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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

Elastin microfibril interfacer 2

EMILIN2, elastin microfibril interfacer 2
Top mentioned proteins: elastin, Emi, CAN, CD45, HAD
Papers on EMILIN2
Diagnostic marker signature for esophageal cancer from transcriptome analysis.
New
Bollschweiler et al., Köln, Germany. In Tumour Biol, Jan 2016
The markers significantly overexpressed already in earlier tumor stages (pT1-2) of both histological subtypes (n = 19) have been clustered in a "diagnostic signature": PLA2G7, PRAME, MMP1, MMP3, MMP12, LIlRB2, TREM2, CHST2, IGFBP2, IGFBP7, KCNJ8, EMILIN2, CTHRC1, EMR2, WDR72, LPCAT1, COL4A2, CCL4, and SNX10.
Multiple-interactions among EMILIN1 and EMILIN2 N- and C-terminal domains.
Doliana et al., Italy. In Matrix Biol, 2015
EMILIN1 and EMILIN2 belong to a family of extracellular matrix glycoproteins characterized by the N-terminal cysteine-rich EMI domain, a long segment with high probabilty for coiled-coil structure formation and a C-terminal gC1q domain.
Genetic variation in the functional ENG allele inherited from the non-affected parent associates with presence of pulmonary arteriovenous malformation in hereditary hemorrhagic telangiectasia 1 (HHT1) and may influence expression of PTPN14.
Akhurst et al., San Francisco, United States. In Front Genet, 2014
EMILIN2, which showed suggestive genetic association with pulmonary AVM, is also reported to interact with Taz in angiogenesis.
EMILIN2 regulates platelet activation, thrombus formation, and clot retraction.
Hoover-Plow et al., Cleveland, United States. In Plos One, 2014
EMILIN2, Elastin Microfibril Interface Located Protein2, was identified as a candidate gene for thrombosis in mouse and human quantitative trait loci studies.
Genome-wide unmasking of epigenetically silenced genes in lung adenocarcinoma from smokers and never smokers.
Belinsky et al., Baltimore, United States. In Carcinogenesis, 2014
The prevalence for methylation of the remaining 38 genes in lung adenocarcinomas from S (n = 97) and NS (n = 75) ranged from 8-89% and significantly differs between S and NS for CPEB1, CST6, EMILIN2, LAYN and MARVELD3 (P < 0.05).
EMILIN2 down-modulates the Wnt signalling pathway and suppresses breast cancer cell growth and migration.
Mongiat et al., Italy. In J Pathol, 2014
EMILIN2 is an extracellular matrix (ECM) protein that exerts contradictory effects within the tumour microenvironment: it induces apoptosis in a number of tumour cells, but it also enhances tumour neo-angiogenesis.
Identification of an interstitial 18p11.32-p11.31 duplication including the EMILIN2 gene in a family with porokeratosis of Mibelli.
Tassano et al., Genova, Italy. In Plos One, 2012
Among these genes, we focused our attention on elastin microfibril interfacer 2 (EMILIN2) gene.
Scalable platform for human embryonic stem cell differentiation to cardiomyocytes in suspended microcarrier cultures.
Oh et al., Singapore, Singapore. In Tissue Eng Part C Methods, 2010
Cells dissociated from differentiated aggregates showed positive staining for cardio-specific markers such as α-actinin, myosin heavy and light chain, troponin I, desmin, and emilin-2.
Methylation profile of single hepatocytes derived from hepatitis B virus-related hepatocellular carcinoma.
Li et al., Hangzhou, China. In Plos One, 2010
Among the 20 most hypermethylated genes in the hepatocytes of HBHC, 7 novel genes (WNK2, EMILIN2, TLX3, TM6SF1, TRIM58, HIST1H4Fand GRASP) were found to be hypermethylated in HBHC and hypomethylated in paired adjacent liver tissues; these findings have not been reported in previous studies on tissue samples.
EMILIN2 (Elastin microfibril interface located protein), potential modifier of thrombosis.
Hoover-Plow et al., Cleveland, United States. In Thromb J, 2010
BACKGROUND: Elastin microfibril interface located protein 2 (EMILIN2) is an extracellular glycoprotein associated with cardiovascular development.
The EMILIN/Multimerin family.
Esposito et al., Italy. In Front Immunol, 2010
Elastin microfibrillar interface proteins (EMILINs) and Multimerins (EMILIN1, EMILIN2, Multimerin1, and Multimerin2) constitute a four member family that in addition to the shared C-terminus gC1q domain typical of the gC1q/TNF superfamily members contain a N-terminus unique cysteine-rich EMI domain.
Mouse chromosome 17 candidate modifier genes for thrombosis.
Hoover-Plow et al., Cleveland, United States. In Mamm Genome, 2010
Seven genes, Twsg1, Zfp161, Dlgap1, Ralbp1, Myom1, Rab31, and Emilin2, of the 23 genes with single nucleotide polymorphisms (SNPs) in the mRNA-UTR had differential expression in B6 and A/J mice.
Annulus cells from more degenerated human discs show modified gene expression in 3D culture compared with expression in cells from healthier discs.
Hanley et al., Charlotte, United States. In Spine J, 2010
Important genes included those related to: 1) the extracellular matrix (ECM) (keratin-associated protein 1-1, hyaluronan synthase 2, and nexin were upregulated; biglycan, collagen type VI alpha 2, thrombospondin 3, laminen alpha 1, fibronectin type III domain-containing protein 1, elastin microfibril interfacer 2, fibulin 2, and nidogen 1 and 2 were downregulated); 2) ECM proteolysis (ADAMTS6 was upregulated); 3) cell proliferation (never in mitosis gene 1-related kinase 3, cell division cycle 2-like 5 [cholinesterase-related cell division controller], RAB42 [member of RAS oncogene family], and cyclin-dependent kinase 6 were upregulated; RAS-like GTP-binding 1 was downregulated); 4) apoptosis (BCL2-like 11 and p53-inducible nuclear protein 1 were upregulated; caspase recruitment domain family, member 10, caspase-1 dominant-negative inhibitor pseudo-ICE, and caspase 9 and FADD-like apoptosis regulator were downregulated); and 5) growth factors, inflammatory mediators, and other genes (fibroblast growth factor 1, pregnancy-associated plasma protein-A, interleukin 1 alpha, and interleukin 7 were upregulated; TGF-beta-induced transcript 1, interleukin 26 and interleukin 1 receptor-like 1, tumor necrosis factor, alpha-induced protein 2, and chemokine (C-X3-C motif) ligand 1 were downregulated).
The extracellular matrix glycoprotein elastin microfibril interface located protein 2: a dual role in the tumor microenvironment.
GeneRIF
Colombatti et al., Italy. In Neoplasia, 2010
The possibility of using EMILIN2 fragments as potent antineoplastic tools for cancer treatment.
EMILINs interact with anthrax protective antigen and inhibit toxin action in vitro.
GeneRIF
Colombatti et al., Italy. In Matrix Biol, 2008
EMILIN1 interacts with anthrax protective antigen and inhibits toxin action in vitro. EMILIN1 may be a potential target and/or a protein useful for countermeasures against B. anthracis toxin lethality.
Regulation of the extrinsic apoptotic pathway by the extracellular matrix glycoprotein EMILIN2.
GeneRIF
Colombatti et al., Italy. In Mol Cell Biol, 2007
Results suggest that the expression of EMILIN2 triggers the apoptosis of different cell lines by activation of death receptors.
An emilin family extracellular matrix protein identified in the cochlear basilar membrane.
GeneRIF
Forrest et al., New York City, United States. In Mol Cell Neurosci, 2003
cochlear emilin-2 mRNA is expressed in the tympanic border cells and an antibody detected protein in the extracellular matrix surrounding the collagenous fibers in the cochlear basilar membrane
The EMILIN protein family.
Review
Spessotto et al., In Matrix Biol, 2000
By using a C-terminal fragment of human EMILIN-1 as a bait in the yeast two-hybrid system, a second family member, EMILIN-2, has also been isolated.
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