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Journal articles on the topic 'MS4A4E'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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1

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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2

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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3

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Naj, Adam C., Gyungah Jun, Gary W. Beecham, Li-San Wang, Badri Narayan Vardarajan, Jacqueline Buros, Paul J. Gallins, et al. "Common variants at MS4A4/MS4A6E, CD2AP, CD33 and EPHA1 are associated with late-onset Alzheimer's disease." Nature Genetics 43, no. 5 (April 3, 2011): 436–41. http://dx.doi.org/10.1038/ng.801.

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12

Xu, Yan, Miao Liu, Yi-hua Gu, Xiao-feng Jia, Yong-Mei Chen, Michelle Santos, Ai-Zhen Wu, Xiao-dong Zhang, Hui-Juan Shi, and Ching-Ling C. Chen. "cDNA cloning and localization of Sp3111 (also called Ms4a14) in the rat testis." REPRODUCTION 148, no. 1 (July 2014): 81–86. http://dx.doi.org/10.1530/rep-14-0087.

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With tetraspanning topology, members of the membrane-spanning four-domain subfamily A (MS4A) may facilitate signaling or ion channel functions in many tissues. In this study, we report the cloning of a full-length cDNA from rat testis, designatedMs4a14(Sp3111), which encodes the MS4A protein with 1139 amino acid residues.In situhybridization and immunohistochemical analyses indicate thatMs4a14is predominantly expressed from round spermatids to spermatozoa at specific stages in the rat testis at both the mRNA and protein level. Immunofluorescence analysis revealed that MS4A14 (SP3111) is located in the acrosome and the midpiece of the flagellum in mature sperm. Previously, we explored and reported the involvement of MS4A14 in reproductive functions, using antibody blockage during IVF and a transgenic RNA interference method in a mouse model. Our results suggested that MS4A14 is involved in fertilization and zygote division. As MS4A14 protein exists in mammals, such as humans, cows, dogs, and rodents, MS4A14 may play a ubiquitous role in mammalian reproduction.

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Kaneko, Takane, Kiyotaka Toshimori, and Hiroshi Iida. "Subcellular localization of MS4A13 isoform 2 in mouse spermatozoa." Reproduction 154, no. 6 (December 2017): 843–57. http://dx.doi.org/10.1530/rep-17-0477.

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To identify upregulated genes during the development of spermatozoa, we performed PCR-selected subtraction analysis of testes RNA samples from 10-day-old and 12-week-old shrews. A transcript, highly homologous to two mouse transcripts, Ms4a13-1 and Ms4a13-2, was differentially regulated. Ms4a13-2, but not Ms4a13-1, was shown to be primarily expressed in mouse testes in an age-dependent manner. Ms4a13-2 cDNA contains an open-reading frame of 522 nucleotides, encoding a protein of 174 amino acids, with predicted molecular mass, 19,345 Da. MS4A13-2 protein was expressed along the periphery of nuclei of round and elongated spermatids (steps 3–16) in adult mouse testes, and in the equatorial region of the heads of fresh mature mouse spermatozoa. In addition, MS4A13-2 was found to localize to the outer acrosomal membrane in the equatorial region of heads in fresh spermatozoa. In acrosome-reacted spermatozoa, the MS4A13-2 expression extended to the entire sperm head including the postacrosomal region and acrosomal cap. MS4A family proteins are known to facilitate intracellular protein–protein interactions as ion channel/adaptor proteins by oligomerization, and have important regulatory roles in cellular growth, survival and activation. We report that the MS4A family member, MS4A13-2, may form oligomers in sperm membranes, which may be involved in an interaction with the zona pellucida or cumulus during fertilization.

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14

Kofler, Julia, Stephanie Bissel, Clayton Wiley, Mark Stauffer, and Geoffrey Murdoch. "O2-09-04: Differential microglial expression of new Alzheimer's disease associated genes MS4A4A and MS4A6A." Alzheimer's & Dementia 8, no. 4S_Part_7 (July 2012): P253. http://dx.doi.org/10.1016/j.jalz.2012.05.675.

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15

Wang, Luqun, Qiong Liu, Hao Li, Li Lizhen, and Xin Wang. "The Establishment of Bortezomib Resistant Myeloma Cell Line KM3/BTZ and Explore the Resistance Mechanism." Blood 124, no. 21 (December 6, 2014): 5226. http://dx.doi.org/10.1182/blood.v124.21.5226.5226.

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Abstract Background: Multiple myeloma (MM) is an incurable B-cell malignancy resulting in significant morbidity and mortality, the incidence of second place in hematological malignancies. The proteasome inhibitor bortezomib inhibits IkappaB degradation, prevents NF-kappaB activation, and induces apoptosis in MM cells, has become first-line drug to MM. Despite its promising activity in traditional chemoresistant myeloma patients, however, some patients are resistant or become refractory to bortezomib. Chauhan D et al reported that Blockade of Hsp27 overcomes bortezomib resistance in lymphoma cells (Chauhan D et al., Cancer Re, 2003). However, bortezomib resistance mechanisms in MM remain controversial, the molecular basis of this reduced responsiveness is currently not fully understood. Objective: To establish a bortezomib-resistant cell line KM3 /BTZ of MM, then search for genes related to bortezomib resistance phenotype by analyzing the differential gene expression patterns with cDNA microarray,and explain the mechanism of bortezomib-resistant multiple myeloma. Methods: Bortezomib-resistant KM3/BTZ cell line was generated by increasing concentration of bortezomib to induce KM3 cells in vitro. MTT assay was employed to detect the cytotoxic effect on KM3 and KM3/BTZ cells. The cells apoptosis were analyzed by flow cytometry. We detect the gene expression profile changes between KM3/BTZ and its parent cell line KM3 cells by CDNA microarray. Combining of molecular annotation system MAS3.0 software and detailed analysis of documented resistance genes were used to analyze the data. Specific differentially-expressed genes were chosen for further verification using real-time RT-PCR. The expression of multi-drug resistance 1(MDR-1) gene mRNA was determined by RT-PCR. Results: The KM3/BTZ cell line was established successfully. Bortezomib resistance index values were significantly higher in KM3/BTZ (IC50 =351.2±3.51ng /ml) when compared to KM3 cells (IC50 = 17.8±1.03ng /ml),and the resistance index is 19.7 (P< 0.05). Through gene expression profiling filtering, compared with KM3,770 significantly differently expressed genes were screened out in the KM3/BTZ cell line, of which up and down regulated genes were 287 and 383 respectively, in which heat shock protein family gene HSPB2 was significantly up-regulated (Ratio=14.7455). Downregulated gene list in KM3/BTZ cell line included transcriptional regulators like ZNF family proteins (Tab 1). Upregulated genes in KM3/BTZ cell line included signal transduction related genes like MS4A family protein (Tab 1) also transcriptional regulators like ZNF family proteins (Tab 1). The expression trend of eight genes for further verification was almost consistent with the microarray, excepting gene of JUN (Fig 1). The expression of MDR-1 mRNA was not observed in either resistant or parental cells (Fig 2). Conclusion: We have successfully established bortezomib-resistant cell line KM3/BTZ. MDR-1 was not involved in bortezomib-resistant multiple myeloma cells.HSPB2, ZNF and MS4A family genes are probably related to bortezomib resistance in KM3/BTZ cells. Our results suggest that they may be new targets to overcome resistance to bortezomib in patients with MM. Table 1. ZNF and MS4A family gene expression in KM3/BTZ and KM3 cells Gene B signal* B detection* A signal* A detection* BvsA signal log ratio* BvsA change* ZNF711 85.08 P 206.16 P 0.41269 D ZNF92 6.75 P 14.57 P 0.46328 D ZNF704 10.7 A 26.78 P 0.39955 D ZNF492 7.08 P 3.48 P 2.03448 I ZNF532 87.93 P 43.54 A 2.01952 I ZNF594 10.25 P 4.63 P 2.21382 I ZNF789 269.79 P 97.3 P 2.77276 I ZNF506 330.36 P 149.48 P 2.21006 I MS4A3 1721.58 P 145.3 P 11.84845 I MS4A4A 2688.23 P 100.8 P 26.66895 I MS4A6A 141.96 P 56.47 M 2.513901 I MS4A1 49.02 P 53.11 P 0.92299 NC P: High expression; A: Low expression; M:Marginally D: Decrease; I: Increase; NC: No change *: A:KM3; B: KM3/BTZ Figure 1 Figure 1. Correlations of gene expression changes between oligonueleotide Microarray and qRT-PCR, showing change of selected gene in KM3/BTZ compared with KM3.The Y-axis indicates the log2 transformed ratio of mRNA expression. Figure 2 Figure 2. The expression level of MDR-1 mRNA in KM3 and KM3/BTZ and K562/A cell lines. M: DNA Marker; 1-2: K562/A cell line; 3-4: KM3cell line; 5-6: KM3/BTZ cell line Disclosures No relevant conflicts of interest to declare.

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Ishibashi, Tomohiko, Takafumi Yokota, Yusuke Satoh, Takao Sudo, Yukiko Doi, Natsuko Fujita, Yasuhiro Nagate, et al. "MS4A3 Marks Early Myeloid Differentiation in Human Hematopoiesis." Blood 124, no. 21 (December 6, 2014): 4319. http://dx.doi.org/10.1182/blood.v124.21.4319.4319.

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Abstract Understanding lineage specific markers contributes to investigation into lineage commitment processes in hematopoiesis. Particularly in the human study, information about hematopoietic lineage divergence is essential to refine hematopoietic lineage tree. Lineage markers are also potentially useful for therapeutic target, such as CD20 in B-cell lymphoma, and CD33 in acute myeloid leukemia. We have recently reported that special AT-rich sequence-binding protein 1 (SATB1), a global chromatin organizer, promotes lymphocyte production from hematopoietic stem cells (HSCs) (Immunity 38;1105, 2013). Expression level of SATB1 increases with early lymphoid differentiation, whereas it is shut off in committed myeloid progenitors. To search a novel cell surface molecule that marks the point of branching lineage along early myeloid and lymphoid differentiation, we performed microarray analyses comparing SATB1-overexpressed HSCs with mock-transduced HSCs. The results drew our attention to membrane-spanning 4-domains, subfamily A, member 3 (MS4A3). MS4A3, also called hematopoietic cell-specific transmembrane 4 (HTm4), is a member of the MS4A family. CD20, encoded by MS4A1 gene, belongs to the same family. We observed that expression level of MS4A3 in SATB1-overexpressed HSCs was decreased almost one tenth of that of mock HSCs. To confirm the relationship of SATB1 and MS4A3 in human hematopoietic cells, we first used chronic myeloid leukemia cell line K562, which was found to clearly express MS4A3 on their cell surface. While SATB1 expression was undetectable in original K562 cells, the exogenous expression of SATB1 significantly reduced their MS4A3 expression level, suggesting that SATB1 negatively regulates MS4A3 expression in human cells. Next, we analyzed MS4A3 expression pattern in primary human hematopoietic stem/progenitor cells. Bone marrow (BM) cells were obtained from healthy donors or patients with acute myeloid leukemia. The Institutional Review Board of Osaka University School of Medicine approved all of protocols, and written informed consents were obtained from all participants. Mononuclear cells were separated from the BM samples by density gradient centrifugation, and subsequently applied to cell sorting for Lineage marker-negative (Lin-) CD34+ CD38- HSCs, Lin- CD34+ CD38+ IL-3 receptor α (IL-3Rα)+ CD45RA- common myeloid progenitors (CMPs), Lin- CD34+ CD38+ IL3-Rα+ CD45RA+ granulocyte-macrophage progenitors (GMPs) and Lin- CD34+ CD38+ IL-3Rα- CD45RA-megakaryocyte-erythroid progenitors (MEPs). MS4A3 expression levels of the sorted cells were analyzed with real-time RT-PCR. We detected more than 10-fold amount of MS4A3 transcripts in CMPs than HSCs. Furthermore, its expression level continuously increased along myeloid lineage differentiation to GMP. On the other hand, megakaryocyte-erythroid lineage differentiation was not accompanied by MS4A3 expression and the amount of MS4A3 transcripts in MEPs was minimum as in HSCs. Flow cytometry analyses confirmed that HSCs and MEPs do not express MS4A3 on their cell surface whereas the MS4A3 expression on CMPs and GMPs is detectable. Further, the Lin- CD34+ CD38+ CD33+ cells could be fractionated according to the intensity of cell surface MS4A3 expression. To investigate the significance of cell surface MS4A3 expression for functional analyses of myeloid progenitor cells, we performed methylcellulose colony-forming assays. We found that MS4A3+ cells in Lin- CD34+ CD38+ CD33+ fraction only produced granulocyte/macrophage colonies, losing erythroid colony- and mixed colony-forming capacity. These results suggest that cell surface expression of MS4A3 is useful to distinguish granulocyte/macrophage lineage-committed progenitors from other lineage-related ones in early human hematopoiesis. We also analyzed MS4A3 expression in BM cells obtained from patients with acute leukemia. Flow cytometry analyses revealed that leukemia cells of some patients expressed substantial amount of cell surface MS4A3. In conclusion, MS4A3 is useful to monitor early stage of myeloid differentiation in human hematopoiesis. In addition, our findings of MS4A3 expression on myeloid leukemia cells, while no expression on normal HSCs, imply that MS4A3 might be a therapeutic target molecule in myelogenous leukemia. Further studies would clarify the application of MS4A3 to anti-leukemia therapy. Disclosures No relevant conflicts of interest to declare.

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Naj, Adam, Gyungah Jun, Jacqueline Buros, Paul Gallins, Lindsay Farrer, Jonathan Haines, Margaret Pericak-Vance, Gerard Schellenberg, and The Alzheimer's Disease Genetics Co. "P1-250: Genome-Wide Association Study of Late-Onset Alzheimer Disease Identifies Disease-Associated Variants in MS4A4/MS4A6E, CD2AP, CD33, and EPHA1." Alzheimer's & Dementia 7 (July 2011): S191. http://dx.doi.org/10.1016/j.jalz.2011.05.530.

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Yan, Yaping, Zichen Li, Guang-Xian Zhang, Mark S. Williams, Gregory B. Carey, Jianke Zhang, Abdolmohamad Rostami, and Hui Xu. "Anti-MS4a4B treatment abrogates MS4a4B-mediated protection in T cells and ameliorates experimental autoimmune encephalomyelitis." Apoptosis 18, no. 9 (June 26, 2013): 1106–19. http://dx.doi.org/10.1007/s10495-013-0870-2.

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19

Michel, J., K. Schönhaar, K. Schledzewski, C. Gkaniatsou, C. Sticht, B. Kellert, F. Lasitschka, C. Géraud, S. Goerdt, and A. Schmieder. "Identification of the novel differentiation marker MS4A8B and its murine homolog MS4A8A in colonic epithelial cells lost during neoplastic transformation in human colon." Cell Death & Disease 4, no. 1 (January 2013): e469-e469. http://dx.doi.org/10.1038/cddis.2012.215.

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Eiring, Anna M., Jamshid S. Khorashad, Anupriya Agarwal, Clinton C. Mason, Fan Yu, Hannah M. Redwine, Amber D. Bowler, et al. "MS4A3 Improves Imatinib Response and Survival in BCR-ABL1 Primary TKI Resistance and in Blastic Transformation of Chronic Myeloid Leukemia." Blood 126, no. 23 (December 3, 2015): 14. http://dx.doi.org/10.1182/blood.v126.23.14.14.

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Abstract Background: Mutations in the BCR-ABL1 kinase domain are a well-documented mechanism of resistance to tyrosine kinase inhibitors (TKIs), but less is known about primary resistance independent of BCR-ABL1 kinase activity. We reported a gene expression classifier of TKI-naïve CD34+ cells from chronic phase chronic myeloid leukemia (CP-CML) patients that predicts cytogenetic response to imatinib (McWeeney et al. Blood 2010). The expression signature associated with primary cytogenetic failure showed overlap with previously reported signatures of blast phase CML (BP-CML), suggesting that primary TKI resistance and advanced disease are biologically similar. Results: To identify critical genes involved in primary TKI resistance, we performed principal component analysis on the expression signature and identified the hematopoietic cell cycle regulator, MS4A3, as a key factor within this classifier. Importantly, low MS4A3 expression not only correlated with primary TKI resistance, but also with shorter overall survival (p<0.01), prompting us to study the role of MS4A3 in more detail. Since the signatures for primary cytogenetic failure and BP-CML overlapped, we next assessed whether MS4A3 expression was downregulated in BP-CML versus CP-CML. qRT-PCR confirmed that MS4A3 mRNA levels are markedly reduced (by >92%) in CD34+ cells from BP-CML patients (n=17; p<0.01) versus CP-CML patients (n=23) and normal controls (n=3). There was no significant difference between normal and chronic phase CD34+ cells, suggesting that MS4A3 is specifically downregulated upon CML blastic transformation. Microarray data from Oehler et al. (unpublished observations) and Zheng et al. (Leukemia 2006) also showed that MS4A3 mRNA levels are reduced in CD34+ cells from BP-CML patients (n=16; p<0.001) compared to CP-CML patients (n=19). Immunoblot analyses confirmed that MS4A3 protein was detectable in CD34+ cells from newly diagnosed CP-CML patients, but not in samples from patients with primary resistance who failed multiple TKIs but lack clinically relevant BCR-ABL1 mutations. Finally, in CP-CML samples from newly diagnosed patients, MS4A3 mRNA levels are 12-fold reduced in primitive CD34+38- stem cells compared to more committed CD34+38+ progenitor cells (n=3; p<0.05), which are innately resistant to BCR-ABL1 inhibition. Consistent with BCR-ABL1 kinase independence, MS4A3 mRNA and protein levels were unaffected by ex vivo TKI treatment. MS4A3 expression is also low in BP-CML cell lines, including K562, KYO-1, BV-173, KCL-22, and KU-812, with the notable exception of LAMA-84 cells. Thus, to understand the functional role of MS4A3 for TKI resistance, we introduced a doxycycline-inducible shRNA targeting MS4A3 (shMS4A3) into LAMA-84 cells. qRT-PCR confirmed 50-90% MS4A3 knockdown in the presence of doxycycline (0.1 µg/mL). Consistent with its role as a tumor suppressor, MTS assays revealed that MS4A3 knockdown increased the imatinib IC50 (n=3; p<0.05) and abolished the effects of imatinib in colony formation assays (n=2; p<0.05). We next assessed the effects of shMS4A3 in CD34+ cells from newly diagnosed CP-CML patients. qRT-PCR confirmed ~50% MS4A3 knockdown in primary cells. Despite the incomplete knockdown, shMS4A3 enhanced colony formation in the presence of imatinib in a dose-dependent manner (n=4; p<0.00001), and abolished imatinib-induced apoptosis (n=3; p<0.001). We also assessed the effects of ectopic MS4A3 expression in CD34+ cells from advanced phase CML (AP-CML) patients. qRT-PCR confirmed >2-fold upregulation of MS4A3. As expected, ectopic MS4A3 reduced colony formation by 55% in AP-CML (n=2; p<0.01), and enhanced sensitivity to imatinib-induced apoptosis by 35% (n=2; p<0.01). Neither shMS4A3 nor ectopic MS4A3 had any effect on survival of normal cord blood CD34+ cells (n=2). Conclusion: Our results suggest that MS4A3 is a tumor suppressor protein in CML that governs TKI responsiveness and is regulated in a BCR-ABL1 kinase-independent manner. MS4A3 loss confers TKI resistance to CP-CML patients destined to exhibit primary cytogenetic failure, and in BP-CML patients with refractory resistance. MS4A3 may also contribute to the innate resistance of primitive CML stem cells. Studies to identify the mechanism of MS4A3 downregulation in TKI resistance and how its loss biochemically impairs TKI response is currently underway and will be reported. Disclosures Agarwal: CTI BioPharma: Research Funding. Deininger:BMS: Other: Consulting & Advisory Role, Research Funding; Novartis: Other: Consulting or Advisory Role, Research Funding; Celgene: Research Funding; Genzyme: Research Funding; Gilead: Research Funding; ARIAD Pharmaceutical Inc.: Other: Consulting or Advisory Role; Incyte: Other: Consulting or Advisory Role; Pfizer: Other: Consulting or Advisory Role.

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Sanyal, Ratna, Maria J. Polyak, Jonathan Zuccolo, Mandip Puri, Lili Deng, Luc Roberts, Ania Zuba, et al. "MS4A4A: a novel cell surface marker for M2 macrophages and plasma cells." Immunology & Cell Biology 95, no. 7 (April 11, 2017): 611–19. http://dx.doi.org/10.1038/icb.2017.18.

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Eiring, Anna M., Jamshid S. Khorashad, Anupriya Agarwal, Clinton C. Mason, Russell Bell, Anna Senina, Anthony D. Pomicter, et al. "MS4A3: A New Player in Leukemic Stem Cell Survival in Chronic Myeloid Leukemia." Blood 128, no. 22 (December 2, 2016): 934. http://dx.doi.org/10.1182/blood.v128.22.934.934.

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Abstract Background: We have previously demonstrated that the transcriptional profile of diagnostic CD34+ cells from chronic phase chronic myeloid leukemia (CP-CML) patients exhibiting primary cytogenetic resistance to imatinib overlaps with that of patients with myeloid blast phase CML (BP-CML) (McWeeney et al. Blood 2010). These data suggest that primary resistance to tyrosine kinase inhibitors (TKIs) and advanced disease are biologically related. The hematopoietic cell cycle regulator, MS4A3, was identified as a principal component of the gene expression classifier predicting response to imatinib. Low MS4A3 correlated not only with primary TKI resistance, but also with shorter overall survival in CP-CML (n=35). Consistently, microarray (n=19 CP-CML; n=16 BP-CML), qRT-PCR (n=22 CP-CML; n=17 BP-CML), and immunoblot (n=3 CP-CML; n=3 BP-CML) analyses demonstrated that MS4A3 mRNA and protein levels are reduced in CD34+ progenitor cells from BP-CML versus CP-CML patients, with no difference between CP-CML and normal CD34+progenitors (n=3) (Eiring et al. ASH 2015 #14). These data suggest that MS4A3 may play a role in both primary TKI resistance and blastic transformation of CML. Results: To assess the functional role of MS4A3 in CML and TKI response, we used ectopic MS4A3 expression and shRNA-mediated MS4A3 knockdown in CD34+ cells from BP-CML and CP-CML patients, respectively. Ectopic expression of MS4A3 in BP-CML CD34+ progenitors (n=5) markedly reduced colony formation in the presence and absence of imatinib, consistent with a tumor suppressor role for MS4A3 in CML. While re-expression of MS4A3 alone did not increase apoptosis compared to empty vector-expressing controls, imatinib-induced apoptosis in BP-CML CD34+ cells was increased by 62%, with no effect on normal CD34+ cord blood cells (n=2). Conversely, shRNA-mediated MS4A3 knockdown (shMS4A3) in CP-CML CD34+ cells (n=7) reduced the effects of imatinib in colony formation and apoptosis assays, with no effect on normal CD34+ progenitors (n=4). In contrast to a previous report (Donato JL, et al. J Clin Invest 2002), we detected no change in cell cycle status of CML or normal CD34+ cells upon MS4A3 ectopic expression or knockdown (n=3). Altogether, these data suggest that MS4A3 positively regulates patient survival and imatinib response in CML progenitor cells. To evaluate MS4A3 in the leukemic stem cell compartment, we performed qRT-PCR on primary CP-CML cells (n=5) and observed that MS4A3 mRNA levels are 22-fold higher in committed CD34+38+ progenitors compared to more primitive CD34+38- stem cells, suggesting a role for MS4A3 in differentiation. Consistently, qRT-PCR, immunoblot, and flow cytometry demonstrated that MS4A3 mRNA and protein were upregulated in CP-CML CD34+ cells upon G-CSF treatment (n=3). Flow cytometry also revealed that shMS4A3 in CP-CML CD34+ cells resulted in a reduction of CD11b+ cells by ~45% in the presence of G-CSF (n=3). To assess the function of MS4A3 in CML stem cells, we performed long-term culture-initiating cell (LTC-IC) assays and xenografts into NSG mice upon MS4A3 knockdown in CP-CML (n=3). shMS4A3 increased Ph+ LTC-IC colony formation in the absence, and even more so in the presence, of imatinib, with no effects on Ph- LTC-ICs. Consistent with these data, shMS4A3 enhanced engraftment of CD34+CD45+GFP+ cells into the bone marrow of NSG recipient mice. Preliminary data in primary TKI-resistant and BP-CML CD34+ cells suggests regulation of this gene by promoter hypermethylation. Conclusions: Altogether, these data suggest that MS4A3 plays a key role in imatinib response of 1) patients with primary TKI resistance, 2) patients with BP-CML, and 3) the CML stem cell compartment. Since the effects of MS4A3 in CML do not involve changes to the cell cycle, experiments are underway to identify the mechanism by which MS4A3 improves imatinib response and survival in CML. Disclosures Druker: Agios: Honoraria; Ambit BioSciences: Consultancy; ARIAD: Patents & Royalties, Research Funding; Array: Patents & Royalties; AstraZeneca: Consultancy; Blueprint Medicines: Consultancy, Equity Ownership, Other: travel, accommodations, expenses ; BMS: Research Funding; CTI: Equity Ownership; Curis: Patents & Royalties; Cylene: Consultancy, Equity Ownership; D3 Oncology Solutions: Consultancy; Gilead Sciences: Consultancy, Other: travel, accommodations, expenses ; Lorus: Consultancy, Equity Ownership; MolecularMD: Consultancy, Equity Ownership, Patents & Royalties; Novartis: Research Funding; Oncotide Pharmaceuticals: Research Funding; Pfizer: Patents & Royalties; Roche: Consultancy. Deininger:Incyte: Consultancy, Membership on an entity's Board of Directors or advisory committees; Gilead: Research Funding; BMS: Consultancy, Research Funding; Pfizer: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; Novartis: Consultancy, Membership on an entity's Board of Directors or advisory committees, Research Funding; CTI BioPharma Corp.: Membership on an entity's Board of Directors or advisory committees; Celgene: Research Funding; Bristol Myers Squibb: Consultancy, Research Funding; Ariad: Consultancy, Membership on an entity's Board of Directors or advisory committees.

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Lefaucheur, Carmen, Denis Viglietti, Luis G. Hidalgo, Lloyd E. Ratner, Serena M. Bagnasco, Ibrahim Batal, Olivier Aubert, et al. "Complement-Activating Anti-HLA Antibodies in Kidney Transplantation: Allograft Gene Expression Profiling and Response to Treatment." Journal of the American Society of Nephrology 29, no. 2 (October 17, 2017): 620–35. http://dx.doi.org/10.1681/asn.2017050589.

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Complement-activating anti-HLA donor-specific antibodies (DSAs) are associated with impaired kidney transplant outcome; however, whether these antibodies induce a specific rejection phenotype and influence response to therapy remains undetermined. We prospectively screened 931 kidney recipients for complement-activating DSAs and used histopathology, immunostaining, and allograft gene expression to assess rejection phenotypes. Effector cells were evaluated using in vitro human cell cultures. Additionally, we assessed the effect of complement inhibition on kidney allograft rejection phenotype and the clinical response to complement inhibition in 116 independent kidney recipients with DSAs at transplant receiving rejection prophylaxis with eculizumab or standard of care (plasma exchange and intravenous Ig) at ten international centers. The histomolecular rejection phenotype associated with complement-activating DSA was characterized by complement deposition and accumulation of natural killer cells and monocytes/macrophages in capillaries and increased expression of five biologically relevant genes (CXCL11, CCL4, MS4A7, MS4A6A, and FCGR3A) indicative of endothelial activation, IFNγ response, CD16-mediated natural killer cell activation, and monocyte/macrophage activation. Compared with standard of care, eculizumab specifically abrogated this histomolecular rejection phenotype and associated with a decreased 3-month rejection incidence rate in patients with complement-activating DSAs (56%; 95% confidence interval [95% CI], 38% to 74% versus 19%; 95% CI, 8% to 35%; P=0.001) but not in those with noncomplement-activating DSAs (9%; 95% CI, 2% to 25% versus 13%; 95% CI, 2% to 40%; P=0.65). In conclusion, circulating complement-activating anti-HLA DSAs are associated with a specific histomolecular kidney allograft rejection phenotype that can be abrogated by complement inhibition.

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Huang, Tinghua, Xiali Huang, Bomei Shi, Xiongyan Liang, Jingbo Luo, and Min Yao. "Relationship among MS4A8 expression, its variants, and the immune response in a porcine model of Salmonella." Canadian Journal of Animal Science 98, no. 4 (December 1, 2018): 778–86. http://dx.doi.org/10.1139/cjas-2017-0037.

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Salmonella colonization often establishes carrier status in infected animals, which decreases their performance. Salmonella-carrying pigs shed large amounts of bacteria in their feces, and thus they have a negative economic impact on the swine industry. The MS4A8 gene (membrane-spanning 4-domains A8) was significantly activated, by up to 119-fold, in peripheral blood after Salmonella inoculation of pigs. The present study analyzed the correlation of peripheral blood expression level and a genetic variant of porcine MS4A8 with Salmonella-infection traits. The result indicated that MS4A8 expression levels correlated significantly with Salmonella shedding counts. Both the expression of MS4A8 and fecal shedding counts correlated with leukocytes, lymphocytes, monocytes, segmented neutrophils, and banded neutrophils. A novel single nucleotide polymorphism of porcine MS4A8 (nonsynonymous, Val > Ala) was associated with Salmonella shedding counts and average daily gain (ADG) of body weight. The TT genotype had higher fecal shedding counts, leukocyte counts, and lymphocyte counts than the TC and CC genotypes. The CC genotype had higher level of ADG than the TC and TT genotype (p < 0.05). Those results indicated that MS4A8 is intriguing and could be used as a prospective genetic marker for Salmonella susceptibility.

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Ye, Lin, Xu-Dong Yao, Fang-Ning Wan, Yuan-Yuan Qu, Zhi-Yu Liu, Xu-Xia Shen, Sheng Li, et al. "MS4A8B promotes cell proliferation in prostate cancer." Prostate 74, no. 9 (April 30, 2014): 911–22. http://dx.doi.org/10.1002/pros.22802.

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Ye, Lin, Xu-Dong Yao, Fang-Ning Wan, Yuan-Yuan Qu, Zhi-Yu Liu, Xu-Xia Shen, Sheng Li, et al. "MS4A8B promotes cell proliferation in prostate cancer." Prostate 74, no. 11 (June 23, 2014): 1160. http://dx.doi.org/10.1002/pros.22852.

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Sui, Yinqiang, and Wenwen Zeng. "MS4A4A Regulates Arginase 1 Induction during Macrophage Polarization and Lung Inflammation in Mice." European Journal of Immunology 50, no. 10 (July 29, 2020): 1602–5. http://dx.doi.org/10.1002/eji.202048585.

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Proitsi, Petroula, Sang Hyuck Lee, Katie Lunnon, Aoife Keohane, John Powell, Claire Troakes, Safa Al-Sarraj, et al. "Alzheimer's disease susceptibility variants in the MS4A6A gene are associated with altered levels of MS4A6A expression in blood." Neurobiology of Aging 35, no. 2 (February 2014): 279–90. http://dx.doi.org/10.1016/j.neurobiolaging.2013.08.002.

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Eiring, Anna M., Anupriya Agarwal, Jamshid S. Khorashad, Clinton C. Mason, David J. Anderson, Fan Yu, Hannah M. Redwine, et al. "The Tumor Suppressors, MS4A3 and G0S2, Are Downregulated in CML Cells with BCR-ABL1 Kinase-Independent Resistance." Blood 124, no. 21 (December 6, 2014): 1786. http://dx.doi.org/10.1182/blood.v124.21.1786.1786.

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Abstract Background: The treatment and survival of chronic myeloid leukemia (CML) patients has greatly improved after the discovery of imatinib; however, disease persistence and drug resistance remain as clinical problems. McWeeney et al. (Blood 2010;115:315-325) identified a gene expression signature predictive of primary cytogenetic resistance to imatinib in treatment-naïve CML chronic phase (CML-CP) patients lacking BCR-ABL1 kinase domain mutations. Comparison of this gene classifier with other studies revealed extensive overlap of resistance genes with genes associated with CML blastic transformation, suggesting that CML-CP patients destined to fail imatinib may exhibit a gene profile reminiscent of advanced CML. Based on rank predictive score from the microarray, the top transcripts found to be dysregulated in newly diagnosed patients who subsequently emerged as imatinib non-responders were: PLCXD2, EGF16, GAS2, RXFP1, ITGA2, MS4A3, FCN1, EMCN, EMCN, CLIP4, ZNF44 and G0S2. Among these, MS4A3 and G0S2 were differentially downregulated in non-responders compared to responders. Conversely, high levels of MS4A3 (p=0.059) and G0S2 (p=0.036) correlated with higher likelihood of major cytogenetic response and longer overall survival. MS4A3 (HTM4) is a hematopoietic cell cycle regulator that inhibits G1/S phase cell cycle transition, whereas G0S2 is proapoptotic mitochondrial protein that interacts with and antagonizes BCL-2. In this study, we investigated the potential role of MS4A3 and G0S2 as tumor suppressors in CML and their influence on TKI resistance and blastic transformation. MS4A3 and CML: Expression of p210BCR-ABL1 in 32Dcl3 or Mo7e myeloid progenitor cells resulted in an 80% reduction of MS4A3 mRNA relative to parental cells by qRT-PCR analysis. Imatinib treatment slightly restored MS4A3 levels in 32D-p210 or Mo7e-p210 cells, but did not return levels to those of normal controls growing with cytokine support. Consistent with a role for MS4A3 in CML blastic transformation, qRT-PCR revealed low levels of MS4A3 in cell line models of blastic phase CML (CML-BP), including K562, KYO-1, and KBM, that were unaffected by treatment with imatinib. Furthermore, qRT-PCR confirmed that MS4A3 is downregulated (~20-fold) in CML CD34+ progenitor cells from CML-BP (n=3) compared to CML-CP (n=5) patients and normal controls (n=3), and that these levels were unaffected by imatinib. We then used tetracycline-inducible shRNA directed against MS4A3 (shMS4A3) to knockdown MS4A3 in primary CML CD34+ cells from newly diagnosed CML-CP patients subsequently responding to TKIs. Western blot and qRT-PCR analyses confirmed MS4A3 downregulation upon exposure to doxycyline (0.1 ug/mL). shMS4A3 upregulated colony formation by 37.6% (p<0.001) in the absence of imatinib, 58.8% (p<0.0001) in 1 µM imatinib, and 138.4% (p<0.001) in 2.5 µM imatinib. Furthermore, shMS4A3 significantly reduced imatinib-induced apoptosis of CML-CP samples in the presence but not absence of doxycycline (p<0.02). G0S2 and CML: Consistent with a role for G0S2 in CML blastic transformation, qRT-PCR revealed that G0S2 mRNA is highly downregulated (~24-fold) in CML CD34+ progenitor cells from CML-BP (n=3) compared to CML-CP (n=5) patients and normal controls (n=3). G0S2 is also downregulated in TKI-resistant K562R and AR230R cells compared to parental TKI-sensitive counterparts. K562R and AR230R cells are resistant to all clinically approved TKIs, but lack BCR-ABL1 kinase domain mutations, implicating BCR-ABL1 kinase-independent TKI resistance. Ectopic expression of a Flag-tagged G0S2 (G0S2-Flag) significantly reduced colony formation in both parental K562 and AR230 cells, but had an even greater effect in TKI-resistant K562R and AR230R cells in the presence of imatinib. G0S2-Flag also impaired colony formation of CML-CP CD34+cells in both the presence (p<0.03) and absence (p<0.01) of imatinib (1 µM). Consistent with a proapoptotic role for G0S2, G0S2-Flag increased Annexin V positivity in all cell lines and patient samples tested. Conclusions:These findings suggest a role for loss of MS4A3 or G0S2 tumor suppressor function in both TKI resistance in the absence of explanatory BCR-ABL1 kinase domain mutations and in CML blastic transformation. Studies to test the effects of restored MS4A3 or G0S2 expression in CML-BP and TKI-resistant patient samples are currently underway. Disclosures Deininger: BMS, Novartis, Celgene, Genzyme, Gilead: Research Funding; BMA, ARIAD, Novartis, Incyte, Pfizer: Advisory Board, Advisory Board Other; BMS, ARIAD, Novartis, Incyte, Pfizer: Consultancy.

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Suenaga, Mitsukuni, Shu Cao, Wu Zhang, Satoshi Matsusaka, Satoshi Okazaki, Martin D. Berger, Yuji Miyamoto, et al. "Role of enterocyte-specific gene polymorphisms in adjuvant treatment for stage III colorectal cancer." Journal of Clinical Oncology 37, no. 4_suppl (February 1, 2019): 550. http://dx.doi.org/10.1200/jco.2019.37.4_suppl.550.

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550 Background: Enterocyte subtype of the Colorectal Cancer (CRC) Assigner classifier is known as favorable to oxaliplatin-based adjuvant treatment for stage III CRC. We previously reported potential predictive value of single nucleotide polymorphisms (SNPs) in enterocyte-related genes in metastatic CRC (Suenaga, ASCO2018). In this study, we examined clinical significance of MS4A12 and CDX2 SNPs in adjuvant treatment (AT) for Stage III CRC. Methods: 350 patients with Stage III CRC were included in this study: 274 received AT (discovery cohort: median age = 62, median follow-up = 59.9 months) and 76 received surgery alone (control: median age = 75, median follow-up = 58.0 months). 68 and 206 patients received FOLFOX and oral fluoriopyrimidine, respectively. SNPs were analyzed by PCR-based direct sequencing. Disease-free survival and overall survival (OS) were analyzed using Kaplan-Meier curves, log-rank test, and Cox proportional hazards regression. Results: In discovery cohort, the G/G variant in MS4A12 rs4939378 was associated with lower 5-y survival rate than any A allele in uni- and multi-variate analyses (70% vs 90%, univariate: HR 2.29, 95% CI: 1.03-5.06, P = 0.035; multivariable: HR 2.58, 95% CI: 1.15-5.76, P = 0.021). Patients with the G/G variant in CDX2 rs3812863 had better OS than those with any A, though not significant in multivariable analysis (5 y-survival rate: 95% vs 82%, univariate: HR 0.34, 95% CI: 0.12-0.97, P = 0.034; multivariable: HR 0.39, 95% CI: 0.13-1.11, P = 0.078). There was no significance in the control, and significant interaction was observed between MS4A12 genotypes and groups (interaction P = 0.007). In addition, there was no interaction between MS4A12 rs4939378 and FOLFOX vs oral fluoropyrimidine. Conclusions: Our findings suggest that MS4A12 and CDX2 gene polymorphisms may predict outcome in patients with Stage III CRC. However, clinical significance of the SNPs for oxaliplatin seems to differ depending on tumor stage. Further research and validation study are warranted to explore the association of the SNPs with carcinogenesis or cancer progression.

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Mattiola, Irene, Federica Tomay, Maria De Pizzol, Rita Silva-Gomes, Benedetta Savino, Tamara Gulic, Andrea Doni, et al. "The macrophage tetraspan MS4A4A enhances dectin-1-dependent NK cell–mediated resistance to metastasis." Nature Immunology 20, no. 8 (July 1, 2019): 1012–22. http://dx.doi.org/10.1038/s41590-019-0417-y.

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Deng, Jianzhao, Xuan Yang, and Bei Zhang. "MS4a6D Exacerbates Immunological Pathology in Experimental Viral Fulminant Hepatitis." International Journal of Sciences 8, no. 02 (2019): 98–104. http://dx.doi.org/10.18483/ijsci.1916.

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Rushton, Christopher K., Sarah E. Arthur, Miguel Alcaide, Matthew Cheung, Aixiang Jiang, Krysta M. Coyle, Kirstie L. S. Cleary, et al. "Genetic and evolutionary patterns of treatment resistance in relapsed B-cell lymphoma." Blood Advances 4, no. 13 (June 26, 2020): 2886–98. http://dx.doi.org/10.1182/bloodadvances.2020001696.

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Abstract Diffuse large B-cell lymphoma (DLBCL) patients are typically treated with immunochemotherapy containing rituximab (rituximab, cyclophosphamide, hydroxydaunorubicin-vincristine (Oncovin), and prednisone [R-CHOP]); however, prognosis is extremely poor if R-CHOP fails. To identify genetic mechanisms contributing to primary or acquired R-CHOP resistance, we performed target-panel sequencing of 135 relapsed/refractory DLBCLs (rrDLBCLs), primarily comprising circulating tumor DNA from patients on clinical trials. Comparison with a metacohort of 1670 diagnostic DLBCLs identified 6 genes significantly enriched for mutations upon relapse. TP53 and KMT2D were mutated in the majority of rrDLBCLs, and these mutations remained clonally persistent throughout treatment in paired diagnostic-relapse samples, suggesting a role in primary treatment resistance. Nonsense and missense mutations affecting MS4A1, which encodes CD20, are exceedingly rare in diagnostic samples but show recurrent patterns of clonal expansion following rituximab-based therapy. MS4A1 missense mutations within the transmembrane domains lead to loss of CD20 in vitro, and patient tumors harboring these mutations lacked CD20 protein expression. In a time series from a patient treated with multiple rounds of therapy, tumor heterogeneity and minor MS4A1-harboring subclones contributed to rapid disease recurrence, with MS4A1 mutations as founding events for these subclones. TP53 and KMT2D mutation status, in combination with other prognostic factors, may be used to identify high-risk patients prior to R-CHOP for posttreatment monitoring. Using liquid biopsies, we show the potential to identify tumors with loss of CD20 surface expression stemming from MS4A1 mutations. Implementation of noninvasive assays to detect such features of acquired treatment resistance may allow timely transition to more effective treatment regimens.

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Cingam, Shashank, Moises Harari-Turquie, Dulcinea Quintana, Leslie Andritsos, and Emrullah Yilmaz. "525 KIT mutation with a low MS4A1/CD20 expression is associated with poor prognosis in melanoma." Journal for ImmunoTherapy of Cancer 8, Suppl 3 (November 2020): A561. http://dx.doi.org/10.1136/jitc-2020-sitc2020.0525.

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BackgroundMelanoma has high response rate to immune checkpoint inhibitors. KIT, a driver mutation in melanoma seen in ~10% of the patients.1 However, the role of the KIT mutation in immune microenvironment of melanoma is not well established yet. Here we report a case with KIT mutation and a likely impaired B cell activity with poor response to Immune-checkpoint inhibitor therapy (ICI). We also describe the overall survival of melanoma depending on KIT mutation and MS4A1/CD20 expression, which encodes CD20, B-lymphocyte-specific membrane protein that plays a role in the development, differentiation, and activation of B-lymphocytes.2MethodsA case with poor response to ICI with KIT mutation and monoclonal B cell lymphocytosis was identified. Clinical and molecular characteristics of melanoma in TCGA was analyzed using cBioPortal web page. TCGA data were analyzed to determine KIT mutation status and MS4A1/CD20 expression in melanoma cohort. Samples in the upper 33 percentile of MS4A1 expression were identified as high expression, and the lower 33 percentile were identified as low expression. Mantel-Cox method was used for overall survival (OS) comparison between the cohorts.Results69-year-old male with initial diagnosis of stage III-B melanoma of the left thumb with local recurrence in the resection site and then lung metastases. Patient was then started on nivolumab/ipilimumab with rapid progression on immunotherapy. He was found to have KIT mutation (exon 13K642EMT), and started on imatinib, but he continued to have progression. He was switched to temozolomide with no response. He also had history of leukopenia, pre-dating the metastatic melanoma and was diagnosed with monoclonal B cell lymphocytosis. With the hypothesis that the patient‘s dysfunctional B cells may have impaired ability of ICI and poor prognosis; we analyzed TCGA database for KIT mutation and MS4A1/CD20 expression- which was used as marker for B cell activity. KIT mutation was seen in 10 of 147 patients with high MS4A1/CD20 expression, and 10 of 135 patients with low MS4A1/CD20 expression. Overall survival was 15 months for the patients with KIT mutation and low MS4A1/CD20 expression, and significantly lower when compared with other groups despite low number of patients. (P<0.0001) (figure 1).Abstract 525 Figure 1KIT mutation and MS41A/CD20 expression - overall survivalLow MS41A/CD20 expression with concurrent KIT mutation is associated with poor overall survivalConclusionsB cells have significant role in immune response to tumor. Lower expression of MS4A1/CD20 is known to be associated with poor prognosis in melanoma and other solid tumors.3 We demonstrated that a concurrent KIT mutation in melanoma with lower expression of MS4A1/CD20 contributes to poor prognosis in melanoma. Therefore, this small subset of aggressive tumors may need combination strategies involving targeting driver pathways with a kinase and immune checkpoint inhibitor.Referencesde Mendonça UB, Cernea CR, Matos LL, de Araujo Lima RR. Analysis of KIT gene mutations in patients with melanoma of the head and neck mucosa: a retrospective clinical report. Oncotarget 2018 May 1;9(33):22886.Tedder TF, Boyd AW, Freedman AS, Nadler LM, Schlossman S. The B cell surface molecule B1 is functionally linked with B cell activation and differentiation. The Journal of Immunology 1985 Aug 1;135(2):973–9.Liu Y, Wang L, Lo KW, Lui VW. Omics-wide quantitative B-cell infiltration analyses identify GPR18 for human cancer prognosis with superiority over CD20. Communications biology 2020 May 12;3(1):1–1.

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Yan, Yaping, Guang-Xian Zhang, Mark S. Williams, Gregory B. Carey, Hongmei Li, Jingxian Yang, Abdolmohamad Rostami, and Hui Xu. "TCR stimulation upregulates MS4a4B expression through induction of AP-1 transcription factor during T cell activation." Molecular Immunology 52, no. 2 (September 2012): 71–78. http://dx.doi.org/10.1016/j.molimm.2012.04.011.

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Xu, Hui, Yaping Yan, Mark S. Williams, Gregory B. Carey, Jingxian Yang, Hongmei Li, Guang-Xian Zhang, and Abdolmohamad Rostami. "MS4a4B, a CD20 Homologue in T Cells, Inhibits T Cell Propagation by Modulation of Cell Cycle." PLoS ONE 5, no. 11 (November 1, 2010): e13780. http://dx.doi.org/10.1371/journal.pone.0013780.

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Cruse, Glenn, Michael A. Beaven, Stephen C. Music, Peter Bradding, and Dean D. Metcalfe. "The Fcεriβ Homologue, MS4A4, Promotes Fcεri-Dependent Human Mast Cell Degranulation By Facilitating PLCγ1 Signaling." Journal of Allergy and Clinical Immunology 135, no. 2 (February 2015): AB240. http://dx.doi.org/10.1016/j.jaci.2014.12.1718.

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Arthur, Greer K., Lauren C. Ehrhardt-Humbert, Douglas B. Snider, Corey Jania, Stephen L. Tilley, Dean D. Metcalfe, and Glenn Cruse. "The FcεRIβ homologue, MS4A4A, promotes FcεRI signal transduction and store-operated Ca2+ entry in human mast cells." Cellular Signalling 71 (July 2020): 109617. http://dx.doi.org/10.1016/j.cellsig.2020.109617.

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Howie, Duncan, Kathleen F. Nolan, Stephen Daley, Emma Butterfield, Elizabeth Adams, Hugo Garcia-Rueda, Claire Thompson, et al. "MS4A4B Is a GITR-Associated Membrane Adapter, Expressed by Regulatory T Cells, Which Modulates T Cell Activation." Journal of Immunology 183, no. 7 (September 14, 2009): 4197–204. http://dx.doi.org/10.4049/jimmunol.0901070.

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Huang, Xiaoyong, Zeqing Feng, Yuanzhong Jiang, Jialin Li, Qun Xiang, Sheng Guo, Chengying Yang, et al. "VSIG4 mediates transcriptional inhibition of Nlrp3 and Il-1β in macrophages." Science Advances 5, no. 1 (January 2019): eaau7426. http://dx.doi.org/10.1126/sciadv.aau7426.

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Hyperactivation of the NLRP3 inflammasome contributes to the pathogenesis of multiple diseases, but the mechanisms underlying transcriptional regulation of Nlrp3 remain elusive. We demonstrate here that macrophages lacking V-set and immunoglobulin domain–containing 4 (Vsig4) exhibit significant increases in Nlrp3 and Il-1β transcription, caspase-1 activation, pyroptosis, and interleukin-1β (IL-1β) secretion in response to NLRP3 inflammasome stimuli. VSIG4 interacts with MS4A6D in the formation of a surface signaling complex. VSIG4 occupancy triggers Ser232 and Ser235 phosphorylation in MS4A6D, leading to activation of JAK2-STAT3-A20 cascades that further results in nuclear factor κB suppression and Nlrp3 and Il-1β repression. Exaggerated NLRP3 and IL-1β expression in Vsig4−/− mice is accountable for deleterious disease severity in experimental autoimmune encephalomyelitis (EAE) and resistance to dextran sulfate sodium (DSS)–induced colitis. The agonistic VSIG4 antibodies (VG11), acting through NLRP3 and IL-1β suppression, show significant therapeutic efficacy in mouse EAE. These findings highlight VSIG4 as a prospective target for treating NLRP3-associated inflammatory disorders.

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Aksu, T., B. Uygur, N. Arat, and H. Kisacik. "MS454 CORONARY ARTERY ECTASIA: CLINICAL AND ANGIOGRAPHICAL EVALUATION." Atherosclerosis Supplements 11, no. 2 (June 2010): 201. http://dx.doi.org/10.1016/s1567-5688(10)70955-7.

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N'Songo, Aurelie, Minerva M. Carrasquillo, Xue Wang, Jeremy D. Burgess, Thuy Nguyen, Yan W. Asmann, Daniel J. Serie, et al. "African American exome sequencing identifies potential risk variants at Alzheimer disease loci." Neurology Genetics 3, no. 2 (April 2017): e141. http://dx.doi.org/10.1212/nxg.0000000000000141.

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Objective:In African Americans, we sought to systematically identify coding Alzheimer disease (AD) risk variants at the previously reported AD genome-wide association study (GWAS) loci genes.Methods:We identified coding variants within genes at the 20 published AD GWAS loci by whole-exome sequencing of 238 African American participants, validated these in 300 additional participants, and tested their association with AD risk in the combined cohort of 538 and with memory endophenotypes in 319 participants.Results:Two ABCA7 missense variants (rs3764647 and rs3752239) demonstrated significant association with AD risk. Variants in MS4A6A, PTK2B, and ZCWPW1 showed significant gene-based association. In addition, coding variants in ZCWPW1 (rs6465770) and NME8 (rs10250905 and rs62001869) showed association with memory endophenotypes.Conclusions:Our findings support a role for ABCA7 missense variants in conferring AD risk in African Americans, highlight allelic heterogeneity at this locus, suggest the presence of AD-risk variants in MS4A6A, PTK2B, and ZCWPW1, nominate additional variants that may modulate cognition, and importantly provide a thorough screen of coding variants at AD GWAS loci that can guide future studies in this population.

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Mehdizadeh, Elham, Mohammad Khalaj-Kondori, Zeinab Shaghaghi-Tarakdari, Saeed Sadigh-Eteghad, Mahnaz Talebi, and Sasan Andalib. "Association of MS4A6A, CD33, and TREM2 gene polymorphisms with the late-onset Alzheimer’s disease." BioImpacts 9, no. 4 (May 22, 2019): 219–25. http://dx.doi.org/10.15171/bi.2019.27.

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Introduction: Alzheimer’s disease (AD), which is a progressive neurodegenerative disorder, causes structural and functional brain disruption. MS4A6A, TREM2, and CD33 gene polymorphisms loci have been found to be associated with the pathobiology of late-onset AD (LOAD). In the present study, we tested the hypothesis of association of LOAD with rs983392, rs75932628, and rs3865444 polymorphisms in MS4A6A, TREM2, CD33 genes, respectively.Methods: In the present study, 113 LOAD patients and 100 healthy unrelated age- and gender-matched controls were selected. DNA was extracted from blood samples by the salting-out method and the genotyping was performed by RFLP-PCR. Electrophoresis was carried out on agarose gel. Sequencing was thereafter utilized for the confirmation of the results. Results: Only CD33 rs3865444 polymorphism revealed a significant difference in the genotypic frequencies of GG (P = 0.001) and GT (P = 0.001), and allelic frequencies of G (P = 0.033) and T (P = 0.03) between LOAD patients and controls. Conclusion: The evidence from the present study suggests that T allele of CD33 rs3865444 polymorphism is associated with LOAD in the studied Iranian population.

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Sugimoto, Takumi, Akihiro Tomita, Junji Hiraga, Kazuyuki Shimada, Hitoshi Kiyoi, Tomohiro Kinoshita, and Tomoki Naoe. "MS4A1 (CD20) Gene Expression Is Down-Regulated by Recruiting the Histone Deacetylase Protein Complex to the Promoter in the CD20-Negative B-Lymphoma Cells After Treatment with Rituximab." Blood 114, no. 22 (November 20, 2009): 1286. http://dx.doi.org/10.1182/blood.v114.22.1286.1286.

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Abstract Abstract 1286 Poster Board I-308 Background Rituximab, a mouse/human chimeric-monoclonal antibody, is now one of the critical molecular targeting drugs for treatment of CD20-positive B-cell lymphomas. Although the survival benefit of rituximab has been proved for several types of CD20-positive B-cell malignancies, resistance to rituximab has also become a considerable problem. Very recently, we reported that down-modulation of CD20 protein expression in CD20-positive B-cell lymphoma patients after treatment with rituximab-containing combination chemotherapies had been observed in 26.3% of re-biopsied patients under relapsed/progress disease (RD/PD) condition (Hiraga et al., 2009, Blood). Interestingly, CD20 expression and the rituximab sensitivity were partially restored by some epigenetic drugs in vitro, suggesting that aberrant down-regulation of MS4A1 gene expression by epigenetic mechanisms may be related to the loss of CD20 protein expression. Aims Analyses of the molecular mechanisms of MS4A1 gene down-regulation after treatment with rituximab-containing chemotherapies. Results Primary B-lymphoma cells and RRBL1 cells (Hiraga et al., 2009, Blood; Tomita et al., 2007, Int J Hematol.), that showed CD20-negative phenotype after using rituximab, were analyzed in these assays. CD20 mRNA and protein expression was partially stimulated by decitabine (DAC), a DNA methyltransferase (DNMT) inhibitor, and the expression was enhanced by trichostation A (TSA), a histone deacetylase (HDAC) inhibitor. Immunoblot analysis indicated that DNMT1 expression was once down-regulated one day after treatment with DAC, and reversed within 3 days. On the other hand, IRF4/Pu.1, the transcription regulators of MS4A1 gene expression, were consistently present with or without DAC. Bisulfite sequencing was performed to check the CpG methylation status of MS4A1 gene promoter, with the result that no significant methylation was confirmed in CD20-negative transformed cells without DAC. Chromatin immunoprecipitation (ChIP) assay indicated that Sin3-HDAC1 co-repressor complex was recruited to MS4A1 gene promoter without DAC/TSA. In the presence of those drugs, Sin3-HDAC1 recruitment was dissociated from the promoter and the histone acetylation of the promoter was confirmed. Under these conditions with/without DAC/TSA, IRF4 and Pu.1 were constantly recruited to the promoter. Immunoprecipitation using whole cell lysate of RRBL1 cells indicated that endogenous Sin3-HDAC1 forms a protein complex, but IRF4 and/or Pu.1 interaction with the complex was not confirmed under this condition. To explore the critical factors for CD20 transcription regulation, expression-profiling assay using cDNA micro array was performed. mRNA from RRBL1 cell with/without DAC/TSA was harvested, and expression profiles were compared. In the presence of DAC or DAC+TSA, 0.7% and 7.0%, respectively, of genes were significantly activated. We are now analyzing some candidates that are critical for the transcription regulation of MS4A1 gene expression. Conclusions Our data indicate that the transcription repression of MS4A1 gene in the CD20-negative phenotypic change after treatment with rituximab is, in part, introduced by the recruitment of Sin3-HDAC1 co-repressor protein complex, not by CpG methylation of the promoter. However, the direct interaction of the complex with IRF4/Pu.1 transcription factors was not confirmed in our assay, and the existence of other transcription factors that interact with Sin3-HDAC1 complex was suggested. To confirm the key regulators of CD20 expression is quite useful for exploring some strategies to overcome the rituximab resistance through CD20-negative transformation after using rituximab. Disclosures Kiyoi: Novartis Pharma Co. Ltd.: Research Funding; Kyowa Hakko Kirin Co. Ltd.: Consultancy. Naoe:Kyowa Hakko Kirin Co., Ltd.: Research Funding; Chugai Pharmaceutical Co., Ltd.: Research Funding; Wyeth K.K.: Research Funding.

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Jeng, Amanda, Celeste Karch, Petra Nowotny, Carlos Cruchaga, and Alison Goate. "P4-085: ABCA7 and MS4A6A expression are upregulated in Alzheimer's disease brains." Alzheimer's & Dementia 8, no. 4S_Part_18 (July 2012): P663. http://dx.doi.org/10.1016/j.jalz.2012.05.1787.

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Ma, Jing, Jin-Tai Yu, and Lan Tan. "MS4A Cluster in Alzheimer’s Disease." Molecular Neurobiology 51, no. 3 (July 1, 2014): 1240–48. http://dx.doi.org/10.1007/s12035-014-8800-z.

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Abou-Raya, S., and A. Abou-Raya. "MS474 PERIPHERAL ARTERY DISEASE AND CARDIOVASCULAR MORBIDITY IN RHEUMATOID ARTHRITIS." Atherosclerosis Supplements 11, no. 2 (June 2010): 205. http://dx.doi.org/10.1016/s1567-5688(10)70975-2.

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Liu, Zhaoyuan, Yaqi Gu, Svetoslav Chakarov, Camille Bleriot, Immanuel Kwok, Xin Chen, Amanda Shin, et al. "Fate Mapping via Ms4a3-Expression History Traces Monocyte-Derived Cells." Cell 178, no. 6 (September 2019): 1509–25. http://dx.doi.org/10.1016/j.cell.2019.08.009.

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Ramirez, Leslie M., Naira Goukasian, Shai Porat, Kristy S. Hwang, Jennifer A. Eastman, Sona Hurtz, Benjamin Wang, et al. "Common variants in ABCA7 and MS4A6A are associated with cortical and hippocampal atrophy." Neurobiology of Aging 39 (March 2016): 82–89. http://dx.doi.org/10.1016/j.neurobiolaging.2015.10.037.

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Koslowski, Michael, Ugur Sahin, Karl Dhaene, Christoph Huber, and Özlem Türeci. "MS4A12 Is a Colon-Selective Store-Operated Calcium Channel Promoting Malignant Cell Processes." Cancer Research 68, no. 9 (May 1, 2008): 3458–66. http://dx.doi.org/10.1158/0008-5472.can-07-5768.

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