Identification and expression of a new type II transmembrane protein in human mast cells

Li, Kang; Wang, Shen Wu; Liu, Yucheng; Martin, Rachel E.; Li, Lixin; Lu, Meisheng; Lamhamedi-Cherradi, Salah-Eddine; Hu, Guanghui; Demissie-Sanders, Sossiena; Zheng, Jie; Chung, Fan; Oates, Thomas; Yao, Zhengbin

doi:10.1016/j.ygeno.2005.03.006

Cited by 37 publications

(42 citation statements)

References 23 publications

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“…Mast cell expressed membrane protein 1 (MCEMP1), also known as C19ORF59, is a transmembrane protein expressed by mast cells, 24 macrophages and other tissues. 25 The exact function of MCEMP1 has yet to be determined; however, the gene's promoter region contains nuclear factor kappa-light-chainenhancer of activated B cell and nuclear factor of activated T-cell binding motifs, similar to many immune receptor genes.…”

Section: Discussionmentioning

confidence: 99%

“…25 The exact function of MCEMP1 has yet to be determined; however, the gene's promoter region contains nuclear factor kappa-light-chainenhancer of activated B cell and nuclear factor of activated T-cell binding motifs, similar to many immune receptor genes. 24 Although limited research has been conducted on MCEMP1, recent findings indicate an emerging role for brain resident mast cells in acute stroke. Experimental stroke studies have reported that mast cells are first responders to cerebral ischemia and act as early regulators of blood-brain barrier permeability.…”

Section: Discussionmentioning

confidence: 99%

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Peripheral Blood MCEMP1 Gene Expression as a Biomarker for Stroke Prognosis

Raman

O’Donnell

Członkowska

et al. 2016

Stroke

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−4). MCEMP1 was also highest soon after symptom onset and had no association with stroke risk factors. Furthermore, MCEMP1 expression independently improved discrimination of 1-month outcome. Indeed, discrimination models for disability and mortality that included MCEMP1 expression, baseline modified Rankin Scale score, and primary stroke type improved discrimination when compared with a model without MCEMP1 (disability Net Reclassification Index, 0.76; P=3.0×10 −6 and mortality Net Reclassification Index, 1.3; P=1.1×10). Significant associations with MCEMP1 were confirmed in an independent validation cohort of 28 stroke cases and 34 controls. Conclusions-This study demonstrates that peripheral blood expression of MCEMP1 may have utility for stroke diagnosis and as a prognostic biomarker of stroke outcome at 1-month. (Stroke. 2016;47:652-658.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Peripheral Blood MCEMP1 Gene Expression as a Biomarker for Stroke Prognosis

Raman

O’Donnell

Członkowska

et al. 2016

Stroke

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“…This supports the notion that resistin is implicated in diabetes pathophysiology. Of note, rs10401670 is located in the second intron of MCEMP1, a gene that encodes a 186 -amino acid protein with a single transmembrane domain expressed mainly by monocytes and mast cell lines (40). Since resistin is mainly expressed by macrophages that evolve from monocytes in adipose tissue, it would be interesting to know if MCEMP1 and its product are functionally influenced by rs10401670 or the SNPs in its 5Ј region and if this protein is involved in resistin and/or glucose metabolism.…”

Section: Discussionmentioning

confidence: 99%

Association of Variants in RETN With Plasma Resistin Levels and Diabetes-Related Traits in the Framingham Offspring Study

et al. 2009

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OBJECTIVE-The RETN gene encodes the adipokine resistin. Associations of RETN with plasma resistin levels, type 2 diabetes, and related metabolic traits have been inconsistent. Using comprehensive linkage disequilibrium mapping, we genotyped tag single nucleotide polymorphisms (SNPs) in RETN and tested associations with plasma resistin levels, risk of diabetes, and glycemic traits. RESEARCH DESIGN AND METHODS-We examined 2,531Framingham Offspring Study participants for resistin levels, glycemic phenotypes, and incident diabetes over 28 years of follow-up. We genotyped 21 tag SNPs that capture common (minor allele frequency Ͼ0.05) or previously reported SNPs at r 2 Ͼ 0.8 across RETN and its flanking regions. We used sex-and age-adjusted linear mixed-effects models (with/without BMI adjustment) to test additive associations of SNPs with traits, adjusted Cox proportional hazards models accounting for relatedness for incident diabetes, and generated empirical P values (P e ) to control for type 1 error.RESULTS-Four tag SNPs (rs1477341, rs4804765, rs1423096, and rs10401670) on the 3Ј side of RETN were strongly associated with resistin levels (all minor alleles associated with higher levels, P e Ͻ0.05 after multiple testing correction). rs10401670 was also associated with fasting plasma glucose (P e ϭ 0.02, BMI adjusted) and mean glucose over follow-up (P e ϭ 0.01; BMI adjusted). No significant association was observed for adiposity traits. On meta-analysis, the previously reported association of SNP Ϫ420C/G (rs1862513) with resistin levels remained significant (P ϭ 0.0009) but with high heterogeneity across studies (P Ͻ 0.0001).CONCLUSIONS-SNPs in the 3Ј region of RETN are associated with resistin levels, and one of them is also associated with glucose levels, although replication is needed. Diabetes 58: 750-756, 2009

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“…MiR-146a could function in braking the immunity via suppressing the level of its target gene, resulting in immune cell immaturation and/or inactivation (31). MCEMP1 encodes a single-pass transmembrane protein and is involved in regulating MC differentiation or immune responses (32). MCEMP1 encodes a single-pass transmembrane protein and is involved in regulating MC differentiation or immune responses (32).…”

Section: Discussionmentioning

confidence: 99%

Silence of long noncoding RNA NEAT1 exerts suppressive effects on immunity during sepsis by promoting microRNA‐125‐dependent MCEMP1 downregulation

2019

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Accumulating studies have recognized microRNAs (miRs) and long noncoding RNAs (lncRNAs) as important molecules involved in the mediation of various biological processes, including innate immunity. In this study, we investigated a novel noncoding RNA regulatory circuitry in the immunity during sepsis. A cecal ligation and puncture‐induced sepsis mouse model was established to determine the expression of mast cell expression membrane protein 1 (MCEMP1). The RNA crosstalk among lncRNA nuclear enriched abundant transcript 1 (NEAT1), miR‐125, and MCEMP1 was validated. Subsequently, the levels of lncRNA NEAT1, miR‐125, and MCEMP1 in T lymphocytes isolated from sepsis mice were up‐ or downregulated by exogenous transfection in an attempt to investigate their effects on the release of inflammatory factors, the expression of immunoglobulins, the activity of T cell subsets and natural killer (NK) cells, as well as T lymphocyte apoptosis. In sepsis mice, MCEMP1 was highly expressed and verified to be a target gene of miR‐125. RNA crosstalk experiment revealed that lncRNA NEAT1 directly inhibited miR‐125 to upregulate MCEMP1. We also observed that elevation of miR‐125, depletion of MCEMP1, or downregulation of lncRNA NEAT1 resulted in promoted T lymphocyte activity, immunoglobulin expression, and NK cell activity, and inhibited release of inflammatory factors and T lymphocyte apoptosis. Taken together, these findings provided evidence that the downregulation of lncRNA NEAT1 could promote miR‐125 to exert an inhibitory effect on the immunity in septic mice by suppressing MCEMP1, highlighting a potential target for the treatment of sepsis. © 2019 IUBMB Life, 2019

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Identification and expression of a new type II transmembrane protein in human mast cells

Cited by 37 publications

References 23 publications

Peripheral Blood MCEMP1 Gene Expression as a Biomarker for Stroke Prognosis

Peripheral Blood MCEMP1 Gene Expression as a Biomarker for Stroke Prognosis

Association of Variants in RETN With Plasma Resistin Levels and Diabetes-Related Traits in the Framingham Offspring Study

Silence of long noncoding RNA NEAT1 exerts suppressive effects on immunity during sepsis by promoting microRNA‐125‐dependent MCEMP1 downregulation

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