to the development of effective strategies to combat this devastating disease.
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Hollingworth, Paul, Denise Harold, Rebecca Sims, Amy Gerrish, Jean-Charles Lambert, Minerva M. Carrasquillo, Richard Abraham, et al. "Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease." Nature Genetics 43, no. 5 (April 3, 2011): 429–35. http://dx.doi.org/10.1038/ng.803.

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Dubey, Harikesh, Kavita Gulati, and Arunabha Ray. "Recent studies on cellular and molecular mechanisms in Alzheimer’s disease: focus on epigenetic factors and histone deacetylase." Reviews in the Neurosciences 29, no. 3 (March 28, 2018): 241–60. http://dx.doi.org/10.1515/revneuro-2017-0049.

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AbstractAlzheimer’s disease (AD) is one of the most common neurodegenerative disorders mainly affecting elderly people. It is characterized by progressive loss of memory and cognitive function. More than 95% of AD cases are related to sporadic or late-onset AD (LOAD). The etiology of LOAD is still unclear. It has been reported that environmental factors and epigenetic alterations play a significant role in AD pathogenesis. Furthermore, recently, genome-wide association studies (GWAS) identified 10 novel risk genes:ABCA7,APOE,BIN1,CD2AP,CD33,CLU,CR1,MS4A6A,MS4A4E, andPICALM, which play an important role for LOAD. In this review, the therapeutic approaches of AD by epigenetic modifications have been discussed. Nowadays, HDAC inhibitors have clinically proven its activity for epigenetic modifications. Furthermore, we try to establish the relationship between HDAC inhibitors and above mentioned LOAD risk genes. Finally, we are hoping that this review may open new area of research for AD treatment.
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Ebbert, Mark T. W., Kevin L. Boehme, Mark E. Wadsworth, Lyndsay A. Staley, Shubhabrata Mukherjee, Paul K. Crane, Perry G. Ridge, and John S. K. Kauwe. "Interaction between variants in CLU and MS4A4E modulates Alzheimer's disease risk." Alzheimer's & Dementia 12, no. 2 (October 5, 2015): 121–29. http://dx.doi.org/10.1016/j.jalz.2015.08.163.

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Deming, Yuetiva, Fabia Filipello, Francesca Cignarella, Claudia Cantoni, Simon Hsu, Robert Mikesell, Zeran Li, et al. "The MS4A gene cluster is a key modulator of soluble TREM2 and Alzheimer’s disease risk." Science Translational Medicine 11, no. 505 (August 14, 2019): eaau2291. http://dx.doi.org/10.1126/scitranslmed.aau2291.

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Soluble triggering receptor expressed on myeloid cells 2 (sTREM2) in cerebrospinal fluid (CSF) has been associated with Alzheimer’s disease (AD). TREM2 plays a critical role in microglial activation, survival, and phagocytosis; however, the pathophysiological role of sTREM2 in AD is not well understood. Understanding the role of sTREM2 in AD may reveal new pathological mechanisms and lead to the identification of therapeutic targets. We performed a genome-wide association study (GWAS) to identify genetic modifiers of CSF sTREM2 obtained from the Alzheimer’s Disease Neuroimaging Initiative. Common variants in the membrane-spanning 4-domains subfamily A (MS4A) gene region were associated with CSF sTREM2 concentrations (rs1582763; P = 1.15 × 10−15); this was replicated in independent datasets. The variants associated with increased CSF sTREM2 concentrations were associated with reduced AD risk and delayed age at onset of disease. The single-nucleotide polymorphism rs1582763 modified expression of the MS4A4A and MS4A6A genes in multiple tissues, suggesting that one or both of these genes are important for modulating sTREM2 production. Using human macrophages as a proxy for microglia, we found that MS4A4A and TREM2 colocalized on lipid rafts at the plasma membrane, that sTREM2 increased with MS4A4A overexpression, and that silencing of MS4A4A reduced sTREM2 production. These genetic, molecular, and cellular findings suggest that MS4A4A modulates sTREM2. These findings also provide a mechanistic explanation for the original GWAS signal in the MS4A locus for AD risk and indicate that TREM2 may be involved in AD pathogenesis not only in TREM2 risk-variant carriers but also in those with sporadic disease.
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Benedet, Andrea Lessa, Aurelie Labbe, Sulantha S. Mathotaarachchi, Kok Pin Ng, Tharick A. Pascoal, Monica Shin, Min-Su Kang, Hanne Struyfs, Serge Gauthier, and Pedro Rosa-Neto. "FUNCTIONAL REGRESSION MODEL UNVEILS THAT GENE INTERACTION BETWEEN NCSTN (AMYLOID METABOLISM) AND MS4A4E (NEUROINFLAMMATION) DETERMINES AMYLOID LOAD SPECIFICALLY ON THE DMN." Alzheimer's & Dementia 13, no. 7 (July 2017): P1489. http://dx.doi.org/10.1016/j.jalz.2017.07.572.

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Pan, Xue, Ying Chen, and Song Gao. "Four genes relevant to pathological grade and prognosis in ovarian cancer." Cancer Biomarkers 29, no. 2 (October 9, 2020): 169–78. http://dx.doi.org/10.3233/cbm-191162.

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BACKGROUND: Ovarian cancer is the common tumor in female, the prognostic of which is influenced by a series of factors. In this study, 4 genes relevant to pathological grade in ovarian cancer were screened out by the construction of weighted gene co-expression network analysis. METHODS: GSE9891 with 298 ovarian cancer cases had been used to construct co-expression networks. Gene Ontology and Kyoto Encyclopedia of Genes and Genomes enrichment analyses was used to analyze the possible mechanism of genes involved in the malignant process of ovarian cancer. Hub genes were validated in other independent datasets, such as GSE63885, GSE26193 and GSE30161. Survival analysis based on the hub genes was performed by website of Kaplan Meier-plotter. RESULTS: The result based on weighted gene co-expression network analysis indicated that turquoise module has the highest association with pathological grade. Gene Ontology enrichment analysis revealed that the genes in turquoise module main enrichment in inflammatory response and immune response. Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that the genes in turquoise module main enrichment in cytokine-cytokine receptor interaction and chemokine signaling pathway. In turquoise module, a total of 4 hub genes (MS4A4A, CD163, CPR65, MS4A6A) were identified. Then, 4 hub genes were effectively verified in the test datasets (GSE63885, GSE26193 and GSE30161) and tissue samples from Shengjing Hospital of China Medical University. Survival analysis indicated that the 4 hub genes were associated with poor progression-free survival of ovarian cancer. CONCLUSIONS: In conclusion, 4 hub genes (MS4A4A, CD163, CPR65, MS4A6A) were verified associated with pathological grade of ovarian cancer. Moreover, MS4A4A, CD163, MS4A6A may serve as a surface marker for M2 macrophages. Targeting the 4 hub genes may can improve the prognosis of ovarian cancer.
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Xu, Hui, Mark S. Williams, and Lisa M. Spain. "Patterns of expression, membrane localization, and effects of ectopic expression suggest a function for MS4a4B, a CD20 homolog in Th1 T cells." Blood 107, no. 6 (March 15, 2006): 2400–2408. http://dx.doi.org/10.1182/blood-2005-08-3340.

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AbstractThe membrane-spanning 4A (MS4A) family of proteins includes CD20, FcϵRIβ, and HTm4, whose genes are grouped in a chromosomal location that is associated with increased susceptibility to allergy and atopic asthma. One family member, Chandra/MS4a4B, was reported to be expressed in T helper 1 (Th1) T cells but not Th2 T cells. In the present study, Ms4a4b was isolated in a screen of genes differentially expressed during thymocyte development. MS4a4B was detected in immature CD4-CD8-CD44+CD25- thymocytes, turned off during further stages of thymocyte development and reexpressed in mature single-positive thymocytes. MS4a4B expression was found in naive CD8+ and CD4+ peripheral T cells and natural killer (NK) cells but not in B cells. MS4a4B is expressed at the cell surface with its C-terminus located in the cytoplasm. When expressed in a T-cell hybridoma by retroviral vector, MS4a4B protein constitutively associated with lipid raft microdomains, whereas in primary T cells endogenous MS4a4B protein became enriched in rafts after T-cell activation. Overexpression of MS4a4B in primary CD4+ T-cell blasts enhanced T-cell receptor (TCR)-induced Th1 cytokine production. These results suggest that MS4a4B expression is tightly regulated during T-cell development and that MS4a4B expression promotes Th1 function and/or differentiation. (Blood. 2006;107:2400-2408)
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Cruse, Glenn, Michael A. Beaven, Stephen C. Music, Peter Bradding, Alasdair M. Gilfillan, and Dean D. Metcalfe. "The CD20 homologue MS4A4 directs trafficking of KIT toward clathrin-independent endocytosis pathways and thus regulates receptor signaling and recycling." Molecular Biology of the Cell 26, no. 9 (May 2015): 1711–27. http://dx.doi.org/10.1091/mbc.e14-07-1221.

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MS4A family members differentially regulate the cell cycle, and aberrant, or loss of, expression of MS4A family proteins has been observed in colon and lung cancer. However, the precise functions of MS4A family proteins and their mechanistic interactions remain unsolved. Here we report that MS4A4 facilitates trafficking of the receptor tyrosine kinase KIT through endocytic recycling rather than degradation pathways by a mechanism that involves recruitment of KIT to caveolin-1–enriched microdomains. Silencing of MS4A4 in human mast cells altered ligand-induced KIT endocytosis pathways and reduced receptor recycling to the cell surface, thus promoting KIT signaling in the endosomes while reducing that in the plasma membrane, as exemplified by Akt and PLCγ1 phosphorylation, respectively. The altered endocytic trafficking of KIT also resulted in an increase in SCF-induced mast cell proliferation and migration, which may reflect altered signaling in these cells. Our data reveal a novel function for MS4A family proteins in regulating trafficking and signaling, which could have implications in both proliferative and immunological diseases.
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Dissertations / Theses on the topic "MS4A4E"

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Ebbert, Mark T. "Role of Epistasis in Alzheimer's Disease Genetics." BYU ScholarsArchive, 2014. https://scholarsarchive.byu.edu/etd/4325.

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Alzheimer's disease is a complex neurodegenerative disease whose basic etiology and genetic structure remains elusive, despite decades of intensive investigation. To date, the significant genetic markers identified have no obvious functional effects, and are unlikely to play a role in Alzheimer's disease etiology, themselves. These markers are likely linked to other genetic variations, rare or common. Regardless of what causal mutations are found, research has demonstrated that no single gene determines Alzheimer's disease development and progression. It is clear that Alzheimer's disease development and progression are based on a set of interactions between genes and environmental variables. This dissertation focuses on gene-gene interactions (epistasis) and their effects on Alzheimer's disease case-control status. We genotyped the top Alzheimer's disease genetic markers as found on AlzGene.org (accessed 2014), and tested for interactions that were associated with Alzheimer's disease case- control status. We identified two potential gene-gene interactions between rs11136000 (CLU) and rs670139 (MS4A4E) (synergy factor = 3.81; p = 0.016), and rs3865444 (CD33) and rs670139 (MS4A4E) (synergy factor = 5.31; p = 0.003). Based on one data set alone, however, it is difficult to know whether the interactions are real. We replicated the CLU-MS4A4E interaction in an independent data set from the Alzheimer's Disease Genetics Consortium (synergy factor = 2.37, p = 0.007) using a meta-analysis. We also identified potential dosage (synergy factor = 2.98, p = 0.05) and APOE ε4 effects (synergy factor = 4.75, p = 0.005) in Cache County that did not replicate independently. The APOE ε4 effect is an association with Alzheimer's disease case-control status in APOE ε4 negative individuals. There is minor evidence both the dosage (synergy factor = 1.73, p = 0.02) and APOE ε4 (synergy factor = 2.08, p = 0.004) effects are real, however, because they replicate when including the Cache County data in the meta-analysis. These results demonstrate the importance of understanding the role of epistasis in Alzheimer's disease. During this research, we also developed a novel tool known as the Variant Tool Chest. The Variant Tool Chest has played an integral part in this research and other projects, and was developed to fill numerous gaps in next-generation sequence data analysis. Critical features include advanced, genotype-aware set operations on single- or multi-sample variant call format (VCF) files. These features are critical for genetics studies using next-generation sequencing data, and were used to perform important analyses in the third study of this dissertation.By understanding the role of epistasis in Alzheimer's disease, researchers will begin to untangle the complex nature of Alzheimer's disease etiology. With this information, therapies and diagnostics will be possible, alleviating millions of patients, their families and caregivers of the painful experience Alzheimer's disease inflicts upon them.
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ALMEIDA, J. F. F. "META-ANÁLISE e Estudo de Associação na Busca de Biomarcadores de Diagnóstico nos Genes Cd2ap e Ms4a4e para a Doença de Alzheimer." Universidade Federal do Espírito Santo, 2018. http://repositorio.ufes.br/handle/10/7115.

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Made available in DSpace on 2018-08-01T21:35:03Z (GMT). No. of bitstreams: 1 tese_12055_Dissertação_Jucimara Ferreira Figueiredo Almeida.pdf: 1594368 bytes, checksum: 88adee5e1c347b9d3fe95a63c1e32395 (MD5) Previous issue date: 2018-02-26
A doença de Alzheimer (DA) é um dos tipos mais comuns de demência. Possui alterações patológicas como placas amilóides e emaranhados de neurofibrilas. A forma esporádica (DAE) representa 98% dos casos da doença de Alzheimer e apresenta etiologia multifatorial. A variante rs670139 do gene MS4A4E e rs9349407 do gene CD2AP foram consideradas, em estudos de Genome wide association studies, como associadas ao risco na DAE. O diagnóstico clínico da DA é difícil e apenas possível quando a doença já está em estágios avançados, sendo assim, estudos buscam encontrar biomarcadores para auxiliar no diagnóstico da doença em estágios precoces. Com isso, nos últimos anos, foram publicados vários estudos caso-controle investigando a associação de rs670139 do gene MS4A4E e rs9349407 do gene CD2AP com DAE em outras populações. Assim, este trabalho teve como objetivo investigar a associação entre o polimorfismo rs670139 MS4A4E e rs9349407 CD2AP com DAE em uma amostra de indivíduos da população da Grande Vitória, ES e realizar um estudo de meta-análise atualizado sobre a associação destas variantes com a doença. O estudo de associação foi realizado com uma amostra composta por 221 indivíduos não consanguíneos, sendo 139 indivíduos saudáveis e 82 pacientes com diagnóstico provável de DAE, pareados em relação à idade e gênero. As amostras foram genotipadas por Polymerase Chain Reaction Restriction Fragment Length Polymorphism. O Equilíbrio de Hardy-Weinberg foi calculado para cada grupo estudado. Os resultados de genotipagem foram validados por sequenciamento em 5% das amostras. Os dados foram analisados pelos testes estatísticos de Qui-quadrado, Odds ratio (Intervalo de confiança de 95%), Mann-Whitney e Regressão logística no programa SPSS (valores de p ≤ 0,05 foram considerados significativos). Na meta-análise a comparação alélica seguindo o modelo genético aditivo foi realizada pelo programa R. Os resultados obtidos neste estudo sugerem que o alelo A de rs670139 MS4A4E está associado ao risco na DAE. Este resultado apoia o papel de risco do rs670139, uma vez que, o polimorfismo, em estudos funcionais, foi correlacionado com o aumento das placas neuríticas. No entanto, não houve associação do polimorfismo rs670139 MS4A4E e rs9349407 CD2AP com DAE na população da Grande Vitória, ES e a meta-análise não encontrou associação para o rs9349407 CD2AP. Os resultados deste trabalho são importantes para ajudar a validar o papel das variantes genéticas sobre o risco de DAE.
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Parker, Wendy. "Distribution and functions of the novel membrane-spanning four-domains, subfamily a member HCA112." 2009. http://hdl.handle.net/2440/59981.

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Members of the membrane-spanning four-domains, subfamily A (MS4A) family are small polypeptides that share the structural features of four-transmembrane domains and unevenly sized extracellular loops. The family includes CD20, FcεRIβ and HtM4, plus a number of relatively uncharacterised proteins / predicted proteins. MS4A proteins are discussed in relation to other protein families, such as the tetraspanins, that are also characterised by four-transmembrane domains. The aim of this study was to identify the cell and tissue distribution, subcellular localisation, and function of a newly discovered member of the MS4A family, hepatocellular carcinoma-associated antigen 112 (HCA112). At a subcellular level, HCA112 was found on the plasma membrane of transfected COS-7 cells, and also within the Golgi complex, trans-Golgi-network, and early endosomes. The molecule is orientated such that the large loop is extracellular and the Nand C-terminal domains are cytoplasmic. The presence of HCA112 associated with components of the endocytic pathway raised the question of whether some originated from the surface membrane. Antibody was used to label a HA epitope tag engineered into the large extracellular loop of HCA112, and the bound antibody was tracked through early endosomes to the recycling compartment. Here it co-localised with internalised transferrin, indicating strongly that HCA112 is internalised via clathrin-dependent mechanisms. Several endocytic sorting motifs within the intracellular domains of HCA112 were investigated for their ability to direct internalisation of HCA112. Deletion of a di-leucine motif was found to slow but not prevent endocytosis, suggesting that it is involved in endocytosis of HCA112, although not essential for the process. When HCA112 expression constructs featuring N- and C-terminal domain truncations were examined, it was found that the N-terminal tail does not affect the subcellular localisation or trafficking of HCA112, while deletion of the C-terminal intracellular domain resulted in retention of the mutant protein in the ER. HCA112 has a wide tissue distribution and is highly expressed in the lining/covering and parenchymal epithelium of some tissues, proximal renal tubules, ductal epithelium in a number of organs, endothelial cells, some steroidogenic endocrine cells, adipocytes, smooth muscle cells, follicular dendritic cells and macrophages. The expression of HCA112 by a wide range of cell types suggests that its function(s) has general importance and is not limited to any specific cell type(s). After reflection on the functions of the HCA112-expressing cells, a common theme that emerged was one of endocytic activity. This lead to speculate that one function of HCA112 might be related to uptake of macromolecules, for instance, in antigen processing and presentation. This might be a general function, such as facilitating uptake of other cell membrane proteins, or directing the traffic of endocytic vesicles. It was noted that HCA112 has a similar cell and tissue distribution to the scavenger receptor and fatty acid translocase FAT/CD36 (Zhang et al., 2003). Furthermore, in cells co-transfected with HCA112 and FAT/CD36, the two molecules co-localise in early endosomes and co-immunoprecipitate, suggesting that the molecules physically and spatially associate. Thus, HCA112 could be involved with (or complement) FAT/CD36 in its functions as a long chain fatty acid transporter and scavenger receptor. A proteomics study of proteins that co-immunoprecipitated with HCA112 detected putative interactions with a number of proteins. These included LR8, transferrin receptor, interferon induced transmembrane proteins 2 and 3, Calpain-6, stomatin, PDGF α receptor, and heat shock 70 kDa protein 8 (HSPA8, formerly known as clathrin un-coating ATPase). Of these, LR8 and the transferrin receptor were investigated in more detail. The results provide strong evidence that HCA112 forms a novel complex with LR8, and that this may be involved in macromolecule internalisation or trafficking of membrane proteins, such as FAT/CD36 or the transferrin receptor. In the case of the transferrin receptor, this traffic appears to involve the clathrin-dependent pathway, but it is possible that when HCA112 is associated with FAT/CD36, it functions within lipid raft domains.
http://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1375454
Thesis (Ph.D.) -- University of Adelaide, School of Molecular and Biomedical Science, 2009
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Books on the topic "MS4A4E"

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Association for Information & Image Mana and Association for Information and Image Management (U.S.). Recommended Practice for Quality Control of Image Scanners: ANSI Aiim Ms44 1988. Association for Information & Image Managemen, 1989.

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Book chapters on the topic "MS4A4E"

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Brown, Kristelle, James Turton, and Kevin Morgan. "Membrane-Spanning 4-Domains Subfamily A, MS4A Cluster." In Genetic Variants in Alzheimer's Disease, 159–79. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7309-1_8.

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Conference papers on the topic "MS4A4E"

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Kuek, Li Eon, Mark Hulett, Donna Davies, and Graham Mackay. "Expression and function of a novel membrane-spanning protein, MS4A8B, in the human airways." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa919.

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Ly, Dalam, Chang-Qi Zhu, Michael Cabanero, Ming-Sound Tsao, and Li Zhang. "Abstract A64: Mast cell expressed FcϵR beta subunit (MS4A2) is prognostic in lung adenocarcinoma." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 20-23, 2016; Boston, MA. American Association for Cancer Research, 2017. http://dx.doi.org/10.1158/2326-6074.tumimm16-a64.

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Zerrouqi, Abdessamad, Beata Pyrzynska, Michal Dwojak, Nina Miazek, Piotr Zapala, Jakub Golab, and Magdalena Winiarska. "Abstract B27: B-cell lymphoma response to anti-CD20 antibodies based therapies is tightly modulated by FOXO1-mediated MS4A1 gene transcription." In Abstracts: AACR Special Conference on Tumor Immunology and Immunotherapy; October 1-4, 2017; Boston, MA. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/2326-6074.tumimm17-b27.

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